FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Maximova, OA
Whitehead, SS
Murphy, BR
Pletnev, AG
AF Maximova, Olga A.
Whitehead, Stephen S.
Murphy, Brian R.
Pletnev, Alexander G.
TI Neuropathogenesis and Neurovirulence of Live Flaviviral Vaccines in
Monkeys Reply
SO JOURNAL OF VIROLOGY
LA English
DT Letter
ID TICK-BORNE ENCEPHALITIS; NONHUMAN-PRIMATES; VIRUS-VACCINE; SAFETY;
RECOMBINANT; MICE
C1 [Maximova, Olga A.; Whitehead, Stephen S.; Murphy, Brian R.; Pletnev, Alexander G.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Pletnev, AG (reprint author), NIAID, Infect Dis Lab, NIH, 33 N Dr,Room 3W10A, Bethesda, MD 20892 USA.
EM apletnev@niaid.nih.gov
NR 19
TC 2
Z9 2
U1 1
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD MAY 15
PY 2009
VL 83
IS 10
BP 5290
EP 5292
PG 3
WC Virology
SC Virology
GA 436IS
UT WOS:000265407700055
ER
PT J
AU Xie, YL
Hassan, SA
Qazi, AM
Tsai-Morris, CH
Dufau, ML
AF Xie, Y. -L.
Hassan, S. A.
Qazi, A. M.
Tsai-Morris, C. H.
Dufau, M. L.
TI Intramolecular Disulfide Bonds of the Prolactin Receptor Short Form Are
Required for Its Inhibitory Action on the Function of the Long Form of
the Receptor
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID SCREENED COULOMB POTENTIALS; ERYTHROPOIETIN RECEPTOR; GROWTH-HORMONE;
DYNAMICS SIMULATIONS; PROMOTER UTILIZATION; SIGNAL-TRANSDUCTION;
KINASE-ACTIVITY; BINDING DOMAIN; PRL RECEPTOR; BETA-CHAIN
AB The short form (S1b) of the prolactin receptor (PRLR) silences prolactin-induced activation of gene transcription by the PRLR long form (LF). The functional and structural contributions of two intramolecular disulfide (S-S) bonds within the extracellular subdomain 1 (D1) of S1b to its inhibitory function on the LF were investigated. Mutagenesis of the paired cysteines eliminated the inhibitory action of S1b. The expression of the mutated S1b (S1bx) on the cell surface was not affected, indicating native-like folding of the receptor. The constitutive JAK2 phosphorylation observed in S1b was not present in cells expressing S1bx, and JAK2 association was disrupted. BRET(50) (BRET(50) represents the relative affinity as acceptor/donor ratio required to reach half-maximal BRET [bioluminescence resonance energy transfer] values) showed decreased LF/S1bx heterodimeric-association and increased affinity in S1bx homodimerization, thus favoring LF homodimerization and prolactin-induced signaling. Computer modeling based on the PRLR crystal structure showed that minor changes in the tertiary structure of D1 upon S-S bond disruption propagated to the quaternary structure of the homodimer, affecting the dimerization interface. These changes explain the higher homodimerization affinity of S1bx and provide a structural basis for its lack of inhibitory function. The PRLR conformation as stabilized by S-S bonds is required for the inhibitory action of S1b on prolactin-induced LF-mediated function and JAK2 association.
C1 [Hassan, S. A.] NIH, Ctr Mol Modeling, DCB CIT, Bethesda, MD 20892 USA.
[Xie, Y. -L.; Qazi, A. M.; Tsai-Morris, C. H.; Dufau, M. L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Endocrinol, Endocrinol & Reprod Res Branch, Program Dev Endocrinol & Genet,NIH, Bethesda, MD 20892 USA.
RP Dufau, ML (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Endocrinol, Endocrinol & Reprod Res Branch, Program Dev Endocrinol & Genet,NIH, Bldg 49,Rm 6A-36,49 Convent Dr,MSC 4510, Bethesda, MD 20892 USA.
EM dufaum@mail.nih.gov
FU NIH Intramural Research Program; Eunice Kennedy Shriver National
Institute of Child Health and Human Development; Center for Information
Technology
FX The study utilized the high-performance computer capabilities of the
Biowulf PC/Linux cluster at the NIH.
NR 36
TC 8
Z9 8
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD MAY 15
PY 2009
VL 29
IS 10
BP 2546
EP 2555
DI 10.1128/MCB.01716-08
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 439ZD
UT WOS:000265665900006
PM 19273600
ER
PT J
AU Kang, HS
Beak, JY
Kim, YS
Herbert, R
Jetten, AM
AF Kang, Hong Soon
Beak, Ju Youn
Kim, Yong-Sik
Herbert, Ronald
Jetten, Anton M.
TI Glis3 Is Associated with Primary Cilia and Wwtr1/TAZ and Implicated in
Polycystic Kidney Disease
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID ZINC-FINGER PROTEIN; NEONATAL DIABETES-MELLITUS; STEM-CELL
DIFFERENTIATION; TRANSCRIPTION FACTOR; REPRESSOR FUNCTIONS; CONGENITAL
HYPOTHYROIDISM; GENE-EXPRESSION; HIPPO PATHWAY; RENAL CYSTS; TAZ
AB In this study, we describe the generation and partial characterization of Kruppel-like zinc finger protein Glis3 mutant (Glis3(zf/zf)) mice. These mice display abnormalities very similar to those of patients with neonatal diabetes and hypothyroidism syndrome, including the development of diabetes and polycystic kidney disease. We demonstrate that Glis3 localizes to the primary cilium, suggesting that Glis3 is part of a cilium-associated signaling pathway. Although Glis3(zf/zf) mice form normal primary cilia, renal cysts contain relatively fewer cells with a primary cilium. We further show that Glis3 interacts with the transcriptional modulator Wwtr1/TAZ, which itself has been implicated in glomerulocystic kidney disease. Wwtr1 recognizes a P/LPXY motif in the C terminus of Glis3 and enhances Glis3-mediated transcriptional activation, indicating that Wwtr1 functions as a coactivator of Glis3. Mutations in the P/LPXY motif abrogate the interaction with Wwtr1 and the transcriptional activity of Glis3, indicating that this motif is part of the transcription activation domain of Glis3. Our study demonstrates that dysfunction of Glis3 leads to the development of cystic renal disease, suggesting that Glis3 plays a critical role in maintaining normal renal functions. We propose that localization to the primary cilium and interaction with Wwtr1 are key elements of the Glis3 signaling pathway.
C1 [Kang, Hong Soon; Beak, Ju Youn; Kim, Yong-Sik; Jetten, Anton M.] NIH, LRB, Cell Biol Sect, Div Intramural Res, Res Triangle Pk, NC 27709 USA.
[Herbert, Ronald] NIEHS, Lab Expt Pathol, NIH, Res Triangle Pk, NC 27709 USA.
RP Jetten, AM (reprint author), NIH, LRB, Cell Biol Sect, Div Intramural Res, Res Triangle Pk, Res Triangle Pk, NC 27709 USA.
EM jetten@niehs.nih.gov
OI Jetten, Anton/0000-0003-0954-4445
FU Intramural Research Program of the NIEHS [Z01-ES-101485]
FX This research was supported by the Intramural Research Program of the
NIEHS (Z01-ES-101485).
NR 57
TC 46
Z9 47
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD MAY 15
PY 2009
VL 29
IS 10
BP 2556
EP 2569
DI 10.1128/MCB.01620-08
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 439ZD
UT WOS:000265665900007
PM 19273592
ER
PT J
AU Padmakumar, VC
Aleem, E
Berthet, C
Hilton, MB
Kaldis, P
AF Padmakumar, V. C.
Aleem, Eiman
Berthet, Cyril
Hilton, Mary Beth
Kaldis, Philipp
TI Cdk2 and Cdk4 Activities Are Dispensable for Tumorigenesis Caused by the
Loss of p53
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID CELL-CYCLE CONTROL; GENE AMPLIFICATION; TUMOR-SUPPRESSOR;
PROTEIN-KINASE; IN-VIVO; C-MYC; CANCER; OVEREXPRESSION; MICE; P21
AB The loss of p53 induces spontaneous tumors in mice, and p53 mutations are found in approximately 50% of human tumors. These tumors are generally caused by a number of events, including genomic instability, checkpoint defects, mitotic defects, deregulation of transcriptional targets, impaired apoptosis, and G(1) deregulation or a combination of these effects. In order to determine the role of proteins involved in G(1) control in tumorigenesis, we focused on Cdk2 and Cdk4, two cyclin-dependent kinases that in association with cyclin E and cyclin D promote the G(1)/S phase transition. We analyzed the consequence of loss of Cdk2 in p53-null animals by generating Cdk2(-/-) p53(-/-) mice. These mice are viable and developed spontaneous tumors, predominantly lymphoblastic lymphomas, similar to p53(-/-) mice. In contrast, the genotypes Cdk4(-/-) p53(-/-) were mostly lethal, with few exceptions, and Cdk2(-/-) Cdk4(-/-) p53(-/-) mice die during embryogenesis at embryonic day 13.5. To study the oncogenic potential, we generated mouse embryonic fibroblasts (MEFs) and found that p53(-/-), Cdk2(-/-) p53(-/-), Cdk4(-/-) p53(-/-), and Cdk2(-/-) Cdk4(-/-) p53(-/-) MEFs grew at similar rates without entering senescence. Ras-transformed MEFs of these genotypes were able to form colonies in vitro and induce tumors in nude mice. Our results suggest that tumorigenicity mediated by p53 loss does not require either Cdk2 or Cdk4, which necessitates considering the use of broad-spectrum cell cycle inhibitors as a means of effective anti-Cdk cancer therapy.
C1 [Kaldis, Philipp] Natl Univ Singapore, Inst Mol & Cell Biol, Canc Lab PRK, Singapore 138673, Singapore.
[Kaldis, Philipp] Natl Univ Singapore, Inst Mol & Cell Biol, Cell Div, Singapore 138673, Singapore.
[Padmakumar, V. C.; Aleem, Eiman; Berthet, Cyril; Hilton, Mary Beth; Kaldis, Philipp] Natl Canc Inst Frederick, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP Kaldis, P (reprint author), Natl Univ Singapore, Inst Mol & Cell Biol, Cell Div, 61 Biopolis Dr, Singapore 138673, Singapore.
EM kaldis@imcb.a-star.edu.sg
RI Kaldis, Philipp/G-2714-2010; ASTAR, IMCB/E-2320-2012; Aleem,
Eiman/I-3777-2012;
OI Kaldis, Philipp/0000-0002-7247-7591; Aleem, Eiman/0000-0002-9215-8213
FU Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 50
TC 19
Z9 21
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD MAY 15
PY 2009
VL 29
IS 10
BP 2582
EP 2593
DI 10.1128/MCB.00952-08
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 439ZD
UT WOS:000265665900009
PM 19307310
ER
PT J
AU Kuwano, Y
Rabinovic, A
Srikantan, S
Gorospe, M
Demple, B
AF Kuwano, Yuki
Rabinovic, Ariel
Srikantan, Subramanya
Gorospe, Myriam
Demple, Bruce
TI Analysis of Nitric Oxide-Stabilized mRNAs in Human Fibroblasts Reveals
HuR-Dependent Heme Oxygenase 1 Upregulation
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID BINDING PROTEIN HUR; MAMMALIAN-CELLS; GENOTOXIC STRESS; RESPONSE
ELEMENT; RICH ELEMENTS; TRANSLATION; DEGRADATION; EXPRESSION; ALPHA;
CYCLOOXYGENASE-2
AB We previously observed that nitric oxide (NO) exposure increases the stability of mRNAs encoding heme oxygenase 1 (HO-1) and TIEG-1 in human and mouse fibroblasts. Here, we have used microarrays to look broadly for changes in mRNA stability in response to NO treatment. Using human IMR-90 and mouse NIH 3T3 fibroblasts treated with actinomycin D to block de novo transcription, microarray analysis suggested that the stability of the majority of mRNAs was unaffected. Among the mRNAs that were stabilized by NO treatment, seven transcripts were found in both IMR-90 and NIH 3T3 cells (CHIC2, GADD45B, HO-1, PTGS2, RGS2, TIEG, and ID3) and were chosen for further analysis. All seven mRNAs showed at least one hit of a signature motif for the stabilizing RNA-binding protein (RBP) HuR; accordingly, ribonucleoprotein immunoprecipitation analysis revealed that all seven mRNAs associated with HuR. In keeping with a functional role of HuR in the response to NO, a measurable fraction of HuR increased in the cytoplasm following NO treatment. However, among the seven transcripts, only HO-1 mRNA showed a robust increase in the level of its association with HuR following NO treatment. In turn, HO-1 mRNA and protein levels were significantly reduced when HuR levels were silenced in IMR-90 cells, and they were elevated when HuR was overexpressed. In sum, our results indicate that NO stabilizes mRNA subsets in fibroblasts, identify HuR as an RBP implicated in the NO response, reveal that HuR alone is insufficient for stabilizing several mRNAs by NO, and show that HO-1 induction by NO is regulated by HuR.
C1 [Rabinovic, Ariel; Demple, Bruce] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02130 USA.
[Kuwano, Yuki; Srikantan, Subramanya; Gorospe, Myriam] NIA, RNA Regulat Sect, Lab Cellular & Mol Biol, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
RP Demple, B (reprint author), Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Room 509,Bldg 1,665 Huntington Ave, Boston, MA 02130 USA.
EM bdemple@hsph.harvard.edu
OI srikantan, subramanya/0000-0003-1810-6519
FU NCI [R01CA082737, T32-CA009078]; National Institute on Aging-Intramural
Research Program, National Institutes of Health
FX Experimental work at Harvard was supported by NCI grant R01CA082737 ( to
B. D.). A. R. was supported by radiation biology training grant NCI
T32-CA009078. M. G., S. S., and Y. K. were supported by the National
Institute on Aging-Intramural Research Program, National Institutes of
Health.
NR 60
TC 20
Z9 20
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD MAY 15
PY 2009
VL 29
IS 10
BP 2622
EP 2635
DI 10.1128/MCB.01495-08
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 439ZD
UT WOS:000265665900012
PM 19289500
ER
PT J
AU Callen, E
Jankovic, M
Wong, N
Zha, S
Chen, HT
Difilippantonio, S
Di Virgilio, M
Heidkamp, G
Alt, FW
Nussenzweig, A
Nussenzweig, M
AF Callen, Elsa
Jankovic, Mila
Wong, Nancy
Zha, Shan
Chen, Hua-Tang
Difilippantonio, Simone
Di Virgilio, Michela
Heidkamp, Gordon
Alt, Frederick W.
Nussenzweig, Andre
Nussenzweig, Michel
TI Essential Role for DNA-PKcs in DNA Double-Strand Break Repair and
Apoptosis in ATM-Deficient Lymphocytes
SO MOLECULAR CELL
LA English
DT Article
ID DEPENDENT PROTEIN-KINASE; CLASS-SWITCH RECOMBINATION; CYTIDINE DEAMINASE
AID; CELL-CYCLE ARREST; ATAXIA-TELANGIECTASIA; B-CELLS; GENOMIC
INSTABILITY; IONIZING-RADIATION; SOMATIC HYPERMUTATION; V(D)J
RECOMBINATION
AB The DNA double-strand break (DSB) repair protein DNA-PKcs and the signal transducer ATM are both activated by DNA breaks and phosphorylate similar substrates in vitro, yet appear to have distinct functions in vivo. Here, we show that ATM and DNA-PKcs have overlapping functions in lymphocytes. Ablation of both kinase activities in cells undergoing immunoglobulin class switch recombination leads to a compound defect in switching and a synergistic increase in chromosomal fragmentation, DNA insertions, and translocations due to aberrant processing of DSBs. These abnormalities are attributed to a compound deficiency in phosphorylation of key proteins required for DNA repair, class switching, and cell death. Notably, both kinases are required for normal levels of p53 phosphorylation in B and T cells and p53-dependent apoptosis. Our experiments reveal a DNA-PKcs-dependent pathway that regulates DNA repair and activation of p53 in the absence of ATM.
C1 [Callen, Elsa; Wong, Nancy; Chen, Hua-Tang; Difilippantonio, Simone; Nussenzweig, Andre] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Zha, Shan; Alt, Frederick W.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Zha, Shan; Alt, Frederick W.] Childrens Hosp, Howard Hughes Med Inst, Program Cellular & Mol Med, Boston, MA 02115 USA.
[Jankovic, Mila; Di Virgilio, Michela; Heidkamp, Gordon; Nussenzweig, Michel] Howard Hughes Med Inst, New York, NY 10065 USA.
[Jankovic, Mila; Di Virgilio, Michela; Heidkamp, Gordon; Nussenzweig, Michel] Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
RP Nussenzweig, A (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM andre_nussenzweig@nih.gov; nussen@mall.rockefeller.edu
FU NIH; National Cancer Institute; Center for Cancer Research
FX We thank Junjie Chen and Anthony Wynshaw-Boris for mice; L. Stapelton
for chromosome painting probes; G. Smith for small molecule inhibitors;
Jeremy Daniel, Davide Robbiani, Oscar Femandez-Capetillo, and Yair
Dorsett for comments on the manuscript; and Rafael Casellas for advice
on ShRNA. A.N. is supported by the Intramural Research program of the
NIH, National Cancer Institute, Center for Cancer Research. F.W.A. is
supported by grants from the NIH. F.W.A. is a Howard Hughes Institute
Investigator. M.C.N. is supported by grants from the NIH. M.C.N. is a
Howard Hughes Institute Investigator.
NR 87
TC 85
Z9 87
U1 0
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD MAY 15
PY 2009
VL 34
IS 3
BP 285
EP 297
DI 10.1016/j.molcel.2009.04.025
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 446TP
UT WOS:000266144400004
PM 19450527
ER
PT J
AU Chang, SE
Kenney, MK
Loucks, TMJ
Ludlow, CL
AF Chang, Soo-Eun
Kenney, Mary Kay
Loucks, Torrey M. J.
Ludlow, Christy L.
TI Brain activation abnormalities during speech and non-speech in
stuttering speakers
SO NEUROIMAGE
LA English
DT Article
DE Stuttering; Speech perception; Planning; Production; Non-speech;
Functional magnetic resonance imaging (fMRI); Auditory-motor
interaction; Forward model
ID POSITRON-EMISSION-TOMOGRAPHY; POSTERIOR PARIETAL CORTEX;
AUDITORY-CORTEX; MOTOR CONTROL; SYLLABLE PRODUCTION; SENSORIMOTOR
INTEGRATION; NEURAL MECHANISMS; FLUENT SPEAKERS; ADULTS; AREAS
AB Although stuttering is regarded as a speech-specific disorder, there is a growing body of evidence suggesting that subtle abnormalities in the motor planning and execution of non-speech gestures exist in stuttering individuals. We hypothesized that people who stutter (PWS) would differ from fluent controls in their neural responses during motor planning and execution of both speech and non-speech gestures that had auditory targets. Using fMRI with sparse sampling, separate BOLD responses were measured for perception, planning, and fluent production of speech and non-speech vocal tract gestures. During both speech and non-speech perception and planning, PWS had less activation in the frontal and temporoparietal regions relative to controls. During speech and non-speech production, PWS had less activation than the controls in the left superior temporal gyrus (STG) and the left pre-motor areas (BA 6) but greater activation in the right STG, bilateral Heschl's gyrus (HG), insula, putamen, and precentral motor regions (BA 4). Differences in brain activation patterns between PWS and controls were greatest in females and less apparent in males. In conclusion, similar differences in PWS from the controls were found during speech and non-speech; during perception and planning they had reduced activation while during production they had increased activity in the auditory area on the right and decreased activation in the left sensorimotor regions. These results demonstrated that neural activation differences in PWS are not speech-specific. Published by Elsevier Inc.
C1 [Chang, Soo-Eun; Kenney, Mary Kay; Loucks, Torrey M. J.; Ludlow, Christy L.] NINDS, Laryngeal & Speech Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Ludlow, CL (reprint author), NINDS, Laryngeal & Speech Sect, Med Neurol Branch, NIH, 10 Ctr Dr MSC 1416 Bldg 10,Room 5D38, Bethesda, MD 20892 USA.
EM ludlowc@ninds.nih.gov
OI Ludlow, Christy/0000-0002-2015-6171
FU Intramural NIH HHS [Z01 NS002980-09]
NR 75
TC 64
Z9 66
U1 0
U2 13
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD MAY 15
PY 2009
VL 46
IS 1
BP 201
EP 212
DI 10.1016/j.neuroimage.2009.01.066
PG 12
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 440TY
UT WOS:000265723800022
PM 19401143
ER
PT J
AU Sayer, JM
Louis, JM
AF Sayer, Jane M.
Louis, John M.
TI Interactions of different inhibitors with active-site aspartyl residues
of HIV-1 protease and possible relevance to pepsin
SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS
LA English
DT Article
DE retroviral protease; aspartic protease; protein structure; calorimetry;
kinetics
ID VIRUS TYPE-1 PROTEASE; HUMAN-IMMUNODEFICIENCY; CANDIDA-ALBICANS;
IN-VITRO; CRYSTAL-STRUCTURE; PLASMODIUM-FALCIPARUM;
PROTEINASE-INHIBITORS; THERMODYNAMIC BASIS; DRUG-RESISTANCE;
MOLECULAR-BASIS
AB The importance of the active site region aspartyl residues 25 and 29 of the mature HIV-1 protease (PR) for the binding of five clinical and three experimental protease inhibitors [symmetric cyclic urea inhibitor DMP323, nonhydrolyzable substrate analog (RPB) and the generic aspartic protease inhibitor acetyl-pepstatin (Ac-PEP)] was assessed by differential scanning calorimetry. Delta T-m values, defined as the difference in T., for a given protein in the presence and absence of inhibitor, for PR with DRV, ATV, SQV, RTV, APV, DMP323, RPB, and Ac-PEP are 22.4, 20.8, 19.3, 15.6, 14.3, 14.7, 8.7, and 6.5 degrees C, respectively. Binding of APV and Ac-PEP is most sensitive to the D25N mutation, as shown by Delta T-m ratios [Delta T-m(PR)/ Delta T-m(PRD25N)] of 35.8 and 16.3, respectively, whereas binding of DMP323 and RPB (Delta T-m ratios of 1-2) is least affected. Binding of the substrate-like inhibitors RPB and Ac-PEP is nearly abolished (Delta T-m(PR)/Delta T-m(PRD29N) >= 44) by the D29N mutation, whereas this mutation only moderately affects binding of the smaller inhibitors (AT. ratios of 1.4-2.2). Of the nine FDA-approved clinical HIV-1 protease inhibitors screened, APV, RTV, and DRV competitively inhibit porcine pepsin with K-i values of 0.3. 0.6, and 2.14 mu M, respectively. DSC results were consistent with this relatively weak binding of APV (Delta T-m 2.7 degrees C) compared with the tight binding of Ac-PEP (Delta T-m >= 17 degrees C). Comparison of superimposed structures of the PR/APV complex with those of PR/Ac-PEP and pepsin/pepstatin A complexes suggests a role for Asp215, Asp32, and Ser219 in pepsin, equivalent to Asp25, Asp25', and Asp29 in PR in the binding and stabilization of the pepsin/APV complex.
C1 [Sayer, Jane M.; Louis, John M.] NIDDK, Chem Phys Lab, NIH, DHHS, Bethesda, MD 20892 USA.
RP Louis, JM (reprint author), NIDDK, Chem Phys Lab, NIH, DHHS, Bldg 5,Room B2-29, Bethesda, MD 20892 USA.
EM johnl@intra.niddk.nih.gov
FU NIDDK; NIH (Intramural Research Program)
FX Grant sponsor: NIDDK, NIH (Intramural Research Program).
NR 53
TC 11
Z9 11
U1 2
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0887-3585
EI 1097-0134
J9 PROTEINS
JI Proteins
PD MAY 15
PY 2009
VL 75
IS 3
BP 556
EP 568
DI 10.1002/prot.22271
PG 13
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 433CJ
UT WOS:000265181000004
PM 18951411
ER
PT J
AU Bhattacharya, S
Black, R
Bourgeois, L
Clemens, J
Cravioto, A
Deen, JL
Dougan, G
Glass, R
Grais, RF
Greco, M
Gust, I
Holmgren, J
Kariuki, S
Lambert, PH
Liu, MA
Longini, I
Nair, GB
Norrby, R
Nossal, GJV
Ogra, P
Sansonetti, P
von Seidlein, L
Songane, F
Svennerholm, AM
Steele, D
Walker, R
AF Bhattacharya, S.
Black, R.
Bourgeois, L.
Clemens, J.
Cravioto, A.
Deen, J. L.
Dougan, Gordon
Glass, R.
Grais, R. F.
Greco, M.
Gust, I.
Holmgren, J.
Kariuki, S.
Lambert, P. -H.
Liu, M. A.
Longini, I.
Nair, G. B.
Norrby, R.
Nossal, G. J. V.
Ogra, P.
Sansonetti, P.
von Seidlein, L.
Songane, F.
Svennerholm, A. -M.
Steele, D.
Walker, R.
TI The Cholera Crisis in Africa
SO SCIENCE
LA English
DT Editorial Material
ID VACCINATION; VACCINES; ZIMBABWE
C1 [Cravioto, A.; Deen, J. L.; von Seidlein, L.] Ctr Diarrhoeal Dis Res, Dhaka 1000, Bangladesh.
[Bhattacharya, S.] Indian Council Med Res, New Delhi, India.
[Black, R.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD 21205 USA.
[Bourgeois, L.; Steele, D.; Walker, R.] PATH, Enter Vaccine Initiat, Seattle, WA 98107 USA.
[Clemens, J.] Int Vaccine Inst, Seoul 151600, South Korea.
[Dougan, Gordon] Wellcome Trust Sanger Inst, Cambridge CB10 1RQ, England.
[Glass, R.] NIH, Fogarty Inst, Bethesda, MD 20892 USA.
[Grais, R. F.] Epictr, FR-75011 Paris, France.
[Gust, I.; Nossal, G. J. V.] Univ Melbourne, Dept Microbiol & Immunol, Melbourne, Vic 3010, Australia.
[Gust, I.; Nossal, G. J. V.] Univ Melbourne, Dept Pathol, Melbourne, Vic 3010, Australia.
[Holmgren, J.; Svennerholm, A. -M.] Univ Gothenburg, SE-40530 Gothenburg, Sweden.
[Kariuki, S.] Kenya Govt Med Res Ctr, Ctr Microbiol Res, Nairobi, Kenya.
[Lambert, P. -H.] Univ Geneva, CH-1211 Geneva 4, Switzerland.
[Liu, M. A.] Karolinska Inst, SE-17177 Stockholm, Sweden.
[Longini, I.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Longini, I.] Univ Washington, Seattle, WA 98109 USA.
[Nair, G. B.] Natl Inst Cholera & Infect Dis, Kolkata 700010, India.
[Norrby, R.] Swedish Inst Infect Dis Control, SE-17182 Solna, Sweden.
[Ogra, P.] SUNY Buffalo, Sch Med & Biomed Sci, Buffalo, NY 14214 USA.
[Sansonetti, P.] Inst Pasteur, INSERM, U786, Unite Pathogenie Microbienne Mol, FR-75724 Paris 15, France.
[Songane, F.] Partnership Maternal Newborn & Child Hlth, CH-1211 Geneva, Switzerland.
RP Deen, JL (reprint author), Ctr Diarrhoeal Dis Res, Dhaka 1000, Bangladesh.
EM jdeen@ivi.int
OI Black, Robert/0000-0001-9926-7984
NR 16
TC 23
Z9 24
U1 1
U2 4
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD MAY 15
PY 2009
VL 324
IS 5929
BP 885
EP 885
DI 10.1126/science.1173890
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 445KD
UT WOS:000266048800018
PM 19443768
ER
PT J
AU Tahiliani, M
Koh, KP
Shen, YH
Pastor, WA
Bandukwala, H
Brudno, Y
Agarwal, S
Iyer, LM
Liu, DR
Aravind, L
Rao, A
AF Tahiliani, Mamta
Koh, Kian Peng
Shen, Yinghua
Pastor, William A.
Bandukwala, Hozefa
Brudno, Yevgeny
Agarwal, Suneet
Iyer, Lakshminarayan M.
Liu, David R.
Aravind, L.
Rao, Anjana
TI Conversion of 5-Methylcytosine to 5-Hydroxymethylcytosine in Mammalian
DNA by MLL Partner TET1
SO SCIENCE
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; GLYCOSYLASE ACTIVITY; CXXC DOMAIN; BASE-J;
DEMETHYLATION; CYTOSINE; METHYLATION; PROTEIN; METHYLTRANSFERASE;
T(10/11)(Q22,Q23)
AB DNA cytosine methylation is crucial for retrotransposon silencing and mammalian development. In a computational search for enzymes that could modify 5-methylcytosine (5mC), we identified TET proteins as mammalian homologs of the trypanosome proteins JBP1 and JBP2, which have been proposed to oxidize the 5-methyl group of thymine. We show here that TET1, a fusion partner of the MLL gene in acute myeloid leukemia, is a 2-oxoglutarate (2OG)- and Fe(II)-dependent enzyme that catalyzes conversion of 5mC to 5-hydroxymethylcytosine (hmC) in cultured cells and in vitro. hmC is present in the genome of mouse embryonic stem cells, and hmC levels decrease upon RNA interference-mediated depletion of TET1. Thus, TET proteins have potential roles in epigenetic regulation through modification of 5mC to hmC.
C1 [Shen, Yinghua; Brudno, Yevgeny; Liu, David R.] Harvard Univ, Dept Chem & Biol Chem, Cambridge, MA 02138 USA.
[Shen, Yinghua; Brudno, Yevgeny; Liu, David R.] Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA.
[Tahiliani, Mamta; Koh, Kian Peng; Pastor, William A.; Bandukwala, Hozefa; Rao, Anjana] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Tahiliani, Mamta; Koh, Kian Peng; Pastor, William A.; Bandukwala, Hozefa; Rao, Anjana] Immune Dis Inst, Boston, MA 02115 USA.
[Agarwal, Suneet] Childrens Hosp Boston, Div Pediat Hematol Oncol, Boston, MA 02115 USA.
[Agarwal, Suneet] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Iyer, Lakshminarayan M.; Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Liu, DR (reprint author), Harvard Univ, Dept Chem & Biol Chem, Cambridge, MA 02138 USA.
EM drliu@fas.harvard.edu; aravind@ncbi.nlm.nih.gov; arao@idi.harvard.edu
RI Waha, Andreas/J-2950-2014
FU NIH [AI44432, K08 HL089150]; a Scholar Award from the Juvenile Diabetes
Research Foundation; Harvard Stem Cell Institute [Seed]; Howard Hughes
Medical Institute; NIH/NIGMS [R01GM065865]; American Heart Association
postdoctoral fellowship; National Library of Medicine, NIH; Lady Tata
Memorial postdoctoral fellowship; NSF Graduate Fellowships; Department
of Defense graduate fellowship
FX We thank K. Kreuzer for the gift of the T4 phage and E. coli ER1656 and
CR63; Charles Richardson, Udi Qimron, and Ben Beauchamp for advice and
assistance in culturing T4 phage; Melissa Call for advice on production
of recombinant proteins in insect cells; and Patrick Hogan for many
helpful discussions. This work was supported by NIH grant AI44432, a
Scholar Award from the Juvenile Diabetes Research Foundation, and a Seed
grant from the Harvard Stem Cell Institute (to A.R.); Howard Hughes
Medical Institute and NIH/NIGMS (R01GM065865) funding (to D.R.L.); an
American Heart Association postdoctoral fellowship (to K.P.K.);
intramural funds of the National Library of Medicine, NIH (to L.A. and
L.M.I.); a Lady Tata Memorial postdoctoral fellowship (to H.B.); NIH
award K08 HL089150 (to S.A.); NSF Graduate Fellowships (to W.A.P. and
Y.B.); and a Department of Defense graduate fellowship (to W.A.P.).
NR 33
TC 2102
Z9 2172
U1 36
U2 318
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD MAY 15
PY 2009
VL 324
IS 5929
BP 930
EP 935
DI 10.1126/science.1170116
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 445KD
UT WOS:000266048800037
PM 19372391
ER
PT J
AU Fan, HY
Liu, ZL
Shimada, M
Sterneck, E
Johnson, PF
Hedrick, SM
Richards, JS
AF Fan, Heng-Yu
Liu, Zhilin
Shimada, Masayuki
Sterneck, Esta
Johnson, Peter F.
Hedrick, Stephen M.
Richards, JoAnne S.
TI MAPK3/1 (ERK1/2) in Ovarian Granulosa Cells Are Essential for Female
Fertility
SO SCIENCE
LA English
DT Article
ID C/EBP-BETA; CUMULUS EXPANSION; KNOCKOUT MICE; MOUSE; EXPRESSION;
OVULATION; FOLLICLE; PHOSPHORYLATION; COMMUNICATION; ACTIVATION
AB A surge of luteinizing hormone (LH) from the pituitary gland triggers ovulation, oocyte maturation, and luteinization for successful reproduction in mammals. Because the signaling molecules RAS and ERK1/2 ( extracellular signal-regulated kinases 1 and 2) are activated by an LH surge in granulosa cells of preovulatory follicles, we disrupted Erk1/2 in mouse granulosa cells and provide in vivo evidence that these kinases are necessary for LH-induced oocyte resumption of meiosis, ovulation, and luteinization. In addition, biochemical analyses and selected disruption of the Cebpb gene in granulosa cells demonstrate that C/EBPb (CCAAT/Enhancer-binding protein-beta) is a critical downstream mediator of ERK1/2 activation. Thus, ERK1/2 and C/EBPb constitute an in vivo LH-regulated signaling pathway that controls ovulation- and luteinization-related events.
C1 [Fan, Heng-Yu; Liu, Zhilin; Richards, JoAnne S.] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA.
[Shimada, Masayuki] Hiroshima Univ, Grad Sch Biosphere Sci, Dept Appl Anim Sci, Higashihiroshima 7398528, Japan.
[Sterneck, Esta] NCI, Lab Cell & Dev Signaling, Ctr Canc Res, Frederick, MD 21702 USA.
[Johnson, Peter F.] NCI, Basic Res Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Hedrick, Stephen M.] Univ Calif San Diego, Dept Cell & Mol Biol, La Jolla, CA 92093 USA.
[Hedrick, Stephen M.] Univ Calif San Diego, Mol Biol Sect, Div Biol Sci, La Jolla, CA 92093 USA.
RP Richards, JS (reprint author), Baylor Coll Med, Dept Mol & Cellular Biol, 1 Baylor Plaza, Houston, TX 77030 USA.
EM joanner@bcm.edu
RI Johnson, Peter/A-1940-2012; Shimada, Masayuki/Q-3673-2016
OI Johnson, Peter/0000-0002-4145-4725; Shimada,
Masayuki/0000-0002-6500-2088
FU NIH [NIH-HD16229, NIH-HD07495, NIH-HD07165]; Project II; Japan Society
for the Promotion of Science [18688016]; Intramural Research Program of
NIH; National Cancer Institute, Center for Cancer Research
FX We thank J. Pouyssegur and J. Shao for providing Erk1 mice and
adenoviral vector of C/EBPSS, respectively. This work was supported by
NIH grants NIH HD16229, NIH HD07495, Project II J.S.R., Grant in Aid for
Scientific Research No. 18688016 from the Japan Society for the
Promotion of Science M.S., Intramural Research Program of NIH, National
Cancer Institute, Center for Cancer Research P.F.J. and E.S., and NIH
Postdoctoral Training Grant NIH HD07165 H.Y.F. The Gene Expression
Omnibus accession number for microarray data is GSE15135.
NR 18
TC 227
Z9 234
U1 2
U2 23
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD MAY 15
PY 2009
VL 324
IS 5929
BP 938
EP 941
DI 10.1126/science.1171396
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 445KD
UT WOS:000266048800039
PM 19443782
ER
PT J
AU Carson, KR
Evens, AM
Richey, EA
Habermann, TM
Focosi, D
Seymour, JF
Laubach, J
Bawn, SD
Gordon, LI
Winter, JN
Furman, RR
Vose, JM
Zelenetz, AD
Mamtani, R
Raisch, DW
Dorshimer, GW
Rosen, ST
Muro, K
Gottardi-Littell, NR
Talley, RL
Sartor, O
Green, D
Major, EO
Bennett, CL
AF Carson, Kenneth R.
Evens, Andrew M.
Richey, Elizabeth A.
Habermann, Thomas M.
Focosi, Daniele
Seymour, John F.
Laubach, Jacob
Bawn, Susie D.
Gordon, Leo I.
Winter, Jane N.
Furman, Richard R.
Vose, Julie M.
Zelenetz, Andrew D.
Mamtani, Ronac
Raisch, Dennis W.
Dorshimer, Gary W.
Rosen, Steven T.
Muro, Kenji
Gottardi-Littell, Numa R.
Talley, Robert L.
Sartor, Oliver
Green, David
Major, Eugene O.
Bennett, Charles L.
TI Progressive multifocal leukoencephalopathy after rituximab therapy in
HIV-negative patients: a report of 57 cases from the Research on Adverse
Drug Events and Reports project
SO BLOOD
LA English
DT Article; Proceedings Paper
CT 44th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY MAY 30-JUN 03, 2008
CL Chicago, IL
SP Amer Soc Clin Oncol
ID B-CELL LYMPHOMA; IDIOPATHIC THROMBOCYTOPENIC PURPURA;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; CHEMOTHERAPY PLUS RITUXIMAB;
MULTIPLE-SCLEROSIS PATIENTS; OF-THE-LITERATURE; JC VIRUS VIREMIA;
ANTIBODY NATALIZUMAB; FOLLICULAR LYMPHOMA; INFECTED PATIENTS
AB Rituximab improves outcomes for persons with lymphoproliferative disorders and is increasingly used to treat immune-mediated illnesses. Recent reports describe 2 patients with systemic lupus erythematosus and 1 with rheumatoid arthritis who developed progressive multifocal leukoencephalopathy (PML) after rituximab treatment. We reviewed PML case descriptions among patients treated with rituximab from the Food and Drug Administration, the manufacturer, physicians, and a literature review from 1997 to 2008. Overall, 52 patients with lymphoproliferative disorders, 2 patients with systemic lupus erythematosus, 1 patient with rheumatoid arthritis, 1 patient with an idiopathic autoimmune pancytopenia, and 1 patient with immune thrombocytopenia developed PML after treatment with rituximab and other agents. Other treatments included hematopoietic stem cell transplantation (7 patients), purine analogs (26 patients), or alkylating agents (39 patients). One patient with an autoimmune hemolytic anemia developed PML after treatment with corticosteroids and rituximab, and 1 patient with an autoimmune pancytopenia developed PML after treatment with corticosteroids, azathioprine, and rituximab. Median time from last rituximab dose to PML diagnosis was 5.5 months. Median time to death after PML diagnosis was 2.0 months. The case-fatality rate was 90%. Awareness is needed of the potential for PML among rituximab-treated persons. (Blood. 2009;113:4834-4840)
C1 [Evens, Andrew M.; Richey, Elizabeth A.; Gordon, Leo I.; Winter, Jane N.; Rosen, Steven T.; Green, David; Bennett, Charles L.] Northwestern Univ, Div Hematol Oncol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Carson, Kenneth R.] Washington Univ, Sch Med, Siteman Comprehens Canc Ctr, St Louis, MO USA.
[Evens, Andrew M.; Gordon, Leo I.; Winter, Jane N.; Rosen, Steven T.; Green, David; Bennett, Charles L.] Robert H Lurie Comprehens Canc Ctr, Chicago, IL USA.
[Habermann, Thomas M.] Mayo Clin, Coll Med, Dept Hematol, Rochester, MN USA.
[Focosi, Daniele] Univ Pisa, Div Hematol, Pisa, Italy.
[Seymour, John F.] Peter MacCallum Canc Ctr, Div Haematol & Med Oncol, Melbourne, Australia.
[Laubach, Jacob] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bawn, Susie D.] Stanford Univ, Sch Med, Div Hematol Oncol, Stanford, CA 94305 USA.
[Furman, Richard R.; Zelenetz, Andrew D.; Mamtani, Ronac] New York Presbyterian Hosp, Cornell Med Ctr, Div Hematol Oncol, New York, NY USA.
[Vose, Julie M.] Univ Nebraska, Med Ctr, Hematol Oncol Sect, Omaha, NE USA.
[Zelenetz, Andrew D.] Mem Sloan Kettering Canc Ctr, Div Hematol Oncol, New York, NY 10021 USA.
[Raisch, Dennis W.] Univ New Mexico, Vet Adm Cooperat Studies Program, Clin Res Pharm Coordinating Ctr, Albuquerque, NM 87131 USA.
[Dorshimer, Gary W.] Univ Penn Hlth Syst, Penn Hosp, Philadelphia, PA USA.
[Muro, Kenji] Northwestern Univ, Dept Neurol Surg, Feinberg Sch Med, Chicago, IL 60611 USA.
[Gottardi-Littell, Numa R.] Northwestern Univ, Dept Pathol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Talley, Robert L.] Kansas City Canc Ctr, Kansas City, MO USA.
[Sartor, Oliver] Tulane Med Sch, New Orleans, LA USA.
[Major, Eugene O.] Natl Inst Neurol Disorders & Stroke, Lab Mol Med & Neurosci, NIH, Bethesda, MD USA.
[Bennett, Charles L.] Jesse Brown VAMC, Vet Adm Ctr Management Complex Chron Condit, Chicago, IL USA.
RP Bennett, CL (reprint author), Northwestern Univ, Div Hematol Oncol, Feinberg Sch Med, 710 N Fairbanks Ct,Olson Pavil,Suite 8-250, Chicago, IL 60611 USA.
EM cbenne@northwestern.edu
OI Zelenetz, Andrew/0000-0003-1403-6883; Focosi,
Daniele/0000-0001-8811-195X; Gordon, Leo/0000-0003-1666-7064
FU NCI NIH HHS [1R01 CA125077-01A1, R01 CA125077]
NR 68
TC 465
Z9 475
U1 9
U2 21
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD MAY 14
PY 2009
VL 113
IS 20
BP 4834
EP 4840
DI 10.1182/blood-2008-10-186999
PG 7
WC Hematology
SC Hematology
GA 445ZT
UT WOS:000266090700007
PM 19264918
ER
PT J
AU Karp, JE
Flatten, K
Feldman, EJ
Greer, JM
Loegering, DA
Ricklis, RM
Morris, LE
Ritchie, E
Smith, BD
Ironside, V
Talbott, T
Roboz, G
Le, SB
Meng, XW
Schneider, PA
Dai, NT
Adjei, AA
Gore, SD
Levis, MJ
Wright, JJ
Garrett-Mayer, E
Kaufmann, SH
AF Karp, Judith E.
Flatten, Karen
Feldman, Eric J.
Greer, Jacqueline M.
Loegering, David A.
Ricklis, Rebecca M.
Morris, Lawrence E.
Ritchie, Ellen
Smith, B. Douglas
Ironside, Valerie
Talbott, Timothy
Roboz, Gail
Le, Son B.
Meng, Xue Wei
Schneider, Paula A.
Dai, Nga T.
Adjei, Alex A.
Gore, Steven D.
Levis, Mark J.
Wright, John J.
Garrett-Mayer, Elizabeth
Kaufmann, Scott H.
TI Active oral regimen for elderly adults with newly diagnosed acute
myelogenous leukemia: a preclinical and phase 1 trial of the
farnesyltransferase inhibitor tipifarnib (R115777, Zarnestra) combined
with etoposide
SO BLOOD
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; FARNESYL TRANSFERASE INHIBITOR; RISK
MYELODYSPLASTIC SYNDROME; COUNCIL AML11 TRIAL; INDUCED APOPTOSIS;
HEMATOLOGIC MALIGNANCIES; IN-VITRO; INTENSIVE CHEMOTHERAPY; TREATMENT
OUTCOMES; CRITICAL TARGET
AB The farnesyltransferase inhibitor tipifarnib exhibits modest activity against acute myelogenous leukemia. To build on these results, we examined the effect of combining tipifarnib with other agents. Tipifarnib inhibited signaling downstream of the farnesylated small G protein Rheb and synergistically enhanced etoposide-induced antiproliferative effects in lymphohematopoietic cell lines and acute myelogenous leukemia isolates. We subsequently conducted a phase 1 trial of tipifarnib plus etoposide in adults over 70 years of age who were not candidates for conventional therapy. A total of 84 patients (median age, 77 years) received 224 cycles of oral tipifarnib (300-600 mg twice daily for 14 or 21 days) plus oral etoposide (100-200 mg daily on days 1-3 and 8-10). Dose-limiting toxicities occurred with 21-day tipifarnib. Complete remissions were achieved in 16 of 54 (30%) receiving 14-day tipifarnib versus 5 of 30 (17%) receiving 21-day tipifarnib. Complete remissions occurred in 50% of two 14-day tipifarnib cohorts: 3A (tipifarnib 600, etoposide 100) and 8A (tipifarnib 400, etoposide 200). In vivo, tipifarnib plus etoposide decreased ribosomal S6 protein phosphorylation and increased histone H2AX phosphorylation and apoptosis. Tipifarnib plus etoposide is a promising orally bioavailable regimen that warrants further evaluation in elderly adults who are not candidates for conventional induction chemotherapy. These clinical studies are registered at www.clinicaltrials.gov as #NCT00112853. (Blood. 2009;113:4841-4852)
C1 [Karp, Judith E.; Greer, Jacqueline M.; Ricklis, Rebecca M.; Smith, B. Douglas; Ironside, Valerie; Gore, Steven D.; Levis, Mark J.] Johns Hopkins Sidney Kimmel Canc Ctr, Div Hematol Malignancies, Baltimore, MD USA.
[Flatten, Karen; Loegering, David A.; Le, Son B.; Meng, Xue Wei; Schneider, Paula A.; Dai, Nga T.; Adjei, Alex A.; Kaufmann, Scott H.] Mayo Clin, Coll Med, Dept Oncol, Rochester, MN USA.
[Feldman, Eric J.; Ritchie, Ellen; Talbott, Timothy; Roboz, Gail] New York Presbyterian Hosp, Cornell Med Ctr, Dept Hematol Oncol, New York, NY USA.
[Morris, Lawrence E.] Bone Marrow Transplant Grp Georgia, Atlanta, GA USA.
[Wright, John J.] NIH, Invest Drug Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Garrett-Mayer, Elizabeth] Med Univ S Carolina, Hollings Canc Ctr, Charleston, SC USA.
RP Karp, JE (reprint author), Johns Hopkins Sidney Kimmel Comprehens Canc Ctr, 1650 Orleans St,CRB 1 Rm 289, Baltimore, MD 21231 USA.
EM jkarp2@jhmi.edu
FU NCI [U01 CA70095]; NCI Translational Research Initiative [24XS126]; NCI
Cancer Center [2P30 CA06973-44]; National Center for Research Resources
[M01-RR0052, R01 CA73709, R01 CA127433]; Leukemia & Lymphoma Society
Translational Research Project [6047-08]
FX The authors thank the Johns Hopkins Sidney Kimmel Cancer Center nursing
staff for superb medical care, and the patients and families, without
whose partnership we could never have conducted the trial and from whom
we have learned critical information that will help us to improve the
treatment of these diseases. This work was supported in part by NCI
(Cooperative Agreement U01 CA70095; J. E. K.), NCI Translational
Research Initiative (contract 24XS126; J. E. K.), NCI Cancer Center
(support grant 2P30 CA06973-44), National Center for Research Resources
(grants M01-RR0052, R01 CA73709, and R01 CA127433), the Leukemia &
Lymphoma Society Translational Research Project (White Plains, NY; grant
6047-08; S. H. K., J. E. K.), and philanthropic funds from Dr Robert
Fischell in memory of his late wife Marian (J. E. K.).
NR 76
TC 42
Z9 42
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD MAY 14
PY 2009
VL 113
IS 20
BP 4841
EP 4852
DI 10.1182/blood-2008-08-172726
PG 12
WC Hematology
SC Hematology
GA 445ZT
UT WOS:000266090700008
PM 19109557
ER
PT J
AU Landgren, O
Gilbert, ES
Rizzo, JD
Socie, G
Banks, PM
Sobocinski, KA
Horowitz, MM
Jaffe, ES
Kingma, DW
Travis, LB
Flowers, ME
Martin, PJ
Deeg, HJ
Curtis, RE
AF Landgren, Ola
Gilbert, Ethel S.
Rizzo, J. Douglas
Socie, Gerard
Banks, Peter M.
Sobocinski, Kathleen A.
Horowitz, Mary M.
Jaffe, Elaine S.
Kingma, Douglas W.
Travis, Lois B.
Flowers, Mary E.
Martin, Paul J.
Deeg, H. Joachim
Curtis, Rochelle E.
TI Risk factors for lymphoproliferative disorders after allogeneic
hematopoietic cell transplantation
SO BLOOD
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; POLYMERASE-CHAIN-REACTION;
VERSUS-HOST-DISEASE; HEMATOLOGIC MALIGNANCIES; IMMUNE RECONSTITUTION;
DEPLETED MARROW; LEUKEMIA; GRAFTS; AGE
AB We evaluated 26 901 patients who underwent allogeneic hematopoietic cell transplantation (HCT) at 271 centers worldwide to define patterns of posttransplantation lymphoproliferative disorders (PTLDs). PTLDs developed in 127 recipients, with 105 (83%) cases occurring within 1 year after transplantation. In multivariate analyses, we confirmed that PTLD risks were strongly associated (P <.001) with T-cell depletion of the donor marrow, antithymocyte globulin (ATG) use, and unrelated or HLA-mismatched grafts (URD/HLA mismatch). Significant associations were also confirmed for acute and chronic graft-versus-host disease. The increased risk associated with URD/HLA-mismatched donors (RR = 3.8) was limited to patients with T-cell depletion or ATG use (P = .004). New findings were elevated risks for age 50 years or older at transplantation (RR = 5.1; P <.001) and second transplantation (RR = 3.5; P <.001). Lower risks were found for T-cell depletion methods that remove both T and B cells (alemtuzumab and elutriation, RR = 3.1; P = .025) compared with other methods (RR = 9.4; P = .005 for difference). The cumulative incidence of PTLDs was low (0.2%) among 21 686 patients with no major risk factors, but increased to 1.1%, 3.6%, and 8.1% with 1, 2, and more than 3 major risk factors, respectively. Our findings identify subgroups of patients who underwent allogeneic HCT at elevated risk of PTLDs for whom prospective monitoring of Epstein-Barr virus activation and early treatment intervention may be particularly beneficial. (Blood. 2009; 113: 4992-5001)
C1 [Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, NIH,Dept Hlth & Human Serv HHS, Bethesda, MD 20892 USA.
[Landgren, Ola; Gilbert, Ethel S.; Curtis, Rochelle E.] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv HHS, NIH, Bethesda, MD 20892 USA.
[Rizzo, J. Douglas; Sobocinski, Kathleen A.; Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Socie, Gerard] Hosp St Louis, Paris, France.
[Banks, Peter M.] Carolinas Med Ctr, Charlotte, NC 28203 USA.
[Jaffe, Elaine S.; Kingma, Douglas W.] NCI, Pathol Lab, Ctr Canc Res, NIH,HHS, Bethesda, MD 20892 USA.
[Travis, Lois B.] Univ Rochester, Dept Radiat Oncol, Rochester, NY 14627 USA.
[Flowers, Mary E.; Martin, Paul J.; Deeg, H. Joachim] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
RP Landgren, O (reprint author), NCI, Med Oncol Branch, Ctr Canc Res, NIH,Dept Hlth & Human Serv HHS, 9000 Rockville Pike,Bldg 10,Rm 13N240F, Bethesda, MD 20892 USA.
EM landgreo@mail.nih.gov
FU NCI [CP-51027, CP-51028, P01-HL36444, P01-CA18029, P01CA102542,
P01-CA15704]; Intramural Research Program of the NIH; Public Health
Service [U24-CA76518]; National Institute of Allergy and Infectious
Diseases; National Heart, Lung and Blood Institute; Office of Naval
Research; Health Services Research Administration [K23 CA82350-05];
Abbott Laboratories; Aetna; American International Group; American Red
Cross; Amgen; Medical College of Wisconsin; AnorMED; Astellas Pharma US;
Baxter International; Berlex Laboratories; Biogen IDEC; BloodCenter of
Wisconsin; Blue Cross and Blue Shield Association; Bristol-Myers Squibb
Company; BRT Laboratories; Cangene; Celgene; CellGenix; Cell
Therapeutics; CelMed Biosciences; Cylex; Cytonome; CytoTherm; DOR
BioPharma; Dynal Biotech; Invitrogen Company; Enzon Pharmaceuticals;
Gambro BCT; Gamida Cell; Genzyme; Gift of Life Bone Marrow Foundation;
GlaxoSmithKline; Histogenetics; HKS Medical Information Systems; Kirin
Brewery; Merck Company; The Medical College of Wisconsin; Millennium
Pharmaceuticals; Miller Pharmacal Group; Milliman USA; Miltenyi Biotec;
MultiPlan; National Marrow Donor Program; Nature Publishing Group;
Novartis Pharmaceuticals; Osiris Therapeutics; Pall Medical; Pfizer;
Pharmion; PDL BioPharma; Roche Laboratories; Sanofi- aventis; Schering
Plough; StemCyte; StemSoft Software; SuperGen; Sysmex; The Marrow
Foundation; THERAKOS; University of Colorado Cord Blood Bank; ViaCell;
ViraCor Laboratories; Wellpoint; Zelos Therapeutics
FX The authors are indebted to the physicians and data professionals at
participating transplant centers who contributed high-quality data to
this study. We are especially grateful to Dr Catherine Metayer from the
University of California, Berkeley, for detailed data review and
statistical analyses for the case-control study. We thank Gary Schoch
from FHCRC, Seattle, and Diane Knutson and Sharon Nell from the CIBMTR,
Milwaukee, for support in data collection. We acknowledge Linda Kaufman,
Kathy Chimes, and Diane Fuchs from Westat (Rockville, MD) for
coordination of field studies, and Nathan Appel, David Hacker, Heather
Bath, and George Geise from Information Management Services (Silver
Spring, MD) for computing support.; This research is supported by
contract nos. CP-51027 and CP-51028 from the NCI; and by the Intramural
Research Program of the NIH and the NCI. The FHCRC investigators are
supported by grants P01-HL36444, P01-CA18029, P01CA102542, and
P01-CA15704 from the NIH. The CIBMTR is supported by Public Health
Service Grant U24-CA76518 from the NCI, the National Institute of
Allergy and Infectious Diseases, and the National Heart, Lung and Blood
Institute; Office of Naval Research; Health Services Research
Administration (HHS); K23 CA82350-05 grant from the NIH; and grants from
Abbott Laboratories; Aetna; American International Group; American Red
Cross; Amgen; anonymous donation to the Medical College of Wisconsin;
AnorMED; Astellas Pharma US; Baxter International; Berlex Laboratories;
Biogen IDEC; BloodCenter of Wisconsin; Blue Cross and Blue Shield
Association; Bristol-Myers Squibb Company; BRT Laboratories; Cangene;
Celgene; CellGenix; Cell Therapeutics; CelMed Biosciences; Cylex;
Cytonome; CytoTherm; DOR BioPharma; Dynal Biotech, an Invitrogen
Company; Enzon Pharmaceuticals; Gambro BCT; Gamida Cell; Genzyme; Gift
of Life Bone Marrow Foundation; GlaxoSmithKline; Histogenetics; HKS
Medical Information Systems; Kirin Brewery; Merck & Company; The Medical
College of Wisconsin; Millennium Pharmaceuticals; Miller Pharmacal
Group; Milliman USA; Miltenyi Biotec; MultiPlan; National Marrow Donor
Program; Nature Publishing Group; Novartis Pharmaceuticals; Osiris
Therapeutics; Pall Medical; Pfizer; Pharmion; PDL BioPharma; Roche
Laboratories; Sanofi- aventis; Schering Plough; StemCyte; StemSoft
Software; SuperGen; Sysmex; The Marrow Foundation; THERAKOS; University
of Colorado Cord Blood Bank; ViaCell; ViraCor Laboratories; Wellpoint;
and Zelos Therapeutics.; The views expressed in this article do not
reflect the official policy or position of the National Institute of
Health, the of the Navy, the Department of Defense, or any other agency
of the US government.
NR 39
TC 150
Z9 162
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD MAY 14
PY 2009
VL 113
IS 20
BP 4992
EP 5001
DI 10.1182/blood-2008-09-178046
PG 10
WC Hematology
SC Hematology
GA 445ZT
UT WOS:000266090700026
PM 19264919
ER
PT J
AU Capitini, CM
Herby, S
Milliron, M
Anver, MR
Mackall, CL
Fry, TJ
AF Capitini, Christian M.
Herby, Sarah
Milliron, Matthew
Anver, Miriam R.
Mackall, Crystal L.
Fry, Terry J.
TI Bone marrow deficient in IFN-gamma signaling selectively reverses
GVHD-associated immunosuppression and enhances a tumor-specific GVT
effect
SO BLOOD
LA English
DT Article
ID VERSUS-HOST-DISEASE; INTERFERON-GAMMA; T-CELLS; IMMUNE RECONSTITUTION;
STEM-CELLS; NK CELLS; GRAFT; TRANSPLANTATION; IMMUNOTHERAPY; VACCINES
AB Vaccine-based expansion of T cells is one approach to enhance the graft-versus-tumor effect of allogeneic bone marrow transplantation (BMT), but the complex immunobiology of the allogeneic environment on responses to tumor vaccines has not been well characterized. We hypothesized that subclinical graft-versus-host disease (GVHD) impairs immunity, but modulation of gamma interferon (IFN-gamma) signaling could reverse this effect. Dendritic cell vaccines and donor lymphocyte infusions (DLIs) were incorporated into a minor histocompatibility antigen-mismatched, T cell-depleted, allogeneic BMT mouse model. Animals were then challenged with H-Y expressing tumors. CD4(+) and CD8(+) responses to H-Y were diminished in vaccinated allogeneic versus syngeneic BMT recipients with DLI doses below the threshold for clinical GVHD, especially in thymectomized hosts. IFN-gamma receptor 1-deficient (IFN-gamma R1(-/-)) T cells cannot cause GVHD but also have diminished vaccine responses. Remarkably, IFN-gamma R1(-/-) bone marrow abrogates GVHD, allowing higher DLI doses to be tolerated, but improves vaccine responses and tumor protection. We conclude that tumor vaccines administered after allogeneic BMT can augment graft-versus-tumor if GVHD is avoided and that prevention of IFN-gamma signaling on donor bone marrow is an effective approach to preventing GVHD while preserving immunocompetence. (Blood. 2009; 113: 5002-5009)
C1 [Capitini, Christian M.; Herby, Sarah; Milliron, Matthew; Mackall, Crystal L.; Fry, Terry J.] NCI, Immunol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Anver, Miriam R.] NCI, Pathol Histotechnol Lab, Sci Applicat Int Corp SAIC Frederick, NIH, Frederick, MD 21701 USA.
[Fry, Terry J.] Childrens Natl Med Ctr, Ctr Canc & Blood Disorders, Washington, DC 20010 USA.
RP Capitini, CM (reprint author), NCI, Immunol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, 10 Ctr Dr,Rm 1W-5832, Bethesda, MD 20892 USA.
EM capitinic@mail.nih.gov
OI Capitini, Christian/0000-0002-2276-6731
FU National Cancer Institute [HHSN261200800001E]; Children's Cancer
Foundation
FX The authors thank Richard Childs and Daniel Fowler for their critical
review of the data and manuscript drafts.; The content of this
publication does not necessarily reflect the views of policies of the
Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the US
government.; This work was supported by intramural research funds at the
National Cancer Institute (C. L. M.), the Children's Cancer Foundation
(T. J. F.), and in part with federal funds from the NCI, NIH, funded by
NCI contract no. HHSN261200800001E (M. R. A.).
NR 40
TC 16
Z9 17
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD MAY 14
PY 2009
VL 113
IS 20
BP 5002
EP 5009
DI 10.1182/blood-2008-11-187385
PG 8
WC Hematology
SC Hematology
GA 445ZT
UT WOS:000266090700027
PM 19258593
ER
PT J
AU Han, Q
Robinson, H
Cai, T
Tagle, DA
Li, JY
AF Han, Qian
Robinson, Howard
Cai, Tao
Tagle, Danilo A.
Li, Jianyong
TI Structural Insight into the Inhibition of Human Kynurenine
Aminotransferase I/Glutamine Transaminase K
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID SPONTANEOUSLY HYPERTENSIVE-RATS; EXCITATORY AMINO-ACIDS;
SUBSTRATE-SPECIFICITY; CRYSTAL-STRUCTURES; TRYPTOPHAN DEGRADATION;
SYNAPTIC-TRANSMISSION; HUNTINGTONS-DISEASE; NICOTINIC RECEPTORS;
QUINOLINIC ACID; DRUG TARGET
AB Human kynurenine aminotransferase I (hKAT I) catalyzes the formation of kynurenic acid, a neuroactive compound. Here, we report three high-resolution crystal structures (1.50-1.55 angstrom) of hKAT I that are in complex with glycerol and each of two inhibitors of hKAT I: indole-3-acetic acid (IAC) and Tris. Because Tris is able to occupy the substrate binding position, we speculate that this may be the basis for hKAT I inhibition. Furthermore, the hKAT/IAC complex structure reveals that the binding moieties of the inhibitor are its indole ring and a carboxyl group. Six chemicals with both binding moieties were tested for their ability to inhibit hKAT I activity; 3-indolepropionic acid and DL-indole-3-lactic acid demonstrated the highest level of inhibition, and as they cannot be considered as substrates of the enzyme, these two inhibitors are promising candidates for future study. Perhaps even more significantly, we report the discovery of two different ligands located simultaneously in the hKAT I active center for the first time.
C1 [Han, Qian; Li, Jianyong] Virginia Tech, Dept Biochem, Blacksburg, VA 24061 USA.
[Robinson, Howard] Brookhaven Natl Lab, Dept Biol, Upton, NY 11973 USA.
[Cai, Tao] NIDCR, OIIB, NIH, Bethesda, MD 20892 USA.
[Tagle, Danilo A.] NINDS, Ctr Neurosci, NIH, Bethesda, MD 20892 USA.
RP Han, Q (reprint author), Virginia Tech, Dept Biochem, Blacksburg, VA 24061 USA.
EM qianhan@vt.edu
RI Han, Qian/J-8696-2014
OI Han, Qian/0000-0001-6245-5252
FU National Synchrotron Light Source; Brookhaven National Laboratory;
Intramural Research Program
FX This work was carried out in part at the National Synchrotron Light
Source, Brookhaven National Laboratory, and supported in part by the
Intramural Research Program of the institutes of NIDCR and NINDS at NIH.
We are grateful to Elizabeth Watson and Graham Richardson (Dr. Jianyong
Li's laboratory, Department-of Biochemistry, Virginia Tech) for critical
reading of this paper.
NR 57
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U1 1
U2 7
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD MAY 14
PY 2009
VL 52
IS 9
BP 2786
EP 2793
DI 10.1021/jm9000874
PG 8
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 443LP
UT WOS:000265911800016
PM 19338303
ER
PT J
AU Grillet, N
Xiong, W
Reynolds, A
Kazmierczak, P
Sato, T
Lillo, C
Dumont, RA
Hintermann, E
Sczaniecka, A
Schwander, M
Williams, D
Kachar, B
Gillespie, PG
Muller, U
AF Grillet, Nicolas
Xiong, Wei
Reynolds, Anna
Kazmierczak, Piotr
Sato, Takashi
Lillo, Concepcion
Dumont, Rachel A.
Hintermann, Edith
Sczaniecka, Anna
Schwander, Martin
Williams, David
Kachar, Bechara
Gillespie, Peter G.
Mueller, Ulrich
TI Harmonin Mutations Cause Mechanotransduction Defects in Cochlear Hair
Cells
SO NEURON
LA English
DT Article
ID SYNDROME TYPE 1D; SYNDROME TYPE 1F; USHER-SYNDROME; RECESSIVE DEAFNESS;
TIP-LINK; SENSORY TRANSDUCTION; PROTOCADHERIN GENE; ALLELIC MUTATIONS;
FAST ADAPTATION; CADHERIN GENE
AB In hair cells, mechanotransduction channels are gated by tip links, the extracellular filaments that consist of cadherin 23 (CDH23) and protocadherin 15 (PCDH15) and connect the stereocilia of each hair cell. However, which molecules mediate cadherin function at tip links is not known. Here we show that the PDZ-domain protein harmonin is a component of the upper tip-link density (UTLD), where CDH23 inserts into the stereociliary membrane. Harmonin domains that mediate interactions with CDH23 and F-actin control harmonin localization in stereocilia and are necessary for normal hearing. In mice expressing a mutant harmonin protein that prevents UTLD formation, the sensitivity of hair bundles to mechanical stimulation is reduced. We conclude that harmonin is a UTLD component and contributes to establishing the sensitivity of mechanotransduction channels to displacement.
C1 [Grillet, Nicolas; Xiong, Wei; Reynolds, Anna; Kazmierczak, Piotr; Hintermann, Edith; Sczaniecka, Anna; Schwander, Martin; Mueller, Ulrich] Scripps Res Inst, Inst Childhood & Neglected Dis, Dept Cell Biol, La Jolla, CA 92037 USA.
[Sato, Takashi; Kachar, Bechara] NIDCD, Lab Cell Struct & Dynam, NIH, Bethesda, MD 20892 USA.
[Lillo, Concepcion; Williams, David] Univ Calif Los Angeles, Sch Med, Jules Stein Eye Inst, Dept Ophthalmol, Los Angeles, CA 90024 USA.
[Lillo, Concepcion; Williams, David] Univ Calif Los Angeles, Sch Med, Jules Stein Eye Inst, Dept Neurobiol, Los Angeles, CA 90024 USA.
[Dumont, Rachel A.; Gillespie, Peter G.] Oregon Hlth & Sci Univ, Oregon Hearing Res Ctr & Vollum Inst, Portland, OR 97239 USA.
RP Muller, U (reprint author), Scripps Res Inst, Inst Childhood & Neglected Dis, Dept Cell Biol, 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM umueller@scripps.edu
RI Wang, Shirong/G-1698-2011; 2009, Secribsal/A-1266-2012; Xiong,
Wei/A-6170-2012; Lillo, Concepcion/A-6321-2009;
OI Lillo, Concepcion/0000-0001-5814-9826; Barr-Gillespie,
Peter/0000-0002-9787-5860
FU NIH [DC005969, DC007704, EYE07042, DC002368]; Skaggs Institute for
Chemical Biology; NHMRC (Australia) [148939]; Bruce Ford and Anne Smith
Bundy Foundation
FX We thank Anthony Ricci for help with electrophysiology and for comments
on the manuscript; C. Ramos, G. Martin, and S. Kupriyanov for assistance
in generating mice; and K. Spencer, M. Wood, and T. Fassel for help with
microscopy and EM. This work was funded by NIH grants DC005969, DC007704
(U. M.), EYE07042 (D.W,), and DC002368 (P.G.); the Skaggs Institute for
Chemical Biology (U.M.); a Jules and Doris Stein RPB professorship
(D.W.); a C.J. Martin fellowship (#148939) NHMRC (Australia) (A.R.); and
a fellowship from the Bruce Ford and Anne Smith Bundy Foundation (A.R.
and W.X).
NR 46
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Z9 66
U1 1
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD MAY 14
PY 2009
VL 62
IS 3
BP 375
EP 387
DI 10.1016/j.neuron.2009.04.006
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 446UG
UT WOS:000266146100009
PM 19447093
ER
PT J
AU Pinsky, PF
AF Pinsky, Paul F.
TI Antioxidant Supplementation and Cancer Prevention
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Pinsky, PF (reprint author), NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
EM pinskyp@mail.nih.gov
NR 4
TC 3
Z9 3
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD MAY 13
PY 2009
VL 301
IS 18
BP 1878
EP 1878
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 444JX
UT WOS:000265978400016
PM 19436011
ER
PT J
AU Volkow, ND
Chandler, RK
Fletcher, BW
AF Volkow, Nora D.
Chandler, Redonna K.
Fletcher, Bennett W.
TI Drug Addiction as a Brain Disorder or Disease Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 [Volkow, Nora D.; Chandler, Redonna K.; Fletcher, Bennett W.] NIDA, Bethesda, MD 20892 USA.
RP Volkow, ND (reprint author), NIDA, Bethesda, MD 20892 USA.
EM nvolkow@nida.nih.gov
NR 6
TC 1
Z9 1
U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD MAY 13
PY 2009
VL 301
IS 18
BP 1881
EP 1882
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 444JX
UT WOS:000265978400023
ER
PT J
AU Zhao, XR
Strong, R
Zhang, J
Sun, GH
Tsien, JZ
Cui, ZZ
Grotta, JC
Aronowski, J
AF Zhao, Xiurong
Strong, Roger
Zhang, Jie
Sun, Guanghua
Tsien, Joe Z.
Cui, Zhenzhong
Grotta, James C.
Aronowski, Jaroslaw
TI Neuronal PPAR gamma Deficiency Increases Susceptibility to Brain Damage
after Cerebral Ischemia
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID ACTIVATED-RECEPTOR-GAMMA; TRANSIENT FOCAL ISCHEMIA; INTRACEREBRAL
HEMORRHAGE TREATMENT; CAUSES INSULIN-RESISTANCE; DEPENDENT
PROTEIN-KINASE; EXPERIMENTAL STROKE; 15-DEOXY-DELTA(12,14)-PROSTAGLANDIN
J(2); 15D-PROSTAGLANDIN J(2); DEVELOPMENTAL-CHANGES; GENE-EXPRESSION
AB Peroxisome proliferator-activated receptor gamma (PPAR gamma) plays a role in regulating a myriad of biological processes in virtually all brain cell types, including neurons. We and others have reported recently that drugs which activate PPAR gamma are effective in reducing damage to brain in distinct models of brain disease, including ischemia. However, the cell type responsible for PPAR gamma-mediated protection has not been established. In response to ischemia, PPAR gamma gene is robustly upregulated in neurons, suggesting that neuronal PPAR gamma may be a primary target for PPAR gamma-agonist-mediated neuroprotection. To understand the contribution of neuronal PPAR gamma to ischemic injury, we generated conditional neuron-specific PPAR gamma knock-out mice (N-PPAR gamma-KO). These mice are viable and appeared to be normal with respect to their gross behavior and brain anatomy. However, neuronal PPAR gamma deficiency caused these mice to experience significantly more brain damage and oxidative stress in response to middle cerebral artery occlusion. The primary cortical neurons harvested from N-PPAR gamma-KO mice, but not astroglia, exposed to ischemia in vitro demonstrated more damage and a reduced expression of numerous key gene products that could explain increased vulnerability, including SOD1 (superoxide dismutase 1), catalase, glutathione S-transferase, uncoupling protein-1, or transcription factor liver X receptor-alpha. Also, PPAR gamma agonist-based neuroprotective effect was lost in neurons from N-PPAR gamma neurons. Therefore, we conclude that PPAR gamma in neurons play an essential protective function and that PPAR gamma agonists may have utility in neuronal self-defense, in addition to their well established anti-inflammatory effect.
C1 [Strong, Roger; Zhang, Jie; Sun, Guanghua; Grotta, James C.; Aronowski, Jaroslaw] Univ Texas Houston, Sch Med, Dept Neurol, Stroke Program, Houston, TX 77030 USA.
[Cui, Zhenzhong] NIMH, Sect Neural Gene Express, NIH, Bethesda, MD 20892 USA.
[Tsien, Joe Z.] Med Coll Georgia, Brain & Behav Discovery Inst, Augusta, GA 30912 USA.
RP Aronowski, J (reprint author), Univ Texas Houston, Sch Med, Dept Neurol, Stroke Program, Houston, TX 77030 USA.
EM J.Aronowski@uth.tmc.edu
FU National Institutes of Health-National Institute of Neurological
Disorders and Stroke [R01NS052791, 1R21NS057284]
FX This project was supported by National Institutes of Health-National
Institute of Neurological Disorders and Stroke Grants R01NS052791 and
1R21NS057284.
NR 65
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Z9 97
U1 1
U2 7
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD MAY 13
PY 2009
VL 29
IS 19
BP 6186
EP 6195
DI 10.1523/JNEUROSCI.5857-08.2009
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 445HU
UT WOS:000266042700016
PM 19439596
ER
PT J
AU Sarin, H
Kanevsky, AS
Fung, SH
Butman, JA
Cox, RW
Glen, D
Reynolds, R
Auh, S
AF Sarin, Hemant
Kanevsky, Ariel S.
Fung, Steve H.
Butman, John A.
Cox, Robert W.
Glen, Daniel
Reynolds, Richard
Auh, Sungyoung
TI Metabolically stable bradykinin B2 receptor agonists enhance
transvascular drug delivery into malignant brain tumors by increasing
drug half-life
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
ID CONVERTING-ENZYME-INHIBITION; GADOLINIUM-DTPA COMPLEX; TO-TISSUE
TRANSPORT; BLOOD-BRAIN; CEREPORT RMP-7; NITRIC-OXIDE; GD-DTPA;
QUANTITATIVE MEASUREMENT; CHEMOTHERAPEUTIC-AGENTS; VASCULAR-PERMEABILITY
AB Background: The intravenous co-infusion of labradimil, a metabolically stable bradykinin B2 receptor agonist, has been shown to temporarily enhance the transvascular delivery of small chemotherapy drugs, such as carboplatin, across the blood-brain tumor barrier. It has been thought that the primary mechanism by which labradimil does so is by acting selectively on tumor microvasculature to increase the local transvascular flow rate across the blood-brain tumor barrier. This mechanism of action does not explain why, in the clinical setting, carboplatin dosing based on patient renal function over-estimates the carboplatin dose required for target carboplatin exposure. In this study we investigated the systemic actions of labradimil, as well as other bradykinin B2 receptor agonists with a range of metabolic stabilities, in context of the local actions of the respective B2 receptor agonists on the blood-brain tumor barrier of rodent malignant gliomas.
Methods: Using dynamic contrast-enhanced MRI, the pharmacokinetics of gadolinium-diethyltriaminepentaacetic acid (Gd-DTPA), a small MRI contrast agent, were imaged in rodents bearing orthotopic RG-2 malignant gliomas. Baseline blood and brain tumor tissue pharmacokinetics were imaged with the 1st bolus of Gd-DTPA over the first hour, and then re-imaged with a 2nd bolus of Gd-DTPA over the second hour, during which normal saline or a bradykinin B2 receptor agonist was infused intravenously for 15 minutes. Changes in mean arterial blood pressure were recorded. Imaging data was analyzed using both qualitative and quantitative methods.
Results: The decrease in systemic blood pressure correlated with the known metabolic stability of the bradykinin B2 receptor agonist infused. Metabolically stable bradykinin B2 agonists, methionine-lysine-bradykinin and labradimil, had differential effects on the transvascular flow rate of Gd-DTPA across the blood-brain tumor barrier. Both methionine-lysine-bradykinin and labradimil increased the blood half-life of Gd-DTPA sufficiently enough to increase significantly the tumor tissue Gd-DTPA area under the time-concentration curve.
Conclusion: Metabolically stable bradykinin B2 receptor agonists, methionine-lysine-bradykinin and labradimil, enhance the transvascular delivery of small chemotherapy drugs across the BBTB of malignant gliomas by increasing the blood half-life of the co-infused drug. The selectivity of the increase in drug delivery into the malignant glioma tissue, but not into normal brain tissue or skeletal muscle tissue, is due to the inherent porous nature of the BBTB of malignant glioma microvasculature.
C1 [Sarin, Hemant] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD 20892 USA.
[Sarin, Hemant; Kanevsky, Ariel S.; Butman, John A.] NIH, Radiol & Imaging Sci Program, Ctr Clin, Bethesda, MD 20892 USA.
[Fung, Steve H.] Massachusetts Gen Hosp, Dept Neuroradiol, Boston, MA 02114 USA.
[Cox, Robert W.; Glen, Daniel; Reynolds, Richard] NIMH, Bethesda, MD 20892 USA.
[Auh, Sungyoung] NINDS, NIH, Bethesda, MD 20892 USA.
RP Sarin, H (reprint author), Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD 20892 USA.
EM sarinh@mail.nih.gov; kanevskya@cc.nih.gov; SFUNG@PARTNERS.ORG;
JButmanA@cc.nih.gov; robertcox@mail.nih.gov; glend@mail.nih.gov;
reynoldr@mail.nih.gov; auhs@ninds.nih.gov
RI Butman, John/A-2694-2008; Butman, John/J-2780-2013;
OI Butman, John/0000-0002-1547-9195; Fung, Steve/0000-0002-1177-682X
FU National Institute of Biomedical Imaging Bioengineering (NIBIB);
Radiology and Imaging Sciences Program (CC)
FX This study was funded by the National Institute of Biomedical Imaging
Bioengineering (NIBIB) and the Radiology and Imaging Sciences Program
(CC). We thank Dr. Matthew Hall for useful discussions.
NR 65
TC 7
Z9 7
U1 0
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD MAY 13
PY 2009
VL 7
AR 33
DI 10.1186/1479-5876-7-33
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 461CA
UT WOS:000267240800001
PM 19439100
ER
PT J
AU Cook, NL
Ayanian, JZ
Orav, EJ
Hicks, LS
AF Cook, Nakela L.
Ayanian, John Z.
Orav, E. John
Hicks, Leroi S.
TI Differences in Specialist Consultations for Cardiovascular Disease by
Race, Ethnicity, Gender, Insurance Status, and Site of Primary Care
SO CIRCULATION
LA English
DT Article
DE coronary disease; healthcare disparities; heart failure; quality of
health care
ID COMMUNITY-HEALTH CENTERS; QUALITY-OF-CARE; ACUTE MYOCARDIAL-INFARCTION;
CORONARY-ARTERY-DISEASE; HEART-FAILURE; ELDERLY-PATIENTS; PHYSICIAN
SPECIALTY; RACIAL-DIFFERENCES; OUTCOMES; DISPARITIES
AB Background-Consultation with cardiologists may improve the quality of ambulatory care and reduce disparities for patients with heart disease. We assessed the use of cardiology consultations and the associated quality by race/ethnicity, gender, insurance status, and site of care.
Methods and Results-In a retrospective cohort, we examined electronic records of 9761 adults with coronary artery disease or congestive heart failure (CHF) receiving primary care at practices affiliated with 2 academic medical centers during 2000 to 2005. During this period, 79.6% of patients with coronary artery disease and 90.3% of patients with CHF had a cardiology consultation. In multivariate analyses, women were less likely to receive a consultation than men for both conditions (coronary artery disease: hazard ratio, 0.89; 95% CI, 0.85 to 0.93; CHF: hazard ratio, 0.93; 95% CI, 0.87 to 0.99). Women also had 15% fewer follow-up consultations than men (P < 0.001). Similarly, patients at community health centers were less likely to receive a consultation (coronary artery disease: hazard ratio, 0.79; 95% CI, 0.74 to 0.84; CHF: hazard ratio, 0.77; 95% CI: 0.71 to 0.84) and had 20% fewer follow-up consultations (P < 0.001) relative to those at hospital-based practices. Black and Hispanic patients with CHF had 13% fewer follow-up consultations than white patients (P = 0.01 and P = 0.04, respectively). In adjusted analyses, consultation was associated with better processes of care compared with no consultation (P < 0.001), particularly for women (P < 0.001 for interaction between consultation and gender).
Conclusions-Among ambulatory patients with coronary artery disease or CHF, women and those at community health centers have less access to cardiologists. Consultation is associated with better quality of care and narrows the gender gap in quality. (Circulation. 2009; 119: 2463-2470.)
C1 [Cook, Nakela L.] NHLBI, Bethesda, MD 20892 USA.
[Hicks, Leroi S.] Brigham & Womens Hosp, Ctr Community Hlth & Hlth Equ, Boston, MA 02115 USA.
[Ayanian, John Z.; Orav, E. John; Hicks, Leroi S.] Brigham & Womens Hosp, Div Gen Med & Primary Care, Boston, MA 02115 USA.
[Ayanian, John Z.; Hicks, Leroi S.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
RP Cook, NL (reprint author), NHLBI, Rockledge 2,Suite 10018,6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM cookn2@nhlbi.nih.gov
FU Agency for Healthcare Research and Quality [5 T32 HS000020-21]
FX Dr Cook was supported by an institutional National Research Service
Award from the Agency for Healthcare Research and Quality (5 T32
HS000020-21) during the conduct of this research.
NR 37
TC 36
Z9 38
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD MAY 12
PY 2009
VL 119
IS 18
BP 2463
EP U76
DI 10.1161/CIRCULATIONAHA.108.825133
PG 9
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 444WP
UT WOS:000266011500007
PM 19398667
ER
PT J
AU Marietta, C
Thompson, LH
Lamerdin, JE
Brooks, PJ
AF Marietta, Cheryl
Thompson, Larry H.
Lamerdin, Jane E.
Brooks, P. J.
TI Acetaldehyde stimulates FANCD2 monoubiquitination, H2AX phosphorylation,
and BRCA1 phosphorylation in human cells in vitro: Implications for
alcohol-related carcinogenesis
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Article
DE Fanconi anemia; Breast cancer; Esophagus; Alcohol
ID DNA CROSS-LINKS; FANCONI-ANEMIA; DAMAGE RESPONSE; ALDEHYDE
DEHYDROGENASE-2; POLYMERASE-KAPPA; HEAVY DRINKERS; CANCER-RISK; ADDUCTS;
REPAIR; CROTONALDEHYDE
AB According to a recent IARC Working Group report, alcohol consumption is causally related to an increased risk of cancer of the upper aerodigestive tract, liver, colorectum, and female breast [R. Baan, K. Straif, Y. Grosse, B. Secretan, F. EI Chissassi, V. Bouvard, A. Altieri, V. Cogliano, Carcinogenicity of alcoholic beverages, Lancet Oncol. 8 (2007) 292-293]. Several lines of evidence indicate that acetalclehyde (AA), the first product of alcohol metabolism, plays a very important role in alcohol-related carcinogenesis, particularly in the esophagus. We previously proposed a model for alcohol-related carcinogenesis in which AA, generated from alcohol metabolism, reacts in cells to generate DNA lesions that form interstrand crosslinks (ICLs) [J.A. Theruvathu, P. Jaruga, R.G. Nath, M. Dizdaroglu, P.J. Brooks, Polyamines stimulate the formation of mutagenic 1, N2-propanodeoxyguanosine adducts from acetalclehyde. Nucleic Acids Res. 33 (2005) 3513-3520]. Since the Fanconi anemia-breast cancer associated (FANC-BRCA) DNA damage response network plays a crucial role in protecting cells against ICLs, in the present work we tested this hypothesis by exposing cells to AA and monitoring activation of this network. We found that AA exposure results in a concentration-dependent increase in FANCD2 monoubiquitination, which is dependent upon the FANC core complex. AA also stimulated BRCA1 phosphorylation at Ser1524 and increased the level of gamma H2AX, with both modifications occurring in a dose-dependent manner. However, AA did not detectably increase the levels of hyperphosphorylated RPA34, a marker of single-stranded DNA exposure at replication forks. These results provide the initial description of the AA-DNA damage response, which is qualitatively similar to the cellular response to mitomycin C, a known DNA crosslinking agent. We discuss the mechanistic implications of these results, as well as their possible relationship to alcohol-related carcinogenesis in different human tissues. (c) 2009 Published by Elsevier B.V.
C1 [Marietta, Cheryl; Brooks, P. J.] NIAAA, Mol Neurobiol Sect, Neurogenet Lab, Rockville, MD 20852 USA.
[Thompson, Larry H.; Lamerdin, Jane E.] Lawrence Livermore Natl Lab, Biosci & Biotechnol Div, Livermore, CA 94551 USA.
[Lamerdin, Jane E.] Odyssey Thera Inc, San Ramon, CA USA.
RP Brooks, PJ (reprint author), NIAAA, Mol Neurobiol Sect, Neurogenet Lab, 5625 Fishers Lane,Room 3S32, Rockville, MD 20852 USA.
EM pjbrooks@mail.nih.gov
FU Intramural NIH HHS [Z01 AA000083-14]
NR 51
TC 26
Z9 27
U1 2
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0027-5107
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD MAY 12
PY 2009
VL 664
IS 1-2
BP 77
EP 83
DI 10.1016/j.mrfmmm.2009.03.011
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 449XM
UT WOS:000266364100011
PM 19428384
ER
PT J
AU Barbey, AK
Krueger, F
Grafman, J
AF Barbey, Aron K.
Krueger, Frank
Grafman, Jordan
TI Structured event complexes in the medial prefrontal cortex support
counterfactual representations for future planning
SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Article
DE structured event complexes; prefrontal cortex; counterfactual reasoning;
planning; prediction; event knowledge
ID ANTERIOR CINGULATE CORTEX; GRASP REPRESENTATIONS; MEMORY; KNOWLEDGE;
SYSTEMS; REGRET; HIPPOCAMPUS; THINKING; HUMANS; BRAIN
AB We propose that counterfactual representations for reasoning about the past or predicting the future depend on structured event complexes (SECs) in the human prefrontal cortex (PFC; 'What would happen if X were performed in the past or enacted in the future?'). We identify three major categories of counterfactual thought (concerning action versus inaction, the self versus other and upward versus downward thinking) and propose that each form of inference recruits SEC representations in distinct regions of the medial PFC. We develop a process model of the regulatory functions these representations serve and draw conclusions about the importance of SECs for explaining the past and predicting the future.
C1 [Barbey, Aron K.; Krueger, Frank; Grafman, Jordan] NINDS, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
[Barbey, Aron K.] Georgetown Univ, Dept Psychol, Washington, DC 20057 USA.
RP Grafman, J (reprint author), NINDS, Cognit Neurosci Sect, NIH, Bldg 10,Room 7D43,10 Ctr Dr,MSC 1440, Bethesda, MD 20892 USA.
EM grafmanj@ninds.nih.gov
RI Barbey, Aron/L-7312-2015;
OI Barbey, Aron/0000-0002-6092-0912; Grafman, Jordan H./0000-0001-8645-4457
FU NINDS
FX The authors are supported by the NINDS Intramural Research Program.
NR 75
TC 50
Z9 50
U1 3
U2 9
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8436
J9 PHILOS T R SOC B
JI Philos. Trans. R. Soc. B-Biol. Sci.
PD MAY 12
PY 2009
VL 364
IS 1521
BP 1291
EP 1300
DI 10.1098/rstb.2008.0315
PG 10
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 425UE
UT WOS:000264662000013
PM 19528010
ER
PT J
AU SanGiovanni, JP
Arking, DE
Iyengar, SK
Elashoff, M
Clemons, TE
Reed, GF
Henning, AK
Sivakumaran, TA
Xu, XM
Dewan, A
Agron, E
Rochtchina, E
Sue, CM
Wang, JJ
Mitchell, P
Hoh, J
Francis, PJ
Klein, ML
Chew, EY
Chakravarti, A
AF SanGiovanni, John Paul
Arking, Dan E.
Iyengar, Sudha K.
Elashoff, Michael
Clemons, Traci E.
Reed, George F.
Henning, Alice K.
Sivakumaran, Theru A.
Xu, Xuming
DeWan, Andrew
Agron, Elvira
Rochtchina, Elena
Sue, Carolyn M.
Wang, Jie Jin
Mitchell, Paul
Hoh, Josephine
Francis, Peter J.
Klein, Michael L.
Chew, Emily Y.
Chakravarti, Aravinda
TI Mitochondrial DNA Variants of Respiratory Complex I that Uniquely
Characterize Haplogroup T2 Are Associated with Increased Risk of
Age-Related Macular Degeneration
SO PLOS ONE
LA English
DT Article
AB Background: Age-related macular degeneration (AMD), a chronic neurodegenerative and neovascular retinal disease, is the leading cause of blindness in elderly people of western European origin. While structural and functional alterations in mitochondria (mt) and their metabolites have been implicated in the pathogenesis of chronic neurodegenerative and vascular diseases, the relationship of inherited variants in the mitochondrial genome and mt haplogroup subtypes with advanced AMD has not been reported in large prospective cohorts.
Methodology/Prinicipal Findings: We examined the relationship of inherited mtDNA variants with advanced AMD in 1168 people using a three-stage design on samples from 12-year and 10-year prospective studies on the natural history of age-related eye disease. In Stage I we resequenced the entire genome in 99 elderly AMD-free controls and 215 people with advanced AMD from the 12-year study. A consistent association with AMD in 14 of 17 SNPs characterizing the mtDNA T haplogroup emerged. Further analysis revealed these associations were driven entirely by the T2 haplogroup, and characterized by two variants in Complex I genes (A11812G of MT-ND4 and A14233G of MT-ND6). We genotyped T haplogroups in an independent sample of 490 cases and 61 controls from the same study (Stage II) and in 56 cases and 246 controls from the 10-year study (Stage III). People in the T2 haplogroup were approximately 2.5 times more likely to have advanced AMD than their peers (odds ratio [OR] = 2.54, 95%CI 1.36-4.80, P <= 0.004) after considering the totality of evidence. Findings persisted after considering the impact of AMD-associated variants A69S and Y402H (OR = 5.19, 95%CI 1.19-22.69, P <= 0.029).
Conclusion: Loci defining the mtDNA T2 haplogroup and Complex I are reasonable targets for novel functional analyses and therapeutic research in AMD.
RP SanGiovanni, JP (reprint author), NEI, NIH, Bethesda, MD 20892 USA.
EM jpsangio@post.harvard.edu
RI Wang, Jie Jin/P-1499-2014; Mitchell, Paul/P-1498-2014
OI Wang, Jie Jin/0000-0001-9491-4898;
FU Intramural NIH HHS [Z99 EY999999, ZIA EY000489-01]; NEI NIH HHS
[01-EY-0-2127, EY015810, R01 EY012203, R01 EY015771, R01 EY015810,
R01-EY12203, R01EY015771]
NR 30
TC 46
Z9 48
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 12
PY 2009
VL 4
IS 5
AR e5508
DI 10.1371/journal.pone.0005508
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 444VZ
UT WOS:000266009800006
PM 19434233
ER
PT J
AU Lou, H
Yeager, M
Li, HC
Bosquet, JG
Hayes, RB
Orr, N
Yu, K
Hutchinson, A
Jacobs, KB
Kraft, P
Wacholder, S
Chatterjee, N
Feigelson, HS
Thun, MJ
Diver, WR
Albanes, D
Virtamo, J
Weinstein, S
Ma, J
Gaziano, JM
Stampfer, M
Schumacher, FR
Giovannucci, E
Cancel-Tassin, G
Cussenot, O
Valeri, A
Andriole, GL
Crawford, ED
Anderson, SK
Tucker, M
Hoover, RN
Fraumeni, JF
Thomas, G
Hunter, DJ
Dean, M
Chanock, SJ
AF Lou, Hong
Yeager, Meredith
Li, Hongchuan
Bosquet, Jesus Gonzalez
Hayes, Richard B.
Orr, Nick
Yu, Kai
Hutchinson, Amy
Jacobs, Kevin B.
Kraft, Peter
Wacholder, Sholom
Chatterjee, Nilanjan
Feigelson, Heather Spencer
Thun, Michael J.
Diver, W. Ryan
Albanes, Demetrius
Virtamo, Jarmo
Weinstein, Stephanie
Ma, Jing
Gaziano, J. Michael
Stampfer, Meir
Schumacher, Fredrick R.
Giovannucci, Edward
Cancel-Tassin, Geraldine
Cussenot, Olivier
Valeri, Antoine
Andriole, Gerald L.
Crawford, E. David
Anderson, Stephen K.
Tucker, Margaret
Hoover, Robert N.
Fraumeni, Joseph F., Jr.
Thomas, Gilles
Hunter, David J.
Dean, Michael
Chanock, Stephen J.
TI Fine mapping and functional analysis of a common variant in MSMB on
chromosome 10q11.2 associated with prostate cancer susceptibility
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE genome-wide association studies; prostate cancer genetics; CREB
transcription factor
ID GENOME-WIDE ASSOCIATION; RADICAL PROSTATECTOMY; RISK LOCUS; PROTEIN;
EXPRESSION; 8Q24; POLYMORPHISMS; EPIDEMIOLOGY; SEQUENCE; DISEASE
AB Two recent genome-wide association studies have independently identified a prostate cancer susceptibility locus on chromosome 10q11.2. The most significant single-nucleotide polymorphism (SNP) marker reported, rs10993994, is 57 bp centromeric of the first exon of the MSMB gene, which encodes beta-microseminoprotein (prostatic secretory protein 94). In this study, a fine-mapping analysis using HapMap SNPs was conducted across a approximate to 65-kb region (chr10: 51168330-51234020) flanking rs10993994 with 13 tag SNPs in 6,118 prostate cancer cases and 6,105 controls of European origin from the Cancer Genetic Markers of Susceptibility (CGEMS) project. rs10993994 remained the most strongly associated marker with prostate cancer risk [P = 8.8 x 10(-18); heterozygous odds ratio (OR) = 1.20, 95% confidence interval (CI): 1.11-1.30; homozygous OR = 1.64, 95% CI: 1.47-1.86 for the adjusted genotype test with 2 df]. In follow-up functional analyses, the T variant of rs10993994 significantly affected expression of in vitro luciferase reporter constructs. In electrophoretic mobility shift assays, the C allele of rs10993994 preferentially binds to the CREB transcription factor. Analysis of tumor cell lines with a CC or CT genotype revealed a high level of MSMB gene expression compared with cell lines with a TT genotype. These findings were specific to the alleles of rs10993994 and were not observed for other SNPs determined by sequence analysis of the proximal promoter. Together, our mapping study and functional analyses implicate regulation of expression of MSMB as a plausible mechanism accounting for the association identified at this locus. Further investigation is warranted to determine whether rs10993994 alone or in combination with additional variants contributes to prostate cancer susceptibility.
C1 [Yeager, Meredith; Bosquet, Jesus Gonzalez; Hayes, Richard B.; Orr, Nick; Yu, Kai; Hutchinson, Amy; Wacholder, Sholom; Chatterjee, Nilanjan; Albanes, Demetrius; Weinstein, Stephanie; Tucker, Margaret; Hoover, Robert N.; Fraumeni, Joseph F., Jr.; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Lou, Hong; Li, Hongchuan; Anderson, Stephen K.; Dean, Michael] NCI, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Lou, Hong; Yeager, Meredith; Hutchinson, Amy] NCI, Core Genotyping Facil, Adv Technol Program, Sci Applicat Int Corp Frederick Inc, Frederick, MD 21702 USA.
[Jacobs, Kevin B.; Thomas, Gilles] Bioinformed Consulting Serv, Gaithersburg, MD 20877 USA.
[Kraft, Peter; Schumacher, Fredrick R.; Hunter, David J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Feigelson, Heather Spencer; Thun, Michael J.; Diver, W. Ryan] Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30303 USA.
[Ma, Jing; Stampfer, Meir; Schumacher, Fredrick R.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, FIN-00300 Helsinki, Finland.
[Gaziano, J. Michael] Harvard Univ, Sch Med, Channing Lab, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Giovannucci, Edward] Harvard Univ, Sch Med, Div Aging, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Cancel-Tassin, Geraldine; Cussenot, Olivier; Valeri, Antoine] Hop Tenon, AP HP, Ctr Rech Pathol Prostat, F-75970 Paris, France.
[Andriole, Gerald L.] Washington Univ, Sch Med, Div Urol Surg, St Louis, MO 63108 USA.
[Crawford, E. David] Univ Colorado Denver & Hlth Sci Ctr, Dept Surg, Denver, CO 80204 USA.
RP Fraumeni, JF (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM fraumenj@mail.nih.gov
RI Anderson, Stephen/B-1727-2012; Dean, Michael/G-8172-2012; Tucker,
Margaret/B-4297-2015; Albanes, Demetrius/B-9749-2015;
OI Anderson, Stephen/0000-0002-7856-4266; Dean,
Michael/0000-0003-2234-0631; Hayes, Richard/0000-0002-0918-661X;
Cancel-Tassin, Geraldine/0000-0002-9583-6382
FU NCI NIH HHS [R01 CA097193]
NR 27
TC 61
Z9 64
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 12
PY 2009
VL 106
IS 19
BP 7933
EP 7938
DI 10.1073/pnas.0902104106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 447RG
UT WOS:000266208900047
PM 19383797
ER
PT J
AU Robbins, JB
Kubler-Kielb, J
Vinogradov, E
Mocca, C
Pozsgay, V
Shiloach, J
Schneerson, R
AF Robbins, John B.
Kubler-Kielb, Joanna
Vinogradov, Evguenii
Mocca, Christopher
Pozsgay, Vince
Shiloach, Joseph
Schneerson, Rachel
TI Synthesis, characterization, and immunogenicity in mice of Shigella
sonnei O-specific oligosaccharide-core-protein conjugates
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE lipopolysaccharide; glycoconjugate; vaccine; Kdo; IgG
ID DYSENTERIAE TYPE-1; FLEXNERI TYPE-2A; POLYSACCHARIDE;
LIPOPOLYSACCHARIDES; ANTIBODIES; VACCINES; CHILDREN
AB Shigellosis, an enteric disease, is on the World Health Organization's priority prevention list. In one study, the Shigella sonnei O-specific polysaccharide (O-SP)-protein conjugate showed 72% protection against disease in Israeli army recruits exposed to high rates (8-14%) of infection. The protection was related to vaccine-induced IgG anti-O-SP levels. Synthetic oligosaccharides of Shigella dysenteriae type 1, bound by their reducing ends to a carrier protein ("sun''-type configuration), induced significantly higher antibody levels than the native O-SP bound to protein by multiple-point attachments ("lattice''-type configuration). Attempts to synthesize the S. sonnei O-SP based oligosaccharides were not successful. Here, we describe the isolation, characterization, and conjugation of low-molecular-mass O-SP-core (O-SPC) fragments. The O-SPC fragments were bound by their reducing ends similar to the preparation of the synthetic S. dysenteriae type 1 conjugates. The O-SPC conjugates used oxime linkages between the terminal Kdo residues at the reducing ends of the S. sonnei saccharides and aminooxy linkers bound to BSA or a recombinant diphtheria toxin. The coupling reaction was carried out at a neutral pH and room temperature. IgG antibody levels induced in young outbred mice by the S. sonnei O-SPC conjugates were significantly higher then those elicited by the O-SP conjugates. Accordingly, we propose to evaluate clinically these conjugates.
C1 [Robbins, John B.; Kubler-Kielb, Joanna; Mocca, Christopher; Pozsgay, Vince; Schneerson, Rachel] NICHHD, NIH, Bethesda, MD 20892 USA.
[Vinogradov, Evguenii] Natl Res Council Canada, Inst Biol Sci, Ottawa, ON K1A 0R6, Canada.
[Shiloach, Joseph] NIAID, NIH, Bethesda, MD 20892 USA.
RP Robbins, JB (reprint author), NICHHD, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM robbinsjo@mail.nih.gov
FU National Institutes of Health; National Institute of Child Health and
Human Development
FX We thank Dr. Vince Pozsgay (National Institutes of Health, Bethesda, MD)
for providing the O-(3- thiopropyl) hydroxylamine linker, Dr. Joseph
Shiloach (National Institutes of Health, Bethesda, MD) for providing
rDT; Dr. Bruce Coxon for assessing sample purities by NMR; Chunyan Guo
for technical assistance; and Dr. Arthur Karpas for statistical analyses
and manuscript review. This work was supported by the Intramural
Research Program of the National Institutes of Health, National
Institute of Child Health and Human Development.
NR 21
TC 36
Z9 36
U1 0
U2 8
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 12
PY 2009
VL 106
IS 19
BP 7974
EP 7978
DI 10.1073/pnas.0900891106
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 447RG
UT WOS:000266208900054
PM 19346477
ER
PT J
AU Nishimura, Y
Sadjadpour, R
Mattapallil, JJ
Igarashi, T
Lee, W
Buckler-White, A
Roederer, M
Chun, TW
Martin, MA
AF Nishimura, Yoshiaki
Sadjadpour, Reza
Mattapallil, Joseph J.
Igarashi, Tatsuhiko
Lee, Wendy
Buckler-White, Alicia
Roederer, Mario
Chun, Tae-Wook
Martin, Malcolm A.
TI High frequencies of resting CD4(+) T cells containing integrated viral
DNA are found in rhesus macaques during acute lentivirus infections
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE HIV; integration; simian immunodeficiency virus; simian/human
immunodeficiency virus
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; HIV-1
INFECTION; TYPE-1 DNA; REVERSE TRANSCRIPTION; GENE-EXPRESSION;
LYMPHOID-TISSUE; REPLICATION; LYMPHOCYTES; MEMORY
AB We and others have reported that the vast majority of virus-producing CD4(+) T cells during the acute infection of rhesus macaques with simian immunodeficiency virus (SIV) or CXCR4 (X4)-using simian/human immunodeficiency viruses (SHIVs) exhibited a nonactivated phenotype. These findings have been extended to show that resting CD4(+) T lymphocytes collected from SIV-or X4-SHIV-infected animals during the first 10 days of infection continue to release virus ex vivo. Furthermore, we observed high frequencies of integrated viral DNA (up to 5.1 x 104 DNA copies per 105 cells) in circulating resting CD4(+) T cells during the first 10 days of the infection. Integration of SIV DNA was detected only in memory CD4(+) T cells and SHIVs preferentially integrated into resting naive CD4(+) T cells. Taken together, these results show that during the acute infection large numbers of resting CD4(+) T cells carry integrated nonhuman primate lentiviral DNA and are the major source of progeny virions irrespective of coreceptor usage. Prompt and sustained interventions are therefore required to block the rapid systemic dissemination of virus and prevent an otherwise fatal clinical outcome.
C1 [Nishimura, Yoshiaki; Sadjadpour, Reza; Igarashi, Tatsuhiko; Lee, Wendy; Buckler-White, Alicia; Martin, Malcolm A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Mattapallil, Joseph J.; Roederer, Mario] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Chun, Tae-Wook] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Martin, MA (reprint author), NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
EM malm@nih.gov
FU National Institute of Allergy and Infectious Diseases; National
Institutes of Health
FX We thank Rahel Petros, Joseph Mckennan, Dhirenkumar Patel, and Dr. Boris
Skopets for diligently assisting in the care and maintenance of our
animals; Robin Kruthers and Ranjini Iyengar for determining viral RNA
levels; Charles Buckler for arranging and scheduling animal experiments;
and Ronald C. Desrosiers (Harvard Medical School, Boston) for providing
molecular clones of SIVmac239 and SIVmac316. This
work was supported by the Intramural Research Program of the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health.
NR 39
TC 20
Z9 20
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 12
PY 2009
VL 106
IS 19
BP 8015
EP 8020
DI 10.1073/pnas.0903022106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 447RG
UT WOS:000266208900061
PM 19416840
ER
PT J
AU Wright, JT
Probstfield, JL
Cushman, WC
Pressel, SL
Cutler, JA
Davis, BR
Einhorn, PT
Rahman, M
Whelton, PK
Ford, CE
Haywood, LJ
Margolis, KL
Oparil, S
Black, HR
Alderman, MH
AF Wright, Jackson T., Jr.
Probstfield, Jeffrey L.
Cushman, William C.
Pressel, Sara L.
Cutler, Jeffrey A.
Davis, Barry R.
Einhorn, Paula T.
Rahman, Mahboob
Whelton, Paul K.
Ford, Charles E.
Haywood, L. Julian
Margolis, Karen L.
Oparil, Suzanne
Black, Henry R.
Alderman, Michael H.
CA ALLHAT Collaborative Res Grp
TI ALLHAT Findings Revisited in the Context of Subsequent Analyses, Other
Trials, and Meta-analyses
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID LIPID-LOWERING TREATMENT; HEART-ATTACK TRIAL;
CONVERTING-ENZYME-INHIBITOR; CALCIUM-CHANNEL BLOCKER;
PROSPECTIVELY-DESIGNED OVERVIEWS; ISOLATED SYSTOLIC HYPERTENSION;
BLOOD-PRESSURE REDUCTION; ANTIHYPERTENSIVE DRUG-TREATMENT; MAJOR
CARDIOVASCULAR EVENTS; HIGH-RISK PATIENTS
AB The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is reevaluated considering information from new clinical trials, meta-analyses, and recent subgroup and explanatory analyses from ALLHAT, especially those regarding heart failure (HF) and the association of drug treatment with new-onset diabetes mellitus (DM) and its cardiovascular disease (CVD) consequences. Chlorthalidone was superior to (1) doxazosin mesylate in preventing combined CVD (CCVD)(risk ratio [RR], 1.20; 95% confidence interval [CI], 1.13-1.27), especially HF (RR, 1.80; 95% CI, 1.40-2.22) and stroke (RR, 1.26; 95% CI, 1.10-1.46); ( 2) lisinopril in preventing CCVD (RR, 1.10; 95% CI, 1.05-1.16), including stroke ( in black persons only) and HF (RR, 1.20; 95% CI, 1.09-1.34); and ( 3) amlodipine besylate in preventing HF, overall (by 28%) and in hospitalized or fatal cases (by 26%). Central independent blinded reassessment of HF hospitalizations confirmed each comparison. Results were consistent by age, sex, race ( except for stroke and CCVD), DM status, metabolic syndrome status, and renal function level. Neither amlodipine nor lisinopril was superior to chlorthalidone in preventing end-stage renal disease overall, by DM status, or by renal function level. In the chlorthalidone arm, new-onset DM was not significantly associated with CCVD (RR, 0.96; 95% CI, 0.88-2.42). Evidence from subsequent analyses of ALLHAT and other clinical outcome trials confirm that neither alpha-blockers, angiotensin-converting enzyme inhibitors, nor calcium channel blockers surpass thiazide-type diuretics (at appropriate dosage) as initial therapy for reduction of cardiovascular or renal risk. Thiazides are superior in preventing HF, and new-onset DM associated with thiazides does not increase CVD outcomes. Arch Intern Med. 2009;169(9):832-842
C1 [Wright, Jackson T., Jr.; Rahman, Mahboob] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Probstfield, Jeffrey L.] Univ Washington, Clin Trial Serv Unit, Seattle, WA 98195 USA.
[Cushman, William C.] Vet Affairs Med Ctr, Memphis, TN USA.
[Pressel, Sara L.] Univ Texas Houston Hlth Sci Ctr, Sch Publ Hlth, Allhat Clin Trials Ctr, Houston, TX 77030 USA.
[Cutler, Jeffrey A.; Einhorn, Paula T.] NHLBI, Bethesda, MD 20892 USA.
[Whelton, Paul K.] Loyola Univ, Med Ctr & Hlth Syst, Maywood, IL 60153 USA.
[Haywood, L. Julian] Univ So Calif, Med Ctr, Los Angeles, CA USA.
[Margolis, Karen L.] Hlth Partners Res Fdn, Minneapolis, MN USA.
[Oparil, Suzanne] Univ Alabama Birmingham, Birmingham, AL USA.
[Black, Henry R.] NYU, Sch Med, New York, NY 10003 USA.
[Alderman, Michael H.] Albert Einstein Coll Med, Dept Epidemiol & Social Med, Bronx, NY 10467 USA.
RP Pressel, SL (reprint author), Univ Texas Houston Hlth Sci Ctr, Sch Publ Hlth, Allhat Clin Trials Ctr, 1200 Herman Pressler St,Ste 801, Houston, TX 77030 USA.
EM Sara.L.Pressel@uth.tmc.edu
FU NHLBI NIH HHS [N01 HC 35130, N01 HC035130, N01HC35130]
NR 62
TC 56
Z9 57
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
EI 1538-3679
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD MAY 11
PY 2009
VL 169
IS 9
BP 832
EP 842
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 444PX
UT WOS:000265994000003
PM 19433694
ER
PT J
AU Cherkin, DC
Sherman, KJ
Avins, AL
Erro, JH
Ichikawa, L
Barlow, WE
Delaney, K
Hawkes, R
Hamilton, L
Pressman, A
Khalsa, PS
Deyo, RA
AF Cherkin, Daniel C.
Sherman, Karen J.
Avins, Andrew L.
Erro, Janet H.
Ichikawa, Laura
Barlow, William E.
Delaney, Kristin
Hawkes, Rene
Hamilton, Luisa
Pressman, Alice
Khalsa, Partap S.
Deyo, Richard A.
TI A Randomized Trial Comparing Acupuncture, Simulated Acupuncture, and
Usual Care for Chronic Low Back Pain
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article; Proceedings Paper
CT 9th International Forum for Primary Care Research on Low Back Pain
CY OCT 06, 2007
CL Mallorca, SPAIN
ID EXPENDITURES; PATTERNS; EFFICACY; OUTCOMES
AB Background: Acupuncture is a popular complementary and alternative treatment for chronic back pain. Recent European trials suggest similar short-term benefits from real and sham acupuncture needling. This trial addresses the importance of needle placement and skin penetration in eliciting acupuncture effects for patients with chronic low back pain.
Methods: A total of 638 adults with chronic mechanical low back pain were randomized to individualized acupuncture, standardized acupuncture, simulated acupuncture, or usual care. Ten treatments were provided over 7 weeks by experienced acupuncturists. The primary outcomes were back-related dysfunction (Roland-Morris Disability Questionnaire score; range, 0-23) and symptom bothersomeness (0-10 scale). Outcomes were assessed at baseline and after 8, 26, and 52 weeks.
Results: At 8 weeks, mean dysfunction scores for the individualized, standardized, and simulated acupuncture groups improved by 4.4, 4.5, and 4.4 points, respectively, compared with 2.1 points for those receiving usual care (P < .001). Participants receiving real or simulated acupuncture were more likely than those receiving usual care to experience clinically meaningful improvements on the dysfunction scale (60% vs 39%; P < .001). Symptoms improved by 1.6 to 1.9 points in the treatment groups compared with 0.7 points in the usual care group (P < .001). After 1 year, participants in the treatment groups were more likely than those receiving usual care to experience clinically meaningful improvements in dysfunction (59% to 65% vs 50%, respectively; P=.02) but not in symptoms (P > .05).
Conclusions: Although acupuncture was found effective for chronic low back pain, tailoring needling sites to each patient and penetration of the skin appear to be unimportant in eliciting therapeutic benefits. These findings raise questions about acupuncture's purported mechanisms of action. It remains unclear whether acupuncture or our simulated method of acupuncture provide physiologically important stimulation or represent placebo or nonspecific effects.
C1 [Cherkin, Daniel C.; Sherman, Karen J.; Erro, Janet H.; Ichikawa, Laura; Barlow, William E.; Delaney, Kristin; Hawkes, Rene] Ctr Hlth Studies, Seattle, WA 98101 USA.
[Avins, Andrew L.; Hamilton, Luisa; Pressman, Alice] No Calif Kaiser Permanente, Div Res, Oakland, CA USA.
[Barlow, William E.] Canc Res & Biostat, Seattle, WA USA.
[Khalsa, Partap S.] Natl Ctr Complementary & Alternat Med, Div Extramural Res & Training, NIH, Bethesda, MD USA.
[Deyo, Richard A.] Oregon Hlth & Sci Univ, Dept Family Med, Portland, OR 97201 USA.
RP Cherkin, DC (reprint author), Ctr Hlth Studies, 1730 Minor Ave,Ste 1600, Seattle, WA 98101 USA.
EM cherkin.d@ghc.org
FU Intramural NIH HHS [Z99 AT999999]; NCCIH NIH HHS [U01 AT 001110, U01
AT001110, U01 AT001110-01A1]
NR 39
TC 178
Z9 190
U1 4
U2 28
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
EI 1538-3679
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD MAY 11
PY 2009
VL 169
IS 9
BP 858
EP 866
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 444PX
UT WOS:000265994000006
PM 19433697
ER
PT J
AU Chakraborty, T
Perlot, T
Subrahmanyam, R
Jani, A
Goff, PH
Zhang, Y
Ivanova, I
Alt, FW
Sen, R
AF Chakraborty, Tirtha
Perlot, Thomas
Subrahmanyam, Ramesh
Jani, Anant
Goff, Peter H.
Zhang, Yu
Ivanova, Irina
Alt, Frederick W.
Sen, Ranjan
TI A 220-nucleotide deletion of the intronic enhancer reveals an epigenetic
hierarchy in immunoglobulin heavy chain locus activation
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID BETA-GLOBIN LOCUS; RECEPTOR-GENE REARRANGEMENT; MOUSE IGH LOCUS; HISTONE
ACETYLATION; CONTROL REGION; V(D)J RECOMBINATION; CORE REGION;
CHROMATIN; METHYLATION; MU
AB A tissue-specific transcriptional enhancer, E mu, has been implicated in developmentally regulated recombination and transcription of the immunoglobulin heavy chain (IgH) gene locus. We demonstrate that deleting 220 nucleotides that constitute the core E. results in partially active locus, characterized by reduced histone acetylation, chromatin remodeling, transcription, and recombination, whereas other hallmarks of tissue-specific locus activation, such as loss of H3K9 dimethylation or gain of H3K4 dimethylation, are less affected. These observations define E mu-independent and E mu-dependent phases of locus activation that reveal an unappreciated epigenetic hierarchy in tissue-specific gene expression.
C1 [Chakraborty, Tirtha; Subrahmanyam, Ramesh; Ivanova, Irina; Sen, Ranjan] NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA.
[Jani, Anant] Yale Univ, Sch Med, Program Immunol, New Haven, CT 06510 USA.
[Perlot, Thomas] Univ Vienna, A-1010 Vienna, Austria.
[Perlot, Thomas; Goff, Peter H.; Zhang, Yu; Alt, Frederick W.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Perlot, Thomas; Goff, Peter H.; Zhang, Yu; Alt, Frederick W.] Childrens Hosp, Howard Hughes Med Inst, Immune Dis Inst, Boston, MA 02115 USA.
RP Sen, R (reprint author), NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA.
EM rs465z@nih.gov
RI Subrahmanyam, Ramesh/K-5503-2012
FU National Institutes of Health [AI2047]; Intramural Research Program of
the National Institute on Aging (Baltimore, MD)
FX T. Perlot is supported by a Boehringer Ingelheim Fonds PhD scholarship.
F. W. Alt is an investigator of the Howard Hughes Medical Institute.
This work was supported by National Institutes of Health grant AI2047
(to F. W. Alt) and by the Intramural Research Program of the National
Institute on Aging (Baltimore, MD). The authors have no conflicting
financial interests.
NR 35
TC 30
Z9 31
U1 0
U2 3
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD MAY 11
PY 2009
VL 206
IS 5
BP 1019
EP 1027
DI 10.1084/jem.20081621
PG 9
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 444WB
UT WOS:000266010000009
PM 19414554
ER
PT J
AU Keele, BF
Li, H
Learn, GH
Hraber, P
Giorgi, EE
Grayson, T
Sun, CX
Chen, YL
Yeh, WW
Letvin, NL
Mascola, JR
Nabel, GJ
Haynes, BF
Bhattacharya, T
Perelson, AS
Korber, BT
Hahn, BH
Shaw, GM
AF Keele, Brandon F.
Li, Hui
Learn, Gerald H.
Hraber, Peter
Giorgi, Elena E.
Grayson, Truman
Sun, Chuanxi
Chen, Yalu
Yeh, Wendy W.
Letvin, Norman L.
Mascola, John R.
Nabel, Gary J.
Haynes, Barton F.
Bhattacharya, Tanmoy
Perelson, Alan S.
Korber, Bette T.
Hahn, Beatrice H.
Shaw, George M.
TI Low-dose rectal inoculation of rhesus macaques by SIVsmE660 or SIVmac251
recapitulates human mucosal infection by HIV-1
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; T-CELL DEPLETION; GASTROINTESTINAL-TRACT;
HETEROSEXUAL TRANSMISSION; TYPE-1 TRANSMISSION; NONHUMAN-PRIMATES; VIRAL
LOAD; MULTIPLE; SIV; DIVERSITY
AB We recently developed a novel strategy to identify transmitted HIV-1 genomes in acutely infected humans using single-genome amplification and a model of random virus evolution. Here, we used this approach to determine the molecular features of simian immunodeficiency virus (SIV) transmission in 18 experimentally infected Indian rhesus macaques. Animals were inoculated intrarectally (i.r.) or intravenously (i.v.) with stocks of SIVmac251 or SIVsmE660 that exhibited sequence diversity typical of early-chronic HIV-1 infection. 987 full-length SIV env sequences ( median of 48 per animal) were determined from plasma virion RNA 1-5 wk after infection. i.r. inoculation was followed by productive infection by one or a few viruses (median 1; range 1-5) that diversified randomly with near starlike phylogeny and a Poisson distribution of mutations. Consensus viral sequences from ramp-up and peak viremia were identical to viruses found in the inocula or differed from them by only one or a few nucleotides, providing direct evidence that early plasma viral sequences coalesce to transmitted/founder viruses. i.v. infection was >2,000-fold more efficient than i.r. infection, and viruses transmitted by either route represented the full genetic spectra of the inocula. These findings identify key similarities in mucosal transmission and early diversification between SIV and HIV-1, and thus validate the SIV-macaque mucosal infection model for HIV-1 vaccine and microbicide research.
C1 [Keele, Brandon F.; Li, Hui; Learn, Gerald H.; Grayson, Truman; Sun, Chuanxi; Chen, Yalu; Hahn, Beatrice H.; Shaw, George M.] Univ Alabama, Birmingham, AL 35223 USA.
[Hraber, Peter; Giorgi, Elena E.; Bhattacharya, Tanmoy; Perelson, Alan S.; Korber, Bette T.] Los Alamos Natl Lab, Los Alamos, NM 87545 USA.
[Bhattacharya, Tanmoy; Korber, Bette T.] Santa Fe Inst, Santa Fe, NM 87501 USA.
[Giorgi, Elena E.] Univ Massachusetts, Amherst, MA 01002 USA.
[Haynes, Barton F.] Duke Univ, Med Ctr, Durham, NC 27710 USA.
[Letvin, Norman L.; Mascola, John R.; Nabel, Gary J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Yeh, Wendy W.; Letvin, Norman L.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Viral Pathogenesis,Dept Med, Boston, MA 02115 USA.
RP Shaw, GM (reprint author), Univ Alabama, Birmingham, AL 35223 USA.
EM gshaw@uab.edu
RI Bhattacharya, Tanmoy/J-8956-2013;
OI Bhattacharya, Tanmoy/0000-0002-1060-652X; Korber,
Bette/0000-0002-2026-5757; Hraber, Peter/0000-0002-2920-4897
FU Center for HIV/AIDS Vaccine Immunology; National Institutes of Health
[AI67854, AI27767]; Bill and Melinda Gates Foundation [37874]; American
Foundation for AIDS Research [106997-3]
FX This work was supported by the Center for HIV/AIDS Vaccine Immunology
and by grants from the National Institutes of Health (AI67854 and
AI27767), the Bill and Melinda Gates Foundation (# 37874), and the
American Foundation for AIDS Research (106997-3).
NR 66
TC 200
Z9 200
U1 1
U2 12
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD MAY 11
PY 2009
VL 206
IS 5
BP 1117
EP 1134
DI 10.1084/jem.20082831
PG 18
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 444WB
UT WOS:000266010000017
PM 19414559
ER
PT J
AU Robison, LL
Armstrong, GT
Boice, JD
Chow, EJ
Davies, SM
Donaldson, SS
Green, DM
Hammond, S
Meadows, AT
Mertens, AC
Mulvihill, JJ
Nathan, PC
Neglia, JP
Packer, RJ
Rajaraman, P
Sklar, CA
Stovall, M
Strong, LC
Yasui, Y
Zeltzer, LK
AF Robison, Leslie L.
Armstrong, Gregory T.
Boice, John D.
Chow, Eric J.
Davies, Stella M.
Donaldson, Sarah S.
Green, Daniel M.
Hammond, Sue
Meadows, Anna T.
Mertens, Ann C.
Mulvihill, John J.
Nathan, Paul C.
Neglia, Joseph P.
Packer, Roger J.
Rajaraman, Preetha
Sklar, Charles A.
Stovall, Marilyn
Strong, Louise C.
Yasui, Yutaka
Zeltzer, Lonnie K.
TI The Childhood Cancer Survivor Study: A National Cancer
Institute-Supported Resource for Outcome and Intervention Research
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 43rd Annual Meeting of the American-Society-of-Clinical-Oncology
CY JUN 01-05, 2007
CL Chicago, IL
SP Amer Soc Clin Oncol
ID LONG-TERM SURVIVORS; ACUTE LYMPHOBLASTIC-LEUKEMIA; QUALITY-OF-LIFE;
BODY-MASS-INDEX; ADULT SURVIVORS; ADOLESCENT CANCER; 5-YEAR SURVIVORS;
GROWTH-HORMONE; HODGKINS-DISEASE; HEALTH-CARE
AB Survival for childhood cancer has increased dramatically over the last 40 years with 5-year survival rates now approaching 80%. For many diagnostic groups, rapid increases in survival began in the 1970s with the broader introduction of multimodality approaches, often including combination chemotherapy with or without radiation therapy. With this increase in rates of survivorship has come the recognition that survivors are at risk for adverse health and quality-of-life outcomes, with risk being influenced by host-, disease-, and treatment-related factors. In 1994, the US National Cancer Institute funded the Childhood Cancer Survivor Study, a multi-institutional research initiative designed to establish a large and extensively characterized cohort of more than 14,000 5-year survivors of childhood and adolescent cancer diagnosed between 1970 and 1986. This ongoing study, which reflects the single most comprehensive body of information ever assembled on childhood and adolescent cancer survivors, provides a dynamic framework and resource to investigate current and future questions about childhood cancer survivors.
C1 [Robison, Leslie L.] St Jude Childrens Hosp, Dept Epidemiol & Canc Control, Memphis, TN 38105 USA.
Natl Canc Inst, Int Epidemiol Inst, Div Canc Epidemiol & Genet, Rockville, MD USA.
Univ Washington, Dept Pediat, Seattle, WA 98195 USA.
Cincinnati Childrens Hosp, Med Ctr, Dept Pediat, Cincinnati, OH USA.
OH State Univ, Sch Med, Dept Pathol, Columbus, OH USA.
Stanford Univ, Med Ctr, Dept Radiat Oncol, Stanford, CA 94305 USA.
Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA.
Emory Univ, Dept Pediat, Atlanta, GA 30322 USA.
Univ Oklahoma, Hlth Sci Ctr, Dept Pediat, Oklahoma City, OK 73190 USA.
Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA.
Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA.
Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
Univ Texas MD Anderson Canc Ctr, Dept Canc Genet, Houston, TX 77030 USA.
Hosp Sick Children, Div Haematol Oncol, Toronto, ON M5G 1X8, Canada.
Univ Alberta, Sch Publ Hlth, Dept Publ Hlth Sci, Edmonton, AB, Canada.
RP Robison, LL (reprint author), St Jude Childrens Hosp, Dept Epidemiol & Canc Control, 262 Danny Thomas Pl,Mail Stop 735, Memphis, TN 38105 USA.
EM les.robison@stjude.org
RI Yasui, Yutaka/E-2564-2015
OI Yasui, Yutaka/0000-0002-7717-8638
FU NCI NIH HHS [U24 CA055727, U24 CA 55727]
NR 103
TC 242
Z9 244
U1 2
U2 12
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 10
PY 2009
VL 27
IS 14
BP 2308
EP 2318
DI 10.1200/JCO.2009.22.3339
PG 11
WC Oncology
SC Oncology
GA 447MM
UT WOS:000266195200002
PM 19364948
ER
PT J
AU Meadows, AT
Friedman, DL
Neglia, JP
Mertens, AC
Donaldson, SS
Stovall, M
Hammond, S
Yasui, Y
Inskip, PD
AF Meadows, Anna T.
Friedman, Debra L.
Neglia, Joseph P.
Mertens, Ann C.
Donaldson, Sarah S.
Stovall, Marilyn
Hammond, Sue
Yasui, Yutaka
Inskip, Peter D.
TI Second Neoplasms in Survivors of Childhood Cancer: Findings From the
Childhood Cancer Survivor Study Cohort
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 43rd Annual Meeting of the American-Society-of-Clinical-Oncology
CY JUN 01-05, 2007
CL Chicago, IL
SP Amer Soc Clin Oncol
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; MALIGNANT NEOPLASMS; FOLLOW-UP; 5-YEAR
SURVIVORS; NONMELANOMA SKIN; HODGKIN-DISEASE; THYROID-CANCER;
BREAST-CANCER; RISK; CHILDREN
AB Purpose To review the reports of subsequent neoplasms (SNs) in the Childhood Cancer Survivor Study (CCSS) cohort that were made through January 1, 2006, and published before July 31, 2008, and to discuss the host-, disease-, and therapy-related risk factors associated with SNs.
Patients and Methods SNs were ascertained by survivor self-reports and subsequently confirmed by pathology findings or medical record review. Cumulative incidence of SNs and standardized incidence ratios for second malignant neoplasms (SMNs) were calculated. The impact of host-, disease-, and therapy-related risk factors was evaluated by Poisson regression.
Results Among 14,358 cohort members, 730 reported 802 SMNs (excluding nonmelanoma skin cancers). This represents a 2.3-fold increase in the number of SMNs over that reported in the first comprehensive analysis of SMNs in the CCSS cohort, which was done 7 years ago. In addition, 66 cases of meningioma and 1,007 cases of nonmelanoma skin cancer were diagnosed. The 30-year cumulative incidence of SMNs was 9.3% and that of nonmelanoma skin cancer was 6.9%. Risk of SNs remains elevated for more than 20 years of follow-up for all primary childhood cancer diagnoses. In multivariate analyses, risks differ by SN subtype, but include radiotherapy, age at diagnosis, sex, family history of cancer, and primary childhood cancer diagnosis. Female survivors whose primary childhood cancer diagnosis was Hodgkin's lymphoma or sarcoma and who received radiotherapy are at particularly increased risk. Analyses of risk associated with radiotherapy demonstrated different dose-response curves for specific SNs.
Conclusion Childhood cancer survivors are at a substantial and increasing risk for SNs, including nonmelanoma skin cancer and meningiomas. Health care professionals should understand the magnitude of these risks to provide individuals with appropriate counseling and follow-up.
C1 [Meadows, Anna T.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
Vanderbilt Univ, Nashville, TN USA.
Univ Minnesota, Minneapolis, MN USA.
Emory Univ, Atlanta, GA 30322 USA.
Stanford Univ, Stanford, CA 94305 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Hammond Univ Alberta, Edmonton, AB, Canada.
Natl Canc Inst, Rockville, MD USA.
RP Meadows, AT (reprint author), Childrens Hosp Philadelphia, 34th St & Civic Ctr Blvd, Philadelphia, PA 19104 USA.
EM meadows@chop.edu
RI Yasui, Yutaka/E-2564-2015
OI Yasui, Yutaka/0000-0002-7717-8638
FU NCI NIH HHS [U24 CA055727, U24 CA55727]
NR 35
TC 202
Z9 203
U1 3
U2 15
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 10
PY 2009
VL 27
IS 14
BP 2356
EP 2362
DI 10.1200/JCO.2008.21.1920
PG 7
WC Oncology
SC Oncology
GA 447MM
UT WOS:000266195200006
PM 19255307
ER
PT J
AU Davis, KL
Gray, ES
Moore, PL
Decker, JM
Salomon, A
Montefiori, DC
Graham, BS
Keefer, MC
Pinter, A
Morris, L
Hahn, BH
Shaw, GM
AF Davis, Katie L.
Gray, Elin S.
Moore, Penny L.
Decker, Julie M.
Salomon, Aidy
Montefiori, David C.
Graham, Barney S.
Keefer, Michael C.
Pinter, Abraham
Morris, Lynn
Hahn, Beatrice H.
Shaw, George M.
TI High titer HIV-1 V3-specific antibodies with broad reactivity but low
neutralizing potency in acute infection and following vaccination
SO VIROLOGY
LA English
DT Article
DE HIV-1; HIV-2; Variable loop 3; Neutralizing antibodies; Acute HIV-1
infection
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SUBTYPE-C INFECTION;
MONOCLONAL-ANTIBODIES; TYPE-1 ENVELOPE; CLADE-A; GP120; DOMAINS;
RESPONSES; EPITOPES; SEQUENCE
AB Identifying the earliest neutralizing antibody specificities that are elicited following infection or vaccination by HIV-1 is an important objective of current HIV/AIDS vaccine research. We have shown previously that transplantation of HIV-1 V3 epitopes into an HIV-2 envelope (Env) scaffold provides a sensitive and specific means to detect and quantify HIV-1 V3 epitope specific neutralizing antibodies (Nabs) in human sera. Here, we employ this HIV-2/HIV-1 V3 scaffolding strategy to study the kinetics of development and breadth of V3-specific Nabs in longitudinal sera from individuals acutely infected with clade C or clade B HIV-1 and in human Subjects immunized with clade B HIV-1 immunogens. HIV-2/HIV-1 chimeras containing V3 sequences matched to virus type (HIV-2 or HIV-1), subtype (clade B or C), or strain (autologous or heterologous) were used as test reagents. We found that by 3-8 weeks post infection, 12 of 14 clade C subjects had a median IC(50) V3-specific Nab titer of 1:700 against chimeric viruses containing a heterologous clade C V3. By 5 months post-infection, all 14 subjects were positive for V3-specific Nabs with median titers of 1:8000 against heterologous clade C V3 and 1:1300 against clade B V3. Two acutely infected clade B patients developed heterologous clade B V3-specific Nabs at titers of 1:300 and 1:1800 by 13 weeks of infection and 1:5000 and 1:11000 by 7 months of infection. Titers were not different against chimeras containing autologous clade B V3 sequences. Each of 10 uninfected normal human volunteers who were immunized with clade B HIV-1 Env immunogens, but none of five sham immunized control subjects, developed V3-specific Nabs titers as high as 1:3000 (median 1: 1300; range 1:700-1:3000). None of the HIV-1 infected or vaccinated subjects had antibodies that neutralized primary HIV-1 virus strains. These results indicate that high-titer, broadly reactive V3-specific antibodies are among the first to be elicited during acute and early HIV-1 infection and following vaccination but these antibodies lack neutralizing potency against primary HIV-1 viruses, which effectively shield V3 from antibody binding to the functional Env trimer. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Decker, Julie M.; Hahn, Beatrice H.; Shaw, George M.] Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
[Davis, Katie L.; Hahn, Beatrice H.; Shaw, George M.] Univ Alabama, Dept Microbiol, Birmingham, AL 35294 USA.
[Gray, Elin S.; Moore, Penny L.; Morris, Lynn] Natl Inst Communicable Dis, AIDS Virus Res Unit, Johannesburg, South Africa.
[Salomon, Aidy; Pinter, Abraham] Publ Hlth Res Inst, Newark, NJ 07103 USA.
[Salomon, Aidy; Pinter, Abraham] Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA.
[Montefiori, David C.] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
[Montefiori, David C.] Duke Univ, Med Ctr, Duke Human Vaccine Inst, Durham, NC 27710 USA.
[Graham, Barney S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Keefer, Michael C.] Univ Rochester, Sch Med & Dent, Rochester, NY 14642 USA.
RP Shaw, GM (reprint author), Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
EM gshaw@uab.edu
OI Moore, Penny/0000-0001-8719-4028; , Lynn/0000-0003-3961-7828; Gray,
Elin/0000-0002-8613-3570
FU Bill and Melinda Gates Foundation [37874, 38619, 38631]; NIH [AI 67854,
AI 27767, AI 46238, U01 AI-46747]
FX we thank the CAPRISA leadership, S. S. Abdool Karim, K. Mlisana, and C.
Williamson, as well as the clinical and laboratory staff at CAPRISA for
serum specimens; L. Corey and J. McElrath for providing HVTN Protocol
203 serum specimens; S. Meleth and H. Kuo for statistical analysis; D.
Edwards for technical assistance; and the clinical and sequencing cores
of the UAB Center for AIDS Research. This work served as partial
fulfillment of the requirements for the Ph. D. degree for K.L. Davis and
was supported by grants from the Bill and Melinda Gates Foundation
(#37874, #38619, #38631) and the NIH (AI 67854, AI 27767, AI 46238, and
U01 AI-46747).
NR 42
TC 50
Z9 50
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD MAY 10
PY 2009
VL 387
IS 2
BP 414
EP 426
DI 10.1016/j.virol.2009.02.022
PG 13
WC Virology
SC Virology
GA 439YF
UT WOS:000265663100020
PM 19298995
ER
PT J
AU Shannon, JG
Cockrell, DC
Takahashi, K
Stahl, GL
Heinzen, RA
AF Shannon, Jeffrey G.
Cockrell, Diane C.
Takahashi, Kazue
Stahl, Gregory L.
Heinzen, Robert A.
TI Antibody-mediated immunity to the obligate intracellular bacterial
pathogen Coxiella burnetii is Fc receptor- and complement-independent
SO BMC IMMUNOLOGY
LA English
DT Article
ID Q-FEVER; RELAPSING FEVER; DENDRITIC CELLS; DEFICIENT MICE; INFECTION;
MACROPHAGES; CLEARANCE; LIPOPOLYSACCHARIDE; MECHANISMS; GENERATION
AB Background: The obligate intracellular bacterial pathogen Coxiella burnetii causes the zoonosis Q fever. The intracellular niche of C. burnetii has led to the assumption that cell-mediated immunity is the most important immune component for protection against this pathogen. However, passive immunization with immune serum can protect naive animals from challenge with virulent C. burnetii, indicating a role for antibody (Ab) in protection. The mechanism of this Ab-mediated protection is unknown. Therefore, we conducted a study to determine whether Fc receptors (FcR) or complement contribute to Ab-mediated immunity (AMI) to C. burnetii.
Results: Virulent C. burnetii infects and replicates within human dendritic cells (DC) without inducing their maturation or activation. We investigated the effects of Ab opsonized C. burnetii on human monocyte-derived and murine bone marrow-derived DC. Infection of DC with Ab-opsonized C. burnetii resulted in increased expression of maturation markers and inflammatory cytokine production. Bacteria that had been incubated with naive serum had minimal effect on DC, similar to virulent C. burnetii alone. The effect of Ab opsonized C. burnetii on DC was FcR dependent as evidenced by a reduced response of DC from FcR knockout (FcR k/o) compared to C57Bl/6 (B6) mice. To address the potential role of FcR in Ab-mediated protection in vivo, we compared the response of passively immunized FcR k/o mice to the B6 controls. Interestingly, we found that FcR are not essential for AMI to C. burnetii in vivo. We subsequently examined the role of complement in AMI by passively immunizing and challenging several different strains of complement-deficient mice and found that AMI to C. burnetii is also complement-independent.
Conclusion: Despite our data showing FcR-dependent stimulation of DC in vitro, Ab-mediated immunity to C. burnetii in vivo is FcR-independent. We also found that passive immunity to this pathogen is independent of complement.
C1 [Shannon, Jeffrey G.; Cockrell, Diane C.; Heinzen, Robert A.] NIAID, Rocky Mt Labs, Intracellular Parasites Lab, NIH,Coxiella Pathogenesis Sect, Hamilton, MT 59840 USA.
[Stahl, Gregory L.] Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, Dept Anesthesiol Perioperat & Pain Med,Sch Med, Boston, MA 02115 USA.
[Takahashi, Kazue] Harvard Univ, Sch Med, Massachusetts Gen Hosp Children, Lab Dev Immunol, Boston, MA USA.
RP Heinzen, RA (reprint author), NIAID, Rocky Mt Labs, Intracellular Parasites Lab, NIH,Coxiella Pathogenesis Sect, Hamilton, MT 59840 USA.
EM jshannon@niaid.nih.gov; dcockrell@niaid.nih.gov;
ktakahashi1@partners.org; gstahl@zeus.bwh.harvard.edu;
rheinzen@niaid.nih.gov
RI Shannon, Jeffrey/A-5735-2009
OI Shannon, Jeffrey/0000-0003-4211-4308
FU Intramural Research Program of the National Institutes of Health
[AI052343, HL56068, HL52886, DE016191, DE017821]; National Institute of
Allergy and Infectious Diseases
FX We thank Shelly Robertson and Harlan Caldwell for critical review of the
manuscript and Gary Hettrick and Anita Mora for graphic illustrations.
This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases (J.G.S., D.C.C, and R.A.H.), NIH grant AI052343
(K.T.), and NIH grants HL56068, HL52886, DE016191 and DE017821 (G.A.S.).
NR 35
TC 19
Z9 20
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2172
J9 BMC IMMUNOL
JI BMC Immunol.
PD MAY 8
PY 2009
VL 10
AR 26
DI 10.1186/1471-2172-10-26
PG 8
WC Immunology
SC Immunology
GA 454PP
UT WOS:000266695000002
PM 19426498
ER
PT J
AU Duncan, CG
Leary, RJ
Lin, JCH
Cummins, J
Di, CH
Schaefer, CF
Wang, TL
Riggins, GJ
Edwards, J
Bigner, D
Kopelovich, L
Vogelstein, B
Kinzler, KW
Velculescu, VE
Yan, H
AF Duncan, Christopher G.
Leary, Rebecca J.
Lin, Jimmy Cheng-Ho
Cummins, Jordan
Di, Chunhui
Schaefer, Carl F.
Wang, Tian-Li
Riggins, Gregory J.
Edwards, Jennifer
Bigner, Darell
Kopelovich, Levy
Vogelstein, Bert
Kinzler, Kenneth W.
Velculescu, Victor E.
Yan, Hai
TI Identification of microbial DNA in human cancer
SO BMC MEDICAL GENOMICS
LA English
DT Article
ID UNRECOGNIZED PATHOGENS; SEARCH; SEQUENCES; TRANSCRIPTOME; SUBTRACTION;
CARCINOMA; DATABASE; GENOMES; TUMOR
AB Background: Microorganisms have been associated with many types of human diseases; however, a significant number of clinically important microbial pathogens remain to be discovered.
Methods: We have developed a genome-wide approach, called Digital Karyotyping Microbe Identification (DK-MICROBE), to identify genomic DNA of bacteria and viruses in human disease tissues. This method involves the generation of an experimental DNA tag library through Digital Karyotyping (DK) followed by analysis of the tag sequences for the presence of microbial DNA content using a compiled microbial DNA virtual tag library.
Results: To validate this technology and to identify pathogens that may be associated with human cancer pathogenesis, we used DK-MICROBE to determine the presence of microbial DNA in 58 human tumor samples, including brain, ovarian, and colorectal cancers. We detected DNA from Human herpesvirus 6 (HHV-6) in a DK library of a colorectal cancer liver metastasis and in normal tissue from the same patient.
Conclusion: DK-MICROBE can identify previously unknown infectious agents in human tumors, and is now available for further applications for the identification of pathogen DNA in human cancer and other diseases.
C1 [Duncan, Christopher G.; Di, Chunhui; Bigner, Darell; Yan, Hai] Duke Univ, Med Ctr, Preston Robert Tisch Brain Tumor Ctr, Dept Pathol,Pediat Brain Tumor Fdn Inst, Durham, NC 27710 USA.
[Leary, Rebecca J.; Lin, Jimmy Cheng-Ho; Cummins, Jordan; Wang, Tian-Li; Vogelstein, Bert; Kinzler, Kenneth W.; Velculescu, Victor E.] Johns Hopkins Kimmel Canc Ctr, Ludwig Ctr Canc Genet & Therapeut, Baltimore, MD 21231 USA.
[Leary, Rebecca J.; Lin, Jimmy Cheng-Ho; Cummins, Jordan; Wang, Tian-Li; Vogelstein, Bert; Kinzler, Kenneth W.; Velculescu, Victor E.] Johns Hopkins Kimmel Canc Ctr, Howard Hughes Med Inst, Baltimore, MD 21231 USA.
[Schaefer, Carl F.] NCI, Ctr Biomed Informat & Informat Technol, Rockville, MD 20852 USA.
[Riggins, Gregory J.; Edwards, Jennifer] Johns Hopkins Univ, Sch Med, Dept Neurosurg, Baltimore, MD 21231 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Yan, H (reprint author), Duke Univ, Med Ctr, Preston Robert Tisch Brain Tumor Ctr, Dept Pathol,Pediat Brain Tumor Fdn Inst, Durham, NC 27710 USA.
EM chris.duncan@duke.edu; rleary1@jhmi.edu; jimmy.lin@jhmi.edu;
jordanmcummins@gmail.com; di.chunhui@duke.edu; schaefec@mail.nih.gov;
tlw@welch.jhu.edu; griggin1@jhmi.edu; jennifer.b.edwards@gmail.com;
bigne001@mc.duke.edu; kopelovl@mail.nih.gov; bertvog@gmail.com;
kinzlke@jhmi.edu; velculescu@jhmi.edu; hai.yan@duke.edu
FU Pediatric Brain Tumor Foundation Institute at Duke; Damon Runyon
Foundation Scholar Award; Southeastern Brain Tumor Foundation Research
Grant; Alex's Lemonade Stand Foundation Innovation Award; V Foundation
Cancer Research; NIH [R01CA118822, R01CA121113, NS20023-21, NS052507,
R37CA11898-34, R37 CA 011898-38]; Brain Tumor Specialized Programs of
Research Excellence [5P20CA096890-02]; Duke Comprehensive Cancer Center
[2P30CA14236]; Accelerate Brain Tumor Cure Foundation; National Cancer
Center, NINDS [5P50 NS20023-25]; NIH SPORE [5P50 CA108786-4]; NCI
[HHSN261200433002C]; Pew Charitable Trusts
FX This work was supported by The Pediatric Brain Tumor Foundation
Institute at Duke; a Damon Runyon Foundation Scholar Award; a
Southeastern Brain Tumor Foundation Research Grant; an Alex's Lemonade
Stand Foundation Innovation Award; a V Foundation Cancer Research Grant;
NIH Grants R01CA118822, R01CA121113, NS20023-21, NS052507 and
R37CA11898-34; Brain Tumor Specialized Programs of Research Excellence
5P20CA096890-02; Duke Comprehensive Cancer Center Support Grant
2P30CA14236; and grants from the Accelerate Brain Tumor Cure Foundation
and the National Cancer Center, NINDS Grant 5P50 NS20023-25, NIH SPORE
Grant 5P50 CA108786-4, NIH Merit Award R37 CA 011898-38, NCI Division of
Cancer Prevention contract HHSN261200433002C, and The Pew Charitable
Trusts.
NR 34
TC 13
Z9 15
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1755-8794
J9 BMC MED GENOMICS
JI BMC Med. Genomics
PD MAY 8
PY 2009
VL 2
AR 22
DI 10.1186/1755-8794-2-22
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 532VD
UT WOS:000272777300001
PM 19426505
ER
PT J
AU Wolf, R
Voscopoulos, C
Winston, J
Dharamsi, A
Goldsmith, P
Gunsior, M
Vonderhaar, BK
Olson, M
Watson, PH
Yuspa, SH
AF Wolf, Ronald
Voscopoulos, Christopher
Winston, Jason
Dharamsi, Alif
Goldsmith, Paul
Gunsior, Michele
Vonderhaar, Barbara K.
Olson, Melanie
Watson, Peter H.
Yuspa, Stuart H.
TI Highly homologous hS100A15 and hS100A7 proteins are distinctly expressed
in normal breast tissue and breast cancer
SO CANCER LETTERS
LA English
DT Article
DE Mammary cancer; Calcium binding proteins; S100; Psoriasis; Myoepithelial
cells
ID PSORIASIN S100A7 EXPRESSION; MESSENGER-RNA; IN-SITU; PROGRESSION; SKIN;
CARCINOMA; RECEPTOR; CELLS; JAB1
AB Human S100A7 (psoriasin) is considered a marker for specific stages of breast cancer. hS100A15 is almost identical to hS100A7 and difficult to discriminate. We developed specific probes to distinguish hS100A7 and hS100A15, and demonstrate their differential distribution in normal breast tissue. Further, hS100A7 and S100A15 transcripts are elevated in ER/PR negative breast cancers, but hS100A15 protein is detected in all cancer specimens while hS100A7 protein is sporadically expressed. The differential regulation, expression and distribution of hS100A7 and hS100A15 and their reported distinct functions are compelling reasons to discriminate among these proteins in normal breast and breast cancers. Published by Elsevier Ireland Ltd.
C1 [Wolf, Ronald; Voscopoulos, Christopher; Winston, Jason; Dharamsi, Alif; Yuspa, Stuart H.] NCI, NIH, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
[Goldsmith, Paul; Gunsior, Michele] NCI, NIH, Antibody & Prot Purificat Unit, Ctr Canc Res, Bethesda, MD 20892 USA.
[Vonderhaar, Barbara K.] NCI, NIH, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Olson, Melanie; Watson, Peter H.] BC Canc Agcy, Deeley Res Ctr, Victoria, BC, Canada.
RP Yuspa, SH (reprint author), NCI, NIH, Lab Canc Biol & Genet, Ctr Canc Res, 37 Convent Dr,MSC 4255,Bldg 37,Room 4068A, Bethesda, MD 20892 USA.
EM yuspas@mail.nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research; German
Research Foundation (DFG); Emmy-Noether Program [Wo 843/2-1]
FX We thank Dr. Akira Oshima for histological evaluation. This research was
supported in part by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research. Ronald Wolf is
funded by the German Research Foundation (DFG), Emmy-Noether Program (Wo
843/2-1).
NR 20
TC 24
Z9 24
U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD MAY 8
PY 2009
VL 277
IS 1
BP 101
EP 107
DI 10.1016/j.canlet.2008.11.032
PG 7
WC Oncology
SC Oncology
GA 432DT
UT WOS:000265114400012
PM 19136201
ER
PT J
AU Son, MJ
Woolard, K
Nam, DH
Lee, J
Fine, HA
AF Son, Myung Jin
Woolard, Kevin
Nam, Do-Hyun
Lee, Jeongwu
Fine, Howard A.
TI SSEA-1 Is an Enrichment Marker for Tumor-Initiating Cells in Human
Glioblastoma
SO CELL STEM CELL
LA English
DT Article
ID CANCER STEM-CELLS; NERVOUS-SYSTEM; PROGENITOR CELLS; CD133; BRAIN;
PROTEIN; GLIOMA; IDENTIFICATION; ANTIGEN; GROWTH
AB CD133+ populations of human glioblastoma multi-forme (GBM) cells are reportedly enriched for tumor stem cells (TSCs) or tumor-initiating cells (TICs). Approximately 40% of freshly isolated GBM specimens, however, do not contain CD133+ tumor cells, raising the possibility that CD133 may not be a universal enrichment marker for GBM TSCs/TiCs. Here we demonstrate that stage-specific embryonic antigen 1(SSEA-1/LeX)+ GBM cells fulfill the functional criteria for TSC/TIC, since (1) SSEA-1+ cells are highly tumorigenic in vivo, unlike SSEA-1-cells; (2) SSEA-1+ cells can give rise to both SSEA-1+ and SSEA-1-cells, thereby establishing a cellular hierarchy; and (3) SSEA-1+ cells have self-renewal and multilineage differentiation potentials. A distinct subpopulation of SSEA-1+ cells was present in all but one of the primary GBMsexamined (n = 24), and most CD133+ tumor cells were also SSEA-1+, suggesting that SSEA-1 may be a general TSC/TIC enrichment marker in human GBMs.
C1 [Son, Myung Jin; Woolard, Kevin; Lee, Jeongwu; Fine, Howard A.] NCI, Neurooncol Branch, NINDS, NIH, Bethesda, MD 20892 USA.
[Nam, Do-Hyun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Neurosurg, Seoul 135710, South Korea.
RP Lee, J (reprint author), NCI, Neurooncol Branch, NINDS, NIH, Bethesda, MD 20892 USA.
EM leejeo@mail.nih.gov; hfine@mail.nih.gov
RI Nam, Do Hyun/C-9656-2011
FU Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research; NINDS FACS Facility; NINDS Light Imaging
Facility
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. We thank Dr.
Dragan Maric (NINDS FACS Facility) for his valuable contributions to
this work. We also thank Dr. Carolyn Smith (NINDS Light Imaging
Facility) and Dr. Hong Sug Kim for their valuable contributions to this
work.
NR 53
TC 313
Z9 319
U1 3
U2 22
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1934-5909
J9 CELL STEM CELL
JI Cell Stem Cell
PD MAY 8
PY 2009
VL 4
IS 5
BP 440
EP 452
DI 10.1016/j.stem.2009.03.003
PG 13
WC Cell & Tissue Engineering; Cell Biology
SC Cell Biology
GA 445SF
UT WOS:000266071100012
PM 19427293
ER
PT J
AU Hanover, JA
Love, DC
Prinz, WA
AF Hanover, John A.
Love, Dona C.
Prinz, William A.
TI Calmodulin-driven Nuclear Entry: Trigger for Sex Determination and
Terminal Differentiation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Review
ID HELIX TRANSCRIPTION FACTORS; TRANSPORT IN-VIVO; PROTEIN IMPORT;
LOCALIZATION SIGNALS; CALCIUM/CALMODULIN INHIBITION; NUCLEOCYTOPLASMIC
TRANSPORT; REVERSING MUTATIONS; CALCIUM REGULATION; FACTOR SEF2-1/E2-2;
BINDING-PROTEIN
AB We originally proposed that Ca(2+)-calmodulin mediates a novel nuclear entry pathway distinct from the canonic Ran-dependent pathway (Sweitzer, T. D., and Hanover, J. A. (1996) Proc. Natl. Acad. Sci. U. S. A. 93, 14574-14579). Although seemingly redundant, Ca(2+)-calmodulin-driven nuclear entry is now known to facilitate nuclear delivery of architectural transcription factors to chromatin. Intriguingly, defects in calmodulin-driven nuclear import of the transcription factors SRY and SOX9 in Sertoli cells lead to human sex reversal diseases with altered male gonad development. Calmodulin-triggered nuclear entry is an evolutionarily ancient feature of eukaryotes observed from yeast to man. Ca(2+)-calmodulin-triggered nuclear entry of key architectural transcription factors is a potentially key epigenetic regulator of terminal differentiation in response to cell signaling.
C1 [Hanover, John A.; Love, Dona C.; Prinz, William A.] NIDDK, Lab Cell Biochem & Biol, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Hanover, JA (reprint author), NIDDK, Lab Cell Biochem & Biol, Natl Inst Hlth, Bethesda, MD 20892 USA.
EM jah@helix.nih.gov
NR 63
TC 25
Z9 25
U1 1
U2 6
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 8
PY 2009
VL 284
IS 19
BP 12593
EP 12597
DI 10.1074/jbc.R800076200
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 440GH
UT WOS:000265688300002
PM 19126540
ER
PT J
AU Salgado, MT
Nagababu, E
Rifkind, JM
AF Salgado, Maria T.
Nagababu, Enika
Rifkind, Joseph M.
TI Quantification of Intermediates Formed during the Reduction of Nitrite
by Deoxyhemoglobin
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID S-NITROSOHEMOGLOBIN; HUMAN CIRCULATION; VASCULAR CONTROL; RED-CELL;
OXIDE; HEMOGLOBIN; MECHANISM; BLOOD; NO; NITROSYLATION
AB Nitric oxide (NO) plays a crucial role in human physiology by regulating vascular tone and blood flow. The short life-span of NO in blood requires a mechanism to retain NO bioactivity in the circulation. Recent studies have suggested a mechanism involving the reduction of nitrite back to NO by deoxyhemoglobin in RBCs. A role for RBCs in transporting NO must, however, bypass the scavenging of NO in RBCs by hemoglobin. To understand how the nitrite reaction can deliver bioactive NO to the vasculature, we have studied the intermediates formed during the reaction. A reliable measure of the total concentration of heme-associated nitrite/NO intermediates formed was provided by combining filtration to measure free nitrite by chemiluminescence and electron paramagnetic resonance to measure the final product Hb(II)NO. By modifying the chemiluminescence method used to detect NO, we have been able to identify two intermediates: 1) a heme-associated nitrite complex that is released as NO in acid solution in the presence of ascorbate and 2) an intermediate that releases NO at neutral pH in the presence of ferricyanide when reacted with an Fe(III) ligand like azide. This species designated as "Hb(II)NO(+)reversible arrow Hb(III)NO" has properties of both isomeric forms resulting in a slower NO dissociation rate and much higher stability than Hb(III)NO, but provides a potential source for bioactive NO, which can be released from the RBC. This detailed analysis of the nitrite reaction with deoxyHb provides important insights into the mechanism for nitrite induced vasodilation by RBCs.
C1 [Salgado, Maria T.; Nagababu, Enika; Rifkind, Joseph M.] NIA, Mol Dynam Sect, Natl Inst Hlth, Baltimore, MD 21224 USA.
RP Rifkind, JM (reprint author), 251 Bayview Blvd,Rm 05B129, Baltimore, MD 21224 USA.
EM rifkindj@mail.nih.gov
FU National Institutes of Health NIA Intramural Research Program
FX This work was supported, in whole or in part, by the National Institutes
of Health NIA Intramural Research Program.
NR 31
TC 30
Z9 30
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 8
PY 2009
VL 284
IS 19
BP 12710
EP 12718
DI 10.1074/jbc.M808647200
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 440GH
UT WOS:000265688300015
PM 19270306
ER
PT J
AU Panchal, RG
Ulrich, RL
Bradfute, SB
Lane, D
Ruthel, G
Kenny, TA
Iversen, PL
Anderson, AO
Gussio, R
Raschke, WC
Bavari, S
AF Panchal, Rekha G.
Ulrich, Ricky L.
Bradfute, Steven B.
Lane, Douglas
Ruthel, Gordon
Kenny, Tara A.
Iversen, Patrick L.
Anderson, Arthur O.
Gussio, Rick
Raschke, William C.
Bavari, Sina
TI Reduced Expression of CD45 Protein-tyrosine Phosphatase Provides
Protection against Anthrax Pathogenesis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; LETHAL TOXIN; BACTERIAL PATHOGENS; SIGNALING
PATHWAYS; DENDRITIC CELLS; HUMAN-DISEASE; MACROPHAGES; INHIBITORS;
SPORES; KINASE
AB The modulation of cellular processes by small molecule inhibitors, gene inactivation, or targeted knockdown strategies combined with phenotypic screens are powerful approaches to delineate complex cellular pathways and to identify key players involved in disease pathogenesis. Using chemical genetic screening, we tested a library of known phosphatase inhibitors and identified several compounds that protected Bacillus anthracis infected macrophages from cell death. The most potent compound was assayed against a panel of sixteen different phosphatases of which CD45 was found to be most sensitive to inhibition. Testing of a known CD45 inhibitor and antisense phosphorodiamidate morpholino oligomers targeting CD45 also protected B. anthracis-infected macrophages from cell death. However, reduced CD45 expression did not protect anthrax lethal toxin ( LT) treated macrophages, suggesting that the pathogen and independently added LT may signal through distinct pathways. Subsequent, in vivo studies with both gene-targeted knockdown of CD45 and genetically engineered mice expressing reduced levels of CD45 resulted in protection of mice after infection with the virulent Ames B. anthracis. Intermediate levels of CD45 expression were critical for the protection, as mice expressing normal levels of CD45 or disrupted CD45 phosphatase activity or no CD45 all succumbed to this pathogen. Mechanism-based studies suggest that the protection provided by reduced CD45 levels results from regulated immune cell homeostasis that may diminish the impact of apoptosis during the infection. To date, this is the first report demonstrating that reduced levels of host phosphatase CD45 modulate anthrax pathogenesis.
C1 [Panchal, Rekha G.; Ulrich, Ricky L.; Bradfute, Steven B.; Ruthel, Gordon; Anderson, Arthur O.; Bavari, Sina] USA, Med Res Inst Infect Dis, Ft Detrick, MD 21702 USA.
[Lane, Douglas; Kenny, Tara A.] NCI, NIH, Target Struct Based Drug Discovery Grp, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Iversen, Patrick L.] AVI BioPharma Inc, Corvallis, OR 97333 USA.
[Gussio, Rick] NCI, NIH, Target Struct Based Drug Discovery Grp, Informat Technol Branch,Dev Therapeut Program, Frederick, MD 21702 USA.
[Raschke, William C.] Sidney Kimmel Canc Ctr, San Diego, CA 92121 USA.
[Raschke, William C.] Virogenics Inc, Del Mar, CA 92014 USA.
RP Panchal, RG (reprint author), USA, Med Res Inst Infect Dis, 1425 Porter St, Ft Detrick, MD 21702 USA.
EM rekha.panchal@amedd.army.mil; sina.bavari@amedd.army.mil
FU National Institutes of Health [N01-CO-12400, R43 A1055102]; Defense
Threat Reduction Agency; NIAID; Developmental Therapeutics Program;
Division of Cancer Treatment and Diagnosis of the NCI
FX This work was supported, in whole or in part, by National Institutes of
Health Grant N01-CO-12400, by the Defense Threat Reduction Agency (to S.
B. and R. G. P.), the NIAID, National Institutes of Health Grant R43
A1055102 (to W. C. R.), and by the Developmental Therapeutics Program in
the Division of Cancer Treatment and Diagnosis of the NCI, National
Institutes of Health.
NR 56
TC 19
Z9 19
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 8
PY 2009
VL 284
IS 19
BP 12874
EP 12885
DI 10.1074/jbc.M809633200
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 440GH
UT WOS:000265688300033
PM 19269962
ER
PT J
AU Qiu, ZJ
Dyer, KD
Xie, ZH
Radinger, M
Rosenberg, HF
AF Qiu, Zhijun
Dyer, Kimberly D.
Xie, Zhihui
Radinger, Madeleine
Rosenberg, Helene F.
TI GATA Transcription Factors Regulate the Expression of the Human
Eosinophil-derived Neurotoxin (RNase 2) Gene
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LEUKEMIA-CELL LINE; INTRONIC ENHANCER; CATIONIC PROTEIN; RIBONUCLEASE
GENES; RNS2 GENE; PROMOTER; FAMILY; DIFFERENTIATION; EVOLUTION; SEQUENCE
AB The transcription factors GATA-1 and GATA-2 have been implicated in promoting differentiation of eosinophilic leukocytes. In this study, we examined the roles of GATA-1 and GATA-2 in activating transcription of the secretory ribonuclease, the eosinophil- derived neurotoxin (EDN/RNase 2). Augmented expression of both GATA-1 and GATA-2 was detected in eosinophil promyelocyte HL-60 clone 15 cells in response to biochemical differentiation with butyric acid. Deletion or mutation of one or both of the two consensus GATA-binding sites in the extended 1000-bp 5' promoter of the EDN gene resulted in profound reduction in reporter gene activity. Antibody-augmented electrophoretic mobility shift and chromatin immunoprecipitation analyses indicate that GATA-1 and GATA-2 proteins bind to both functional GATA consensus sequences in the EDN promoter. Interestingly, RNA silencing of GATA-1 alone had no impact on EDN expression; silencing of GATA-2 resulted in diminished expression of EDN, and also diminished expression of GATA-1 in both butyric acid-induced HL-60 clone 15 cells and in differentiating human eosinophils derived from CD34(+) hematopoietic progenitors. Likewise, overexpression of GATA-2 in uninduced HL-60 clone 15 cells resulted in augmented transcription of both EDN and GATA-1. Taken together, our data suggest that GATA-2 functions directly via interactions with the EDN promoter and also indirectly, via its ability to regulate the expression of GATA-1 in differentiating eosinophils and eosinophil cell lines.
C1 [Qiu, Zhijun; Dyer, Kimberly D.; Xie, Zhihui; Radinger, Madeleine; Rosenberg, Helene F.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
RP Rosenberg, HF (reprint author), NIAID, Lab Allerg Dis, NIH, Bldg 10,Rm 11C215,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM hrosenberg@niaid.nih.gov
FU National Institutes of Health [AI00941, AI00942]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants AI00941 and AI00942 NIAID (Division of Intramural
Research).
NR 49
TC 13
Z9 14
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 8
PY 2009
VL 284
IS 19
BP 13099
EP 13109
DI 10.1074/jbc.M807307200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 440GH
UT WOS:000265688300057
PM 19279013
ER
PT J
AU Weisz, A
Mazzola, EP
Ito, Y
AF Weisz, Adrian
Mazzola, Eugene P.
Ito, Yoichiro
TI Preparative separation of di- and trisulfonated components of Quinoline
Yellow using affinity-ligand pH-zone-refining counter-current
chromatography
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article; Proceedings Paper
CT 5th International Conference on Countercurrent Chromatography
CY JUL 26-29, 2008
CL Rio de Janeiro, BRAZIL
DE Counter-current chromatography; pH-zone-refining CCC; Quinoline Yellow;
D&C Yellow No. 10; Sulfonic acids; Disulfonic acids; Trisulfonic acid;
Isomers; Ligand; Dyes; NMR
ID TANDEM MASS-SPECTROMETRY; ACIDS; PURIFICATION
AB Four positionally isomeric 2-(2-quinolinyl)-1H-indene-1,3(2H)-dionedisulfonic acids (SA) and one triSA, components of the color additive Quinoline Yellow (QY, Color Index No. 47005), were isolated from the dye mixture by affinity-ligand pH-zone-refining counter-current chromatography (CCC) through complementary use of ion-exchange and ion-pair reagents as the ligand. The added ligands facilitated the partitioning oft lie very polar polysulfonated components into the organic stationary phase of the two-phase solvent systems that consisted of isoamyl alcohol-methyl tert-butyl ether-acetonitrile-water (3:5:1 :7).(3:4: 1:7) or (3:11:5). Thus. separation of a 5-g portion Of QY using Sulfuric acid as the retainer and dodecylanime as the ligand (an ion-exchange reagent, 20% in the stationary phase), resulted in 1.21 g of 6',5-diSA and 1.69 g of 6',8',5-triSA, both of over 99% purity. A minor component, 8',4-diSA, not previously reported was also obtained (4.8 mg of over 94% purity) through a similar separation of a different batch Of QY using hydrochloric acid as the retainer and 10% dodecylamine as the ligand in the stationary phase. Two components that co-eluted (0.55 g) in the 5 g separation were separated when trifluoroacetic acid was used as the retainer and tetrabutylammonium hydroxide (an ion-pair reagent) as the ligand. The separation resulted in 20.7 mg of 6',4-diSA, not previously reported, and 111.8 mg of 8'.5-diSA, both of over 98% purity. The isolated Compounds were characterized by high-resolution mass spectrometry and proton nuclear magnetic resonance with correlated spectroscopy assignments. Published by Elsevier B.V.
C1 [Weisz, Adrian] US FDA, Off Cosmet & Colors, Ctr Food Safety & Appl Nutr, College Pk, MD 20740 USA.
[Mazzola, Eugene P.] US FDA, Off Regulatory Sci, Ctr Food Safety & Appl Nutr, College Pk, MD 20740 USA.
[Ito, Yoichiro] NHLBI, Bioseparat Technol Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Weisz, A (reprint author), US FDA, Off Cosmet & Colors, Ctr Food Safety & Appl Nutr, College Pk, MD 20740 USA.
EM adrian.weisz@fda.hhs.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 26
TC 18
Z9 20
U1 5
U2 24
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD MAY 8
PY 2009
VL 1216
IS 19
BP 4161
EP 4168
DI 10.1016/j.chroma.2009.02.064
PG 8
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 444BU
UT WOS:000265955900005
PM 19281993
ER
PT J
AU Ito, Y
Clary, R
Powell, J
Knight, M
Finn, TM
AF Ito, Y.
Clary, R.
Powell, J.
Knight, M.
Finn, T. M.
TI Improved spiral tube assembly for high-speed counter-current
chromatography
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article; Proceedings Paper
CT 5th International Conference on Countercurrent Chromatography
CY JUL 26-29, 2008
CL Rio de Janeiro, BRAZIL
DE Spiral tube support assembly; High-speed counter-current chromatography;
Separation of proteins and peptides; Polymer phase system (TPAS)
AB The original spiral tube support (STS) assembly is improved by changing the shape of the tubing, with I cm presses perpendicularly along the length. This modification interrupts the laminar flow of the mobile phase. The tubing in the four return grooves to the center of the rotor is flattened by a specially made pressing tool to increase the number of spiral layers and decrease the dead space Volume, thus increasing the column efficiency. The performance of this spiral tube assembly was tested in separations of dipeptides and proteins with Suitable polar two-phase solvent systems. The results revealed that the present system yields high partition efficiency with a satisfactory level of stationary phase retention in a short elution time. The present high-speed counter-current chromatographic (HSCCC) system will be efficiently applied to a broad spectrum of two-phase solvent systems including aqueous-aqueous polymer phase systems (TPAS) which are used for separation of biopolymers such as proteins and nucleic acids. Published by Elsevier B.V.
C1 [Ito, Y.] NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
[Knight, M.; Finn, T. M.] CC Biotech LLC, Rockville, MD 20850 USA.
RP Ito, Y (reprint author), NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, 10 Ctr Dr,Bldg 10,Room 8N230, Bethesda, MD 20892 USA.
EM itoy2@mail.nih.gov
OI Knight, Martha/0000-0003-4863-8858
FU Intramural NIH HHS [Z99 HL999999]
NR 7
TC 26
Z9 26
U1 1
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD MAY 8
PY 2009
VL 1216
IS 19
BP 4193
EP 4200
DI 10.1016/j.chroma.2008.10.126
PG 8
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 444BU
UT WOS:000265955900010
PM 19062024
ER
PT J
AU Baldermann, S
Fleischmann, P
Bolten, M
Watanabe, N
Winterhalter, P
Ito, Y
AF Baldermann, Susanne
Fleischmann, Peter
Bolten, Mareike
Watanabe, Naoharu
Winterhalter, Peter
Ito, Yoichiro
TI Centrifugal precipitation chromatography, a powerful technique for the
isolation of active enzymes from tea leaves (Camellia sinensis)
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article; Proceedings Paper
CT 5th International Conference on Countercurrent Chromatography
CY JUL 26-29, 2008
CL Rio de Janeiro, BRAZIL
DE Centrifugal precipitation chromatography; CCD; Carotenoid cleavage; Tea;
Camellia sinensis
ID CAROTENOID CLEAVAGE DIOXYGENASE; FUNCTIONAL-CHARACTERIZATION;
AMMONIUM-SULFATE; FRACTIONATION; IDENTIFICATION; PIGMENTS
AB Centrifugal precipitation chromatography was developed approximately 10 years ago. In contrast to other counter-current chromatographic techniques, the centrifugal precipitation chromatography system is operated With two Mutually miscible Solutions separated by a cut-off membrane. Centrifugal precipitation chromatography was firstly introduced for the separation of proteins using all ammonium sulfate gradient. In this study we describe a novel approach using solvent-based protein precipitation for the isolation of active plant enzymes from tea leaves (Camellia sinensis) by centrifugal precipitation chromatography. We developed a gradient based oil acetone and Tris-buffer, because the biological activity of carotenases in tea leaves cannot be preserved in the presence of ammonium sulfate. Parameters Such as the critical solvent concentration, flow rate, buffer concentration, and sample load were determined and/or optimized. Subsequently, the newly developed separation protocol was successfully used for the isolation Of active carotenoid cleavage enzymes from tea leaves. The isolated enzymes showed high enzymatic activities and purities and could be directly used for enzymatic assays and structure elucidation. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Baldermann, Susanne; Watanabe, Naoharu] Shizuoka Univ, Grad Sch Sci & Technol, Integrated Biosci Sect, Suruga Ku, Shizuoka 4228529, Japan.
[Baldermann, Susanne; Fleischmann, Peter; Bolten, Mareike; Winterhalter, Peter] Tech Univ Carolo Wilhelmina Braunschweig, Inst Food Chem, D-38106 Braunschweig, Germany.
[Ito, Yoichiro] NHLBI, Bioseparat Technol Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Baldermann, S (reprint author), Shizuoka Univ, Grad Sch Sci & Technol, Integrated Biosci Sect, Suruga Ku, 836 Ohya, Shizuoka 4228529, Japan.
EM s.baldermann@tu-bs.de
RI Baldermann, Susanne/C-4292-2014
OI Baldermann, Susanne/0000-0002-1501-4320
FU Intramural NIH HHS [Z01 HL001047-09]
NR 23
TC 6
Z9 6
U1 0
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD MAY 8
PY 2009
VL 1216
IS 19
BP 4263
EP 4267
DI 10.1016/j.chroma.2009.01.102
PG 5
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 444BU
UT WOS:000265955900020
PM 19233373
ER
PT J
AU Wei, Y
Xie, QQ
Dong, WT
Ito, Y
AF Wei, Yun
Xie, Qianqian
Dong, Wanting
Ito, Yoichiro
TI Separation of epigallocatechin and flavonoids from Hypericum perforatum
L. by high-speed counter-current chromatography and preparative
high-performance liquid chromatography
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article; Proceedings Paper
CT 5th International Conference on Countercurrent Chromatography
CY JUL 26-29, 2008
CL Rio de Janeiro, BRAZIL
DE High-speed counter-current chromatography; Preparative high-performance
liquid chromatography; Hypericum perforatum L.; Flavonoids;
Epigallocatechin
ID CONSTITUENTS
AB High-speed counter-current chromatography (HSCCC) and preparative high-performance liquid chromatography (prep-HPLC) were successively used for the separation of epigallocatechin and flavonoids from Hypericum perforatum L. The two-phase solvent system composed of ethyl acetate-methanol-water (10:1:10, v/v) was used for HSCCC. About 900 mg of the crude extract was separated by HSCCC, yielding 7.8 mg of quercitrin at a purity of over 97%, 12.6 mg of quercetin at a purity of over 93%, and 38.9 mg of a mixture of hyperoside, isoquercitrin and miquelianin constituting over 97% of the fraction. A mixture of epigallocatechin arid avicularin pooled from three HSCCC runs, a total amount of 54.3 mg, was further separated by prep-HPLC yielding 23.4 mg of epigallocatechin and 15.3 mg of avicularin each at a purity of over 97%. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Wei, Yun; Xie, Qianqian; Dong, Wanting] Beijing Univ Chem Technol, State Key Lab Chem Resource Engn, Beijing 100029, Peoples R China.
[Ito, Yoichiro] NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Wei, Y (reprint author), Beijing Univ Chem Technol, State Key Lab Chem Resource Engn, 15 Beisanhuan E Rd, Beijing 100029, Peoples R China.
EM weiyun@mail.buct.edu.cn
FU Intramural NIH HHS [Z99 HL999999]
NR 14
TC 42
Z9 46
U1 0
U2 20
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD MAY 8
PY 2009
VL 1216
IS 19
BP 4313
EP 4318
DI 10.1016/j.chroma.2008.12.056
PG 6
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 444BU
UT WOS:000265955900028
PM 19150073
ER
PT J
AU Beilhartz, GL
Wendeler, M
Baichoo, N
Rausch, J
Le Grice, S
Gotte, M
AF Beilhartz, Greg L.
Wendeler, Michaela
Baichoo, Noel
Rausch, Jason
Le Grice, Stuart
Goette, Matthias
TI HIV-1 Reverse Transcriptase Can Simultaneously Engage Its DNA/RNA
Substrate at Both DNA Polymerase and RNase H Active Sites: Implications
for RNase H Inhibition
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE HIV; reverse transcriptase; RNase H; drug resistance; inhibitors
ID HUMAN-IMMUNODEFICIENCY-VIRUS; UNNATURAL AMINO-ACIDS; RIBONUCLEASE-H;
CRYSTAL-STRUCTURE; CLEAVAGE SPECIFICITY; DRUG-RESISTANCE; RATCHET MODEL;
PRIMER; TRANSLOCATION; MECHANISM
AB Reverse transcriptase of the human immunodeficiency virus possesses DNA polymerase and ribonuclease (RNase) H activities. Although the nucleic acid binding cleft separating these domains can accommodate structually diverse duplexes, it is currently unknown whether regular DNA/RNA hybrids can simultaneously contact both active sites. In this study, we demonstrate that ligands capable of trapping the T-end of the primer at the polymerase active site affect the specificity of RNase H cleavage without altering the efficiency of the reaction. Experiments under single-turnover Conditions reveal that complexes with a bound nucleotide substrate show specific RNase H cleavage at template position -18, while complexes with the pyrophosphate analogue foscarnet show a specific cut at position -19. This pattern is indicative of post-translocated and pre-translocated conformations. The data are inconsistent with models postulating that the substrate toggles between both active sites, such that the primer 3'-terminus is disengaged from the polymerase active site when the template is in contact with the RNase H active site. In contrast, our findings provide strong evidence to suggest that the nucleic acid substrate can engage both active sites at the same time. As a consequence, the bound and intact DNA/RNA hybrid can restrict access of RNase H active site inhibitors. We have mapped the binding site of the recently discovered inhibitor beta-thujaplicinol between the RNase H active site and Y501 of the RNase H primer grip, and have shown that the inhibitor is unable to bind to a preformed reverse transcriptase-DNA/RNA complex. In conclusion, the bound nucleic acid substrate and in turn, active DNA synthesis can represent an obstacle to RNase H inhibition with compounds that bind to the RNase H active site. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Beilhartz, Greg L.; Goette, Matthias] McGill Univ, Dept Microbiol & Immunol, Montreal, PQ H3A 2B4, Canada.
[Wendeler, Michaela; Baichoo, Noel; Rausch, Jason; Le Grice, Stuart] NCI, RT Biochem Sect, HIV Drug Resistance Program, Frederick, MD 21701 USA.
RP Gotte, M (reprint author), McGill Univ, Dept Microbiol & Immunol, Duff Med Bldg D-6,3775 Univ St, Montreal, PQ H3A 2B4, Canada.
EM matthias.gotte@mcgill.ca
FU Canadian Association; Canadian Institutes of Health Research; Center for
Cancer Research, National Cancer Center, National Institutes of Health
FX The authors would like to thank Suzanne McCormick and Jennifer T. Miller
for excellent technical assistance. This; work was funded by a grant
from the Canadian Association for AIDS Research to M. G. M.G. was the
recipient of a national career award from the Canadian Institutes of
Health Research. S. L.G. was supported by the intramural research
program of the Center for Cancer Research, National Cancer Center,
National Institutes of Health.
NR 48
TC 39
Z9 40
U1 1
U2 5
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD MAY 8
PY 2009
VL 388
IS 3
BP 462
EP 474
DI 10.1016/j.jmb.2009.03.025
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 447GD
UT WOS:000266178700004
PM 19289131
ER
PT J
AU Bhaumik, P
Xiao, HG
Parr, CL
Kiso, Y
Gustchina, A
Yada, RY
Wlodawer, A
AF Bhaumik, Prasenjit
Xiao, Huogen
Parr, Charity L.
Kiso, Yoshiaki
Gustchina, Alla
Yada, Rickey Y.
Wlodawer, Alexander
TI Crystal Structures of the Histo-Aspartic Protease (HAP) from Plasmodium
falciparum
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE aspartic proteases; inhibitor binding; crystal structure
ID HYDROXYMETHYLCARBONYL HMC ISOSTERE; VIRUS TYPE-1 PROTEASE; ACTIVE-SITE;
PLASMEPSIN-II; MOLECULAR REPLACEMENT; MACROMOLECULAR STRUCTURES;
HISTOASPARTIC PROTEASE; MAXIMUM-LIKELIHOOD; MALARIA PARASITE; CATALYTIC
SITE
AB The structures of recombinant histo-aspartic protease (HAP) from malariacausing parasite Plasmodium falciparum as apoenzyme and in complex with two inhibitors, pepstatin A and KNI-10006, were solved at 2.5-, 3.3-, and 3.05-angstrom resolutions, respectively. In the apoenzyme crystals, HAP forms a tight dimer not seen previously in any aspartic protease. The interactions between the monomers affect the conformation of two flexible loops, the functionally important "flap" (residues 70-83) and its structural equivalent in the C-terminal domain (residues 238-245), as well as the orientation of helix 225-235. The flap is found in an open conformation in the apoenzyme. Unexpectedly, the active site of the apoenzyme contains a zinc ion tightly bound to His32 and Asp215 from one monomer and to Glu278A from the other monomer, with the coordination of Zn resembling that seen in metalloproteases. The flap is closed in the structure of the pepstatin A complex, whereas it is open in the complex with KNI-10006. Although the binding mode of pepstatin A is significantly different from that in other pepsin-like aspartic proteases, its location in the active site makes unlikely the previously proposed hypothesis that HAP is a serine protease. The binding mode of KNI-10006 is unusual compared with the binding of other inhibitors from the KNI series to aspartic proteases. The novel features of the HAP active site could facilitate design of specific inhibitors used in the development of antimalarial drugs. Published by Elsevier Ltd.
C1 [Bhaumik, Prasenjit; Gustchina, Alla; Wlodawer, Alexander] NCI, Prot Struct Sect, Macromol Crystallog Lab, Frederick, MD 21702 USA.
[Xiao, Huogen; Parr, Charity L.; Yada, Rickey Y.] Univ Guelph, Dept Food Sci, Guelph, ON N1G 2W1, Canada.
[Kiso, Yoshiaki] Kyoto Pharmaceut Univ, Dept Med Chem, Ctr Frontier Res Med Sci, Yamashina Ku, Kyoto 6078412, Japan.
RP Gustchina, A (reprint author), NCI, Prot Struct Sect, Macromol Crystallog Lab, Frederick, MD 21702 USA.
EM alla@ncifcrf.gov
RI Yada, Rickey/A-8289-2013
FU U.S. Department of Energy, Office of Science, Office of Basic Energy
Sciences [31-109-Eng-38]; Natural Sciences and Engineering Research
Council of Canada
FX Diffraction data were collected at the SER-CAT beamline 22-ID, located
at the Advanced Photon Source, Argonne National Laboratory. Use of the
Advanced Photon Source was supported by the U.S. Department of Energy,
Office of Science, Office of Basic Energy Sciences, under contract no.
W-31-109-Eng-38. This project was supported in part by the Intramural
Research Program of the National Institutes of Health, National Cancer
Institute, Center for Cancer Research. Financial support from the
Natural Sciences and Engineering Research Council of Canada and that
from the Canada Research Chairs
NR 58
TC 24
Z9 24
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD MAY 8
PY 2009
VL 388
IS 3
BP 520
EP 540
DI 10.1016/j.jmb.2009.03.011
PG 21
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 447GD
UT WOS:000266178700008
PM 19285084
ER
PT J
AU Zhang, J
Jima, DD
Jacobs, C
Fischer, R
Gottwein, E
Huang, G
Lugar, PL
Lagoo, AS
Rizzieri, DA
Friedman, DR
Weinberg, JB
Lipsky, PE
Dave, SS
AF Zhang, Jenny
Jima, Dereje D.
Jacobs, Cassandra
Fischer, Randy
Gottwein, Eva
Huang, Grace
Lugar, Patricia L.
Lagoo, Anand S.
Rizzieri, David A.
Friedman, Daphne R.
Weinberg, J. Brice
Lipsky, Peter E.
Dave, Sandeep S.
TI Patterns of microRNA expression characterize stages of human B-cell
differentiation
SO BLOOD
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; TRANSCRIPTION FACTOR; GENE-EXPRESSION;
BURKITTS-LYMPHOMA; PROTEIN-SYNTHESIS; BLIMP-1; PROLIFERATION;
MICROARRAY; PREDICTION; PROFILES
AB Mature B-cell differentiation provides an important mechanism for the acquisition of adaptive immunity. Malignancies derived from mature B cells constitute the majority of leukemias and lymphomas. These malignancies often maintain the characteristics of the normal B cells that they are derived from, a feature that is frequently used in their diagnosis. The role of microRNAs in mature B cells is largely unknown. Through concomitant microRNA and mRNA profiling, we demonstrate a potential regulatory role for microRNAs at every stage of the mature B-cell differentiation process. In addition, we have experimentally identified a direct role for the microRNA regulation of key transcription factors in B-cell differentiation: LMO2 and PRDM1 (Blimp1). We also profiled the microRNA of B-cell tumors derived from diffuse large B-cell lymphoma, Burkitt lymphoma, and chronic lymphocytic leukemia. We found that, in contrast to many other malignancies, common B-cell malignancies do not down-regulate microRNA expression. Although these tumors could be distinguished from each other with use of microRNA expression, each tumor type maintained the expression of the lineage-specific microRNAs. Expression of these lineage-specific microRNAs could correctly predict the lineage of B-cell malignancies in more than 95% of the cases. Thus, our data demonstrate that microRNAs may be important in maintaining the mature B-cell phenotype in normal and malignant B cells. (Blood. 2009;113:4586-4594)
C1 [Zhang, Jenny; Jima, Dereje D.; Jacobs, Cassandra; Huang, Grace; Dave, Sandeep S.] Duke Univ, Duke Inst Genome Sci & Policy, Durham, NC 27710 USA.
[Fischer, Randy; Lugar, Patricia L.; Lipsky, Peter E.] NIAMSD, Autoimmun Branch, Bethesda, MD 20892 USA.
[Gottwein, Eva] Duke Univ, Dept Mol Genet & Microbiol, Durham, NC 27710 USA.
[Gottwein, Eva] Duke Univ, Ctr Virol, Durham, NC 27710 USA.
[Lugar, Patricia L.; Rizzieri, David A.; Friedman, Daphne R.; Weinberg, J. Brice; Dave, Sandeep S.] Duke Univ, Dept Med, Durham, NC 27710 USA.
[Lagoo, Anand S.] Duke Univ, Dept Pathol, Durham, NC 27710 USA.
RP Dave, SS (reprint author), Duke Univ, Duke Inst Genome Sci & Policy, 101 Sci Dr,Box 3382, Durham, NC 27710 USA.
EM sandeep.dave@duke.edu
FU Doris Duke Charitable Foundation (New York, NY); National Institutes of
Health [K12]; Duke Cancer Center Development
FX S. S. D. was supported by the Doris Duke Charitable Foundation (New
York, NY), National Institutes of Health grant K12, and a Duke Cancer
Center Development Grant. We thank Dr Joseph Nevins for a critical
review of the manuscript, and Laszlo Jakoi and Chaitanya Acharya for
technical assistance. We also thank Wayne Terrell and Dr Raj Dash for
assistance with pathology specimens, and Tri-Tin Le (Applied
Biosystems), Chris Miller (Applied Biosystems), and John Alexandrou
(Exiqon) for advice and technical support.
NR 50
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U2 7
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD MAY 7
PY 2009
VL 113
IS 19
BP 4586
EP 4594
DI 10.1182/blood-2008-09-178186
PG 9
WC Hematology
SC Hematology
GA 443LC
UT WOS:000265910300021
PM 19202128
ER
PT J
AU Lucas, DM
Edwards, RB
Lozanski, G
West, DA
Shin, JD
Vargo, MA
Davis, ME
Rozewski, DM
Johnson, AJ
Su, BN
Goettl, VM
Heerema, NA
Lin, TS
Lehman, A
Zhang, XL
Jarjoura, D
Newman, DJ
Byrd, JC
Kinghorn, AD
Grever, MR
AF Lucas, David M.
Edwards, Ryan B.
Lozanski, Gerard
West, Derek A.
Shin, Jungook D.
Vargo, Melissa A.
Davis, Melanie E.
Rozewski, Darlene M.
Johnson, Amy J.
Su, Bao-Ning
Goettl, Virginia M.
Heerema, Nyla A.
Lin, Thomas S.
Lehman, Amy
Zhang, Xiaoli
Jarjoura, David
Newman, David J.
Byrd, John C.
Kinghorn, A. Douglas
Grever, Michael R.
TI The novel plant-derived agent silvestrol has B-cell selective activity
in chronic lymphocytic leukemia and acute lymphoblastic leukemia in
vitro and in vivo
SO BLOOD
LA English
DT Article
ID ROCAGLAMIDE DERIVATIVES; HISTONE DEACETYLASE; MULTIPLE-MYELOMA;
DOWN-REGULATION; BCL-2 FAMILY; T-CELLS; APOPTOSIS; MCL-1; PROTEIN;
FLAVOPIRIDOL
AB Therapeutic options for advanced B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are limited. Available treatments can also deplete T lymphocytes, leaving patients at risk of life-threatening infections. In the National Cancer Institute cell line screen, the structurally unique natural product silvestrol produces an unusual pattern of cytotoxicity that suggests activity in leukemia and selectivity for B cells. We investigated silvestrol efficacy using primary human B-leukemia cells, established B-leukemia cell lines, and animal models. In CLL cells, silvestrol LC(50) (concentration lethal to 50%) is 6.9 nM at 72 hours. At this concentration, there is no difference in sensitivity of cells from patients with or without the del( 17p13.1) abnormality. In isolated cells and whole blood, silvestrol is more cytotoxic toward B cells than T cells. Silvestrol causes early reduction in Mcl-1 expression due to translational inhibition with subsequent mitochondrial damage, as evidenced by reactive oxygen species generation and membrane depolarization. In vivo, silvestrol causes significant B-cell reduction in E mu-Tcl-1 transgenic mice and significantly extends survival of 697 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity. These data indicate silvestrol has efficacy against B cells in vitro and in vivo and identify translational inhibition as a potential therapeutic target in B-cell leukemias. (Blood. 2009;113:4656-4666)
C1 [Lucas, David M.; Edwards, Ryan B.; West, Derek A.; Shin, Jungook D.; Vargo, Melissa A.; Davis, Melanie E.; Rozewski, Darlene M.; Johnson, Amy J.; Goettl, Virginia M.; Lin, Thomas S.; Byrd, John C.; Grever, Michael R.] Ohio State Univ, Dept Internal Med, Columbus, OH 43210 USA.
[Lozanski, Gerard; Heerema, Nyla A.] Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA.
[Su, Bao-Ning; Byrd, John C.; Kinghorn, A. Douglas] Ohio State Univ, Coll Pharm, Columbus, OH 43210 USA.
[Lehman, Amy; Zhang, Xiaoli; Jarjoura, David] Ohio State Univ, Ctr Biostat, Columbus, OH 43210 USA.
[Newman, David J.] NCI, Nat Prod Branch, Frederick, MD 21701 USA.
RP Lucas, DM (reprint author), OSUCCC Bldg,Rm 455,410 W 12th Ave, Columbus, OH 43210 USA.
EM david.lucas@osumc.edu
RI Johnson, Amy/A-5662-2009; Lucas, David/E-3555-2011;
OI Kinghorn, A. Douglas/0000-0002-6647-8707
FU CLL Global Research Foundation (Houston, TX) [NCI (P01 CA081534)];
American Cancer Society (Atlanta, GA; Institutional Research Grant);
Samuel Waxman Cancer Research Foundation (New York, NY); Leukemia &
Lymphoma Society (White Plains, NY); Warren Brown Foundation (Columbus,
OH); National Cooperative Drug Discovery Group [CA52956, CA125066]
FX This work was supported in part by the NCI (P01 CA081534), the CLL
Global Research Foundation (Houston, TX), the American Cancer Society
(Atlanta, GA; Institutional Research Grant), the Samuel Waxman Cancer
Research Foundation (New York, NY), the Leukemia & Lymphoma Society
(White Plains, NY), and the D. Warren Brown Foundation (Columbus, OH).
Silvestrol was provided through a National Cooperative Drug Discovery
Group (CA52956) and NCI P01 (CA125066; A. D. K.).
NR 57
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U1 0
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD MAY 7
PY 2009
VL 113
IS 19
BP 4656
EP 4666
DI 10.1182/blood-2008-09-175430
PG 11
WC Hematology
SC Hematology
GA 443LC
UT WOS:000265910300028
PM 19190247
ER
PT J
AU Brander, C
Marincola, FM
AF Brander, Christian
Marincola, Francesco M.
TI AAAS joins the Translational Medicine family
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
AB The AAAS has announced the launch of Science Translational Medicine. This is further and critical recognition of this discipline and we are deeply gratified that translational medicine has risen to the level of recognition by one of the world's most prestigious scientific organizations. We believe that Science Translational Medicine will provide another valuable venue for the rapid and broad dissemination of important articles in the field and contribute to enhancing the effectiveness of translational medicine overall.
It has been almost six years since we launched the Journal of Translational Medicine as an open-access journal with Biomed Central [1]. At the beginning, we faced the inevitable skepticism and received several inquires among others also from Science reporters questioning both the significance of translational medicine in today's biomedical world and the need for a new journal dedicated to it.
C1 [Brander, Christian] Hosp Univ Germans Trias & Pujol, Fundacio IrsiCaixa, Lab Retrovirol, Badalona 08916, Spain.
[Brander, Christian] Inst Catalana Recerca & Estudis Avancats, Barcelona, Catalonia, Spain.
[Marincola, Francesco M.] NIH, IDIS, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Marincola, Francesco M.] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
RP Brander, C (reprint author), Hosp Univ Germans Trias & Pujol, Fundacio IrsiCaixa, Lab Retrovirol, Ctra Canyet S-N, Badalona 08916, Spain.
EM cbrander@irsicaixa.es; fmarincola@mail.cc.nih.gov
OI Brander, Christian/0000-0002-0548-5778
NR 7
TC 2
Z9 2
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD MAY 7
PY 2009
VL 7
AR 32
DI 10.1186/1479-5876-7-32
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 447BK
UT WOS:000266166400001
PM 19422684
ER
PT J
AU Nienborg, H
Cumming, BG
AF Nienborg, Hendrikje
Cumming, Bruce G.
TI Decision-related activity in sensory neurons reflects more than a
neuron's causal effect
SO NATURE
LA English
DT Article
ID EARLY VISUAL-CORTEX; PERCEPTUAL DECISION; TASK STRATEGY; V2 NEURONS;
AREA MT; CHOICE; RESPONSES; DISCRIMINATION; REPRESENTATION; VARIABILITY
AB During perceptual decisions, the activity of sensory neurons correlates with a subject's percept, even when the physical stimulus is identical(1-9). The origin of this correlation is unknown. Current theory proposes a causal effect of noise in sensory neurons on perceptual decisions(10-12), but the correlation could result from different brain states associated with the perceptual choice(13) (a top-down explanation). These two schemes have very different implications for the role of sensory neurons in forming decisions(14). Here we use white-noise analysis(15) to measure tuning functions of V2 neurons associated with choice and simultaneously measure how the variation in the stimulus affects the subjects' (two macaques) perceptual decisions(16-18). In causal models, stronger effects of the stimulus upon decisions, mediated by sensory neurons, are associated with stronger choice-related activity. However, we find that over the time course of the trial these measures change in different directions-at odds with causal models. An analysis of the effect of reward size also supports this conclusion. Finally, we find that choice is associated with changes in neuronal gain that are incompatible with causal models. All three results are readily explained if choice is associated with changes in neuronal gain caused by top-down phenomena that closely resemble attention(19). We conclude that top-down processes contribute to choice-related activity. Thus, even forming simple sensory decisions involves complex interactions between cognitive processes and sensory neurons.
C1 [Nienborg, Hendrikje; Cumming, Bruce G.] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
RP Nienborg, H (reprint author), NEI, Sensorimotor Res Lab, NIH, 49 Convent Dr, Bethesda, MD 20892 USA.
EM hnienb@gmail.com
FU US National Institutes of Health; National Eye Institute
FX This research was supported by the Intramural Research Program of the US
National Institutes of Health, National Eye Institute. We are grateful
to J.A. Movshon and M. Shadlen for discussions and to the members of the
Laboratory of Sensorimotor Research for comments on an earlier version
of this manuscript. We also thank D. Parker and B. Nagy for excellent
animal care.
NR 31
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U1 4
U2 17
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD MAY 7
PY 2009
VL 459
IS 7243
BP 89
EP U93
DI 10.1038/nature07821
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441WN
UT WOS:000265801300035
PM 19270683
ER
PT J
AU He, LM
Xue, L
Xu, JH
McNeil, BD
Bai, L
Melicoff, E
Adachi, R
Wu, LG
AF He, Liming
Xue, Lei
Xu, Jianhua
McNeil, Benjamin D.
Bai, Li
Melicoff, Ernestina
Adachi, Roberto
Wu, Ling-Gang
TI Compound vesicle fusion increases quantal size and potentiates synaptic
transmission
SO NATURE
LA English
DT Article
ID MULTIVESICULAR RELEASE; POSTTETANIC POTENTIATION; TRANSMITTER RELEASE;
RIBBON SYNAPSE; RAT CALYX; 2 MODES; EXOCYTOSIS; NEURONS; ENDOCYTOSIS;
CAPACITANCE
AB Exocytosis at synapses involves fusion between vesicles and the plasma membrane(1). Although compound fusion between vesicles(2,3) was proposed to occur at ribbon-type synapses(4,5), whether it exists, how it is mediated, and what role it plays at conventional synapses remain unclear. Here we report the existence of compound fusion, its underlying mechanism, and its role at a nerve terminal containing conventional active zones in rats and mice. We found that high potassium application and high frequency firing induced giant capacitance up-steps, reflecting exocytosis of vesicles larger than regular ones, followed by giant down-steps, reflecting bulk endocytosis. These intense stimuli also induced giant vesicle-like structures, as observed with electron microscopy, and giant miniature excitatory postsynaptic currents (mEPSCs), reflecting more transmitter release. Calcium and its sensor for vesicle fusion, synaptotagmin, were required for these giant events. After high frequency firing, calcium/synaptotagmin-dependent mEPSC size increase was paralleled by calcium/synaptotagmin-dependent post-tetanic potentiation. These results suggest a new route of exocytosis and endocytosis composed of three steps. First, calcium/synaptotagmin mediates compound fusion between vesicles. Second, exocytosis of compound vesicles increases quantal size, which increases synaptic strength and contributes to the generation of post-tetanic potentiation. Third, exocytosed compound vesicles are retrieved via bulk endocytosis. We suggest that this vesicle cycling route be included in models of synapses in which only vesicle fusion with the plasma membrane is considered(1).
C1 [He, Liming; Xue, Lei; Xu, Jianhua; McNeil, Benjamin D.; Bai, Li; Wu, Ling-Gang] NINDS, Bethesda, MD 20892 USA.
[Melicoff, Ernestina; Adachi, Roberto] Univ Texas MD Anderson Canc Ctr, Dept Pulm Med, Houston, TX 77030 USA.
RP Wu, LG (reprint author), NINDS, 35 Convent Dr,Bldg 35,Room 2B 1012, Bethesda, MD 20892 USA.
EM wul@ninds.nih.gov
OI Xu, Jianhua/0000-0003-0084-8856; McNeil, Benjamin/0000-0001-7545-3598
FU National Institute of Neurological Disorders and Stroke Intramural
Research Program; American Heart Association
FX We thank J. Diamond and K. Paradiso for comments on the manuscript, and
S. Cheng, R. Azzam and V. Crocker for help in EM. This work was
supported by the National Institute of Neurological Disorders and Stroke
Intramural Research Program (L.-G. W.) and the American Heart
Association (R. A.).
NR 33
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U1 2
U2 23
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD MAY 7
PY 2009
VL 459
IS 7243
BP 93
EP U99
DI 10.1038/nature07860
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441WN
UT WOS:000265801300036
PM 19279571
ER
PT J
AU Adams, GB
Alley, IR
Chung, U
Chabner, KT
Jeanson, NT
Lo Celso, C
Marsters, ES
Chen, M
Weinstein, LS
Lin, CP
Kronenberg, HM
Scadden, DT
AF Adams, Gregor B.
Alley, Ian R.
Chung, Ung-il
Chabner, Karissa T.
Jeanson, Nathaniel T.
Lo Celso, Cristina
Marsters, Emily S.
Chen, Min
Weinstein, Lee S.
Lin, Charles P.
Kronenberg, Henry M.
Scadden, David T.
TI Haematopoietic stem cells depend on G alpha(s)-mediated signalling to
engraft bone marrow
SO NATURE
LA English
DT Article
ID IN-VIVO; CHOLERA-TOXIN; MICE; DIFFERENTIATION; LYMPHOPOIESIS;
MYELOPOIESIS; MIGRATION; SELECTINS; CXCR4
AB Haematopoietic stem and progenitor cells (HSPCs) change location during development(1) and circulate in mammals throughout life(2), moving into and out of the bloodstream to engage bone marrow niches in sequential steps of homing, engraftment and retention(3-5). Here we show that HSPC engraftment of bone marrow in fetal development is dependent on the guanine-nucleotide-binding protein stimulatory a subunit (G alpha(s)). HSPCs from adult mice deficient in G alpha(s) (G alpha(-/-)(s)) differentiate and undergo chemotaxis, but also do not home to or engraft in the bone marrow in adult mice and demonstrate a marked inability to engage the marrow microvasculature. If deleted after engraftment, G alpha(s) deficiency did not lead to lack of retention in the marrow, rather cytokine-induced mobilization into the blood was impaired. Testing whether activation of G alpha(s) affects HSPCs, pharmacological activators enhanced homing and engraftment in vivo. G alpha(s) governs specific aspects of HSPC localization under physiological conditions in vivo and may be pharmacologically targeted to improve transplantation efficiency.
C1 [Adams, Gregor B.; Alley, Ian R.; Chabner, Karissa T.; Jeanson, Nathaniel T.; Lo Celso, Cristina; Marsters, Emily S.; Scadden, David T.] Harvard Univ, Sch Med, Ctr Regenerat Med, Boston, MA 02114 USA.
[Chung, Ung-il; Kronenberg, Henry M.] Harvard Univ, Sch Med, Endocrine Unit, Boston, MA 02114 USA.
[Lin, Charles P.] Harvard Univ, Sch Med, Adv Microscopy Program, Ctr Syst Biol, Boston, MA 02114 USA.
[Lin, Charles P.] Harvard Univ, Sch Med, Wellman Ctr Photomed, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Adams, Gregor B.; Lo Celso, Cristina; Scadden, David T.] Harvard Univ, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
[Scadden, David T.] Harvard Univ, Sch Med, Dept Stem Cell & Regenerat Biol, Boston, MA 02114 USA.
[Chen, Min; Weinstein, Lee S.] NIDDKD, Bethesda, MD 20892 USA.
RP Scadden, DT (reprint author), Harvard Univ, Sch Med, Ctr Regenerat Med, Boston, MA 02114 USA.
EM dscadden@mgh.harvard.edu
FU Burroughs Wellcome Fund, Doris Duke Charitable Trust; Harvard Stem Cell
Institute; National Institutes of Health
FX Financial support for this work was provided by the Burroughs Wellcome
Fund, Doris Duke Charitable Trust (D. T. S.), the Harvard Stem Cell
Institute (C. P. L.) and the National Institutes of Health (G. B. A., C.
P. L., H. M. K., D. T. S.).
NR 21
TC 41
Z9 42
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD MAY 7
PY 2009
VL 459
IS 7243
BP 103
EP U111
DI 10.1038/nature07859
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441WN
UT WOS:000265801300038
PM 19322176
ER
PT J
AU Heintzman, ND
Hon, GC
Hawkins, RD
Kheradpour, P
Stark, A
Harp, LF
Ye, Z
Lee, LK
Stuart, RK
Ching, CW
Ching, KA
Antosiewicz-Bourget, JE
Liu, H
Zhang, XM
Green, RD
Lobanenkov, VV
Stewart, R
Thomson, JA
Crawford, GE
Kellis, M
Ren, B
AF Heintzman, Nathaniel D.
Hon, Gary C.
Hawkins, R. David
Kheradpour, Pouya
Stark, Alexander
Harp, Lindsey F.
Ye, Zhen
Lee, Leonard K.
Stuart, Rhona K.
Ching, Christina W.
Ching, Keith A.
Antosiewicz-Bourget, Jessica E.
Liu, Hui
Zhang, Xinmin
Green, Roland D.
Lobanenkov, Victor V.
Stewart, Ron
Thomson, James A.
Crawford, Gregory E.
Kellis, Manolis
Ren, Bing
TI Histone modifications at human enhancers reflect global
cell-type-specific gene expression
SO NATURE
LA English
DT Article
ID HUMAN GENOME; BINDING-SITES; TRANSCRIPTION; PROMOTERS; ELEMENTS;
SEQUENCE; RECEPTOR; MAP
AB The human body is composed of diverse cell types with distinct functions. Although it is known that lineage specification depends on cell-specific gene expression, which in turn is driven by promoters, enhancers, insulators and other cis-regulatory DNA sequences for each gene(1-3), the relative roles of these regulatory elements in this process are not clear. We have previously developed a chromatin-immunoprecipitation-based microarray method (ChIP-chip) to locate promoters, enhancers and insulators in the human genome(4-6). Here we use the same approach to identify these elements in multiple cell types and investigate their roles in cell-type-specific gene expression. We observed that the chromatin state at promoters and CTCF-binding at insulators is largely invariant across diverse cell types. In contrast, enhancers are marked with highly cell-type-specific histone modification patterns, strongly correlate to cell-type-specific gene expression programs on a global scale, and are functionally active in a cell-type-specific manner. Our results define over 55,000 potential transcriptional enhancers in the human genome, significantly expanding the current catalogue of human enhancers and highlighting the role of these elements in cell-type-specific gene expression.
C1 [Heintzman, Nathaniel D.; Hon, Gary C.; Hawkins, R. David; Harp, Lindsey F.; Ye, Zhen; Lee, Leonard K.; Stuart, Rhona K.; Ching, Christina W.; Ching, Keith A.; Ren, Bing] Univ Calif San Diego, Sch Med, Ludwig Inst Canc Res, La Jolla, CA 92093 USA.
[Heintzman, Nathaniel D.] Univ Calif San Diego, Sch Med, Biomed Sci Grad Program, La Jolla, CA 92093 USA.
[Hon, Gary C.] Univ Calif San Diego, Sch Med, Bioinformat Program, La Jolla, CA 92093 USA.
[Ren, Bing] Univ Calif San Diego, Sch Med, Dept Cellular & Mol Med, La Jolla, CA 92093 USA.
[Kheradpour, Pouya; Stark, Alexander; Kellis, Manolis] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
[Stark, Alexander; Kellis, Manolis] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
[Antosiewicz-Bourget, Jessica E.; Stewart, Ron; Thomson, James A.] Morgridge Inst Res, Madison, WI 53707 USA.
[Liu, Hui; Zhang, Xinmin; Green, Roland D.] Roche NimbleGen Inc, Madison, WI 53719 USA.
[Lobanenkov, Victor V.] NIAID, Rockville, MD 20852 USA.
[Thomson, James A.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI 53706 USA.
[Crawford, Gregory E.] Duke Univ, Inst Genome Sci & Policy, Durham, NC 27708 USA.
[Crawford, Gregory E.] Duke Univ, Dept Pediat, Durham, NC 27708 USA.
RP Ren, B (reprint author), Univ Calif San Diego, Sch Med, Ludwig Inst Canc Res, 9500 Gilman Dr, La Jolla, CA 92093 USA.
EM biren@ucsd.edu
RI Stark, Alexander/D-1473-2012;
OI Stark, Alexander/0000-0003-2611-0841; Lobanenkov,
Victor/0000-0001-6665-3635; Stuart, Rhona/0000-0001-5916-9693
FU American Cancer Society; NIAID; LICR; NHGRI; NCI; CIRM
FX We thank members of the Ren laboratory for comments. This work was
supported by funding from American Cancer Society (R. D. H.), NIAID
Intramural Research Program (V. V. L.), LICR (B. R.), NHGRI (B. R.), NCI
(B. R.) and CIRM (B. R.).
NR 25
TC 1087
Z9 1106
U1 9
U2 85
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD MAY 7
PY 2009
VL 459
IS 7243
BP 108
EP 112
DI 10.1038/nature07829
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441WN
UT WOS:000265801300039
PM 19295514
ER
PT J
AU Saini, P
Eyler, DE
Green, R
Dever, TE
AF Saini, Preeti
Eyler, Daniel E.
Green, Rachel
Dever, Thomas E.
TI Hypusine-containing protein eIF5A promotes translation elongation
SO NATURE
LA English
DT Article
ID SYNTHESIS INITIATION-FACTORS; PEPTIDE-BOND SYNTHESIS;
SACCHAROMYCES-CEREVISIAE; DECAY PATHWAY; YEAST; PURIFICATION;
PROGRESSION; MECHANISM; MUTANTS; BINDING
AB Translation elongation factors facilitate protein synthesis by the ribosome. Previous studies identified two universally conserved translation elongation factors, EF-Tu in bacteria (known as eEF1A in eukaryotes) and EF-G (eEF2), which deliver aminoacyl-tRNAs to the ribosome and promote ribosomal translocation, respectively(1). The factor eIF5A (encoded by HYP2 and ANB1 in Saccharomyces cerevisiae), the sole protein in eukaryotes and archaea to contain the unusual amino acid hypusine (N(epsilon)-(4-amino-2-hydroxybutyl)lysine)(2), was originally identified based on its ability to stimulate the yield (endpoint) of methionylpuromycin synthesis-a model assay for first peptide bond synthesis thought to report on certain aspects of translation initiation(3,4). Hypusine is required for eIF5A to associate with ribosomes(5,6) and to stimulate methionyl-puromycin synthesis(7). Because eIF5A did not stimulate earlier steps of translation initiation(8), and depletion of eIF5A in yeast only modestly impaired protein synthesis(9), it was proposed that eIF5A function was limited to stimulating synthesis of the first peptide bond or that eIF5A functioned on only a subset of cellular messenger RNAs. However, the precise cellular role of eIF5A is unknown, and the protein has also been linked to mRNA decay, including the nonsense-mediated mRNA decay pathway(10,11), and to nucleocytoplasmic transport(12,13). Here we use molecular genetic and biochemical studies to show that eIF5A promotes translation elongation. Depletion or inactivation of eIF5A in the yeast S. cerevisiae resulted in the accumulation of polysomes and an increase in ribosomal transit times. Addition of recombinant eIF5A from yeast, but not a derivative lacking hypusine, enhanced the rate of tripeptide synthesis in vitro. Moreover, inactivation of eIF5A mimicked the effects of the eEF2 inhibitor sordarin, indicating that eIF5A might function together with eEF2 to promote ribosomal translocation. Because eIF5A is a structural homologue of the bacterial protein EF-P(14,15), we propose that eIF5A/EF-P is a universally conserved translation elongation factor.
C1 [Saini, Preeti; Dever, Thomas E.] NICHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
[Eyler, Daniel E.; Green, Rachel] Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, Howard Hughes Med Inst, Baltimore, MD 21205 USA.
RP Dever, TE (reprint author), NICHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
EM tdever@nih.gov
OI Dever, Thomas/0000-0001-7120-9678
FU HHMI; NIH; NICHD
FX Acknowledgements We thank T. G. Kinzy for providing anti-yeast eEF1A,
eEF2 and eEF3 antisera, as well as constructs for the purification of
eEF2 and eEF3; J. Lorsch for providing constructs for purification of
yeast initiation factors; J. Dinmann for frameshifting reporter vectors,
and A. Hinnebusch, T. G. Kinzy, A. Jivotovskaya, D. Shelton, C. Grant,
J. Lorsch and members of the Dever and Hinnebusch laboratories for
comments and discussion. Salary support provided by HHMI (R. G.) and NIH
(D. E. E.). This work was supported in part by the Intramural Research
Program of the NIH, NICHD (to T. E. D.).
NR 35
TC 185
Z9 194
U1 0
U2 18
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD MAY 7
PY 2009
VL 459
IS 7243
BP 118
EP U129
DI 10.1038/nature08034
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441WN
UT WOS:000265801300041
PM 19424157
ER
PT J
AU Bockenhauer, D
Feather, S
Stanescu, HC
Bandulik, S
Zdebik, AA
Reichold, M
Tobin, J
Lieberer, E
Sterner, C
Landoure, G
Arora, R
Sirimanna, T
Thompson, D
Cross, JH
van't Hoff, W
Al Masri, O
Tullus, K
Yeung, S
Anikster, Y
Klootwijk, E
Hubank, M
Dillon, MJ
Heitzmann, D
Arcos-Burgos, M
Knepper, MA
Dobbie, A
Gahl, WA
Warth, R
Sheridan, E
Kleta, R
AF Bockenhauer, Detlef
Feather, Sally
Stanescu, Horia C.
Bandulik, Sascha
Zdebik, Anselm A.
Reichold, Markus
Tobin, Jonathan
Lieberer, Evelyn
Sterner, Christina
Landoure, Guida
Arora, Ruchi
Sirimanna, Tony
Thompson, Dorothy
Cross, J. Helen
van't Hoff, William
Al Masri, Omar
Tullus, Kjell
Yeung, Stella
Anikster, Yair
Klootwijk, Enriko
Hubank, Mike
Dillon, Michael J.
Heitzmann, Dirk
Arcos-Burgos, Mauricio
Knepper, Mark A.
Dobbie, Angus
Gahl, William A.
Warth, Richard
Sheridan, Eamonn
Kleta, Robert
TI Epilepsy, Ataxia, Sensorineural Deafness, Tubulopathy, and KCNJ10
Mutations.
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID DISTAL CONVOLUTED TUBULE; WIDE LINKAGE ANALYSIS; NA-CL COTRANSPORTER;
BARTTERS-SYNDROME; K+ CHANNEL; POTASSIUM CHANNEL; BLOOD-PRESSURE;
HYPOKALEMIC ALKALOSIS; BASOLATERAL MEMBRANE; KNOCK-OUT
AB Background: Five children from two consanguineous families presented with epilepsy beginning in infancy and severe ataxia, moderate sensorineural deafness, and a renal salt-losing tubulopathy with normotensive hypokalemic metabolic alkalosis. We investigated the genetic basis of this autosomal recessive disease, which we call the EAST syndrome (the presence of epilepsy, ataxia, sensorineural deafness, and tubulopathy).
Methods: Whole-genome linkage analysis was performed in the four affected children in one of the families. Newly identified mutations in a potassium-channel gene were evaluated with the use of a heterologous expression system. Protein expression and function were further investigated in genetically modified mice.
Results: Linkage analysis identified a single significant locus on chromosome 1q23.2 with a lod score of 4.98. This region contained the KCNJ10 gene, which encodes a potassium channel expressed in the brain, inner ear, and kidney. Sequencing of this candidate gene revealed homozygous missense mutations in affected persons in both families. These mutations, when expressed heterologously in xenopus oocytes, caused significant and specific decreases in potassium currents. Mice with Kcnj10 deletions became dehydrated, with definitive evidence of renal salt wasting.
Conclusions: Mutations in KCNJ10 cause a specific disorder, consisting of epilepsy, ataxia, sensorineural deafness, and tubulopathy. Our findings indicate that KCNJ10 plays a major role in renal salt handling and, hence, possibly also in blood-pressure maintenance and its regulation.
N Engl J Med 2009;360:1960-70.
C1 [Bockenhauer, Detlef; Stanescu, Horia C.; Zdebik, Anselm A.; Tobin, Jonathan; Landoure, Guida; Arora, Ruchi; Sirimanna, Tony; Thompson, Dorothy; Cross, J. Helen; van't Hoff, William; Tullus, Kjell; Klootwijk, Enriko; Hubank, Mike; Dillon, Michael J.; Kleta, Robert] UCL, Great Ormond St Hosp, London NW3 2PF, England.
[Feather, Sally; Yeung, Stella; Dobbie, Angus; Sheridan, Eamonn] Univ Leeds, Leeds Hosp, Leeds, W Yorkshire, England.
[Feather, Sally; Yeung, Stella; Dobbie, Angus; Sheridan, Eamonn] Univ Leeds, Bradford Teaching Hosp, Leeds, W Yorkshire, England.
[Stanescu, Horia C.; Landoure, Guida; Anikster, Yair; Klootwijk, Enriko; Arcos-Burgos, Mauricio; Knepper, Mark A.; Gahl, William A.; Kleta, Robert] NIH, Bethesda, MD 20892 USA.
[Bandulik, Sascha; Reichold, Markus; Lieberer, Evelyn; Sterner, Christina; Heitzmann, Dirk; Warth, Richard] Univ Regensburg, Inst Physiol, Regensburg, Germany.
[Landoure, Guida] Univ Bamako, Dept Neurol, Bamako, Mali.
[Al Masri, Omar] Sheikh Khalifa Med City, Abu Dhabi, U Arab Emirates.
[Anikster, Yair] Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
[Arcos-Burgos, Mauricio] Univ Miami, Miami, FL USA.
RP Kleta, R (reprint author), UCL, Royal Free Hosp, Ctr Nephrol, Rowland Hill St, London NW3 2PF, England.
EM r.kleta@ucl.ac.uk
RI Bockenhauer, Detlef/C-5951-2008; Hubank, Michael/C-1837-2008; Warth,
Richard/N-7119-2014; Reichold, Markus/J-9933-2015; Bandulik,
Sascha/L-7365-2015;
OI Bockenhauer, Detlef/0000-0001-5878-941X; Hubank,
Michael/0000-0002-2901-0742; Warth, Richard/0000-0001-6084-0659;
Thompson, Dorothy/0000-0001-5491-3911
FU Intramural NIH HHS [Z01 HL001285-22, Z99 HL999999, ZIA HL001285-23, ZIA
HL001285-24, Z01 HL001285-21]
NR 41
TC 208
Z9 213
U1 1
U2 15
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD MAY 7
PY 2009
VL 360
IS 19
BP 1960
EP 1970
DI 10.1056/NEJMoa0810276
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 441QN
UT WOS:000265784400006
PM 19420365
ER
PT J
AU Upton, TG
Kashemirov, BA
McKenna, CE
Goodman, MF
Prakash, GKS
Kultyshev, R
Batra, VK
Shock, DD
Pedersen, LC
Beard, WA
Wilson, SH
AF Upton, Thomas G.
Kashemirov, Boris A.
McKenna, Charles E.
Goodman, Myron F.
Prakash, G. K. Surya
Kultyshev, Roman
Batra, Vinod K.
Shock, David D.
Pedersen, Lars C.
Beard, William A.
Wilson, Samuel H.
TI alpha,beta-Difluoromethylene Deoxynucleoside 5 '-Triphosphates: A
Convenient Synthesis of Useful Probes for DNA Polymerase beta Structure
and Function
SO ORGANIC LETTERS
LA English
DT Article
ID VIRUS-1 REVERSE-TRANSCRIPTASE; PHOSPHONATE ANALOGS; NUCLEOSIDE
TRIPHOSPHATE; PERCHLORYL FLUORIDE; ATP ANALOGS; FIDELITY; ACID;
NUCLEOTIDES; SPECIFICITY; DERIVATIVES
AB alpha,beta-Difluoromethylene deoxynucleoside 5'-triphosphates (dNTPs, N = A or C) are advantageously obtained via phosphorylation of corresponding dNDP analogues using catalytic ATP, PEP, nucleoside diphosphate kinase, and pyruvate kinase. DNA pol beta K(d) values for the alpha,beta-CF(2) and unmodified dNTPs, alpha,beta-NH dUTP, and the alpha,beta-CH(2) analogues of dATP and dGTP are discussed in relation to the conformations of alpha,beta-CF(2) dTTP versus alpha,beta-NH dUTP bound into the enzyme active site.
C1 [Upton, Thomas G.; Kashemirov, Boris A.; McKenna, Charles E.; Goodman, Myron F.; Prakash, G. K. Surya; Kultyshev, Roman] Univ So Calif, Dept Biol & Chem, Los Angeles, CA 90089 USA.
[Batra, Vinod K.; Shock, David D.; Pedersen, Lars C.; Beard, William A.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP McKenna, CE (reprint author), Univ So Calif, Dept Biol & Chem, Los Angeles, CA 90089 USA.
EM mckenna@usc.edu
RI Upton, Thomas/E-3749-2012
FU NIH [5-U19-CA105010]; National Institute of Environmental Health
Sciences
FX We thank Dr. Ron New (Mass Spectrometry Facility, University of
California, Riverside) for assistance in obtaining high resolution mass
spectra of nucleotide analogues, Ms. Keriann Oertell (University of
Southern California) for verifying the DNA synthesis background activity
in 9 after dual-HPLC purification, and Prof. George L. Kenyon
(University of Michigan) for helpful discussions. This research was
supported by the Intramural Research Program of the NIH, National
Institute of Environmental Health Sciences and by NIH program project
grant 5-U19-CA105010.
NR 43
TC 26
Z9 26
U1 1
U2 18
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1523-7060
J9 ORG LETT
JI Org. Lett.
PD MAY 7
PY 2009
VL 11
IS 9
BP 1883
EP 1886
DI 10.1021/ol701755k
PG 4
WC Chemistry, Organic
SC Chemistry
GA 438AT
UT WOS:000265529000005
PM 19351147
ER
PT J
AU Xu, SG
White, HD
Offer, GW
Yu, LC
AF Xu, Sengen
White, Howard D.
Offer, Gerald W.
Yu, Leepo C.
TI Stabilization of Helical Order in the Thick Filaments by Blebbistatin:
Further Evidence of Coexisting Multiple Conformations of Myosin
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID ADENOSINE-TRIPHOSPHATE; MOTOR DOMAIN; SKELETAL-MUSCLE; CROSS-BRIDGES;
INHIBITION; MECHANISM; STATES; CROSSBRIDGES; DISSOCIATION; SPECIFICITY
AB The degree of helical order of the thick filament of mammalian skeletal muscle is highly dependent on temperature and the nature of the ligand. Previously, we showed that there was a close correlation between the conformation of the myosin heads on the surface of the thick filaments and the extent of their helical order. Helical order required the heads to be in the closed conformation. In addition, we showed that, with the same ligand bound at the active site, three conformations of myosin coexisted in equilibrium. Hitherto, however, there was no detectable helical order as measured by x-ray diffraction under the temperatures studied for myosin with MgADP and the nucleotide-free myosin, raising the possibility that the concept of multiple conformations has I mited validity. In this study, blebbistatin was used to stabilize the closed conformation of myosin. The degree of helical order is substantially improved with MgATP at low temperature or with MgADP or in the absence of nucleotide. The thermodynamic parameters of the disorder-order transition and the characteristics of the ordered array were not significantly altered by binding blebbistatin. The simplest explanation is that the binding of blebbistatin increases the proportion of myosin in the closed conformation from being negligible to substantial. These results provide further evidence for the coexistence of multiple conformations of myosin under a wide range of conditions and for the closed conformation being directly coupled to helical order.
C1 [Xu, Sengen; Yu, Leepo C.] NIAMSD, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[White, Howard D.] E Virginia Med Sch, Norfolk, VA USA.
[Offer, Gerald W.] Univ Bristol, Dept Physiol & Pharmacol, Bristol, Avon, England.
RP Yu, LC (reprint author), NIAMSD, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM yule@mail.nih.gov
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases of
the National Institutes of Health; National Institutes of Health
[EB00209, HL040864]
FX This research was supported in part by the Intramural Research Program
of the National Institute of Arthritis and Musculoskeletal and Skin
Diseases of the National Institutes of Health and in part by National
Institutes of Health grants (No. EB00209 and HL040864 to H.D.W.).
NR 29
TC 14
Z9 14
U1 1
U2 3
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD MAY 6
PY 2009
VL 96
IS 9
BP 3673
EP 3681
DI 10.1016/j.bpj.2009.01.049
PG 9
WC Biophysics
SC Biophysics
GA 450JV
UT WOS:000266397700020
PM 19413972
ER
PT J
AU Mattson, MP
Maudsley, S
AF Mattson, Mark P.
Maudsley, Stuart
TI Live Longer sans the AT(1A) Receptor
SO CELL METABOLISM
LA English
DT Editorial Material
ID II TYPE-1 RECEPTOR; STRESS
AB Excessive activation of the AT(1A) receptor (AT(1A)R) by angiotensin II (Ang II) is implicated in the age-related development of hypertension, diabetes, and kidney disease. AT(1A)R-deficient mice live longer and have lower levels of oxidative stress than wild-type mice (Benigni et al., 2009), suggesting a role for AT(1A)R signaling in the aging process.
C1 [Mattson, Mark P.; Maudsley, Stuart] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
RI Mattson, Mark/F-6038-2012
FU Intramural NIH HHS [ZIA AG000318-04, Z01 AG000314-07]
NR 10
TC 9
Z9 9
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD MAY 6
PY 2009
VL 9
IS 5
BP 403
EP 405
DI 10.1016/j.cmet.2009.04.002
PG 3
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 442LC
UT WOS:000265841700003
PM 19416709
ER
PT J
AU Wang, XL
Suzuki, R
Lee, K
Tran, T
Gunton, JE
Saha, AK
Patti, ME
Goldfine, A
Ruderman, NB
Gonzalez, FJ
Kahn, CR
AF Wang, Xiaohui L.
Suzuki, Ryo
Lee, Kevin
Tran, Thien
Gunton, Jenny E.
Saha, Asish K.
Patti, Mary-Elizabeth
Goldfine, Allison
Ruderman, Neil B.
Gonzalez, Frank J.
Kahn, C. Ronald
TI Ablation of ARNT/HIF1 beta in Liver Alters Gluconeogenesis, Lipogenic
Gene Expression, and Serum Ketones
SO CELL METABOLISM
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; HYPOXIA-INDUCIBLE FACTOR-1; ARYL-HYDROCARBON
RECEPTOR; HEPATIC GLUCONEOGENESIS; INSULIN-RESISTANCE; LIPID
HOMEOSTASIS; MALONYL-COA; PPAR-ALPHA; IN-VIVO; ACID
AB We have previously shown that expression of the transcription factor ARNT/HIF1 beta is reduced in islets of humans with type 2 diabetes. We have now found that ARNT is also reduced in livers of diabetics. To study the functional effect of its reduction, we created mice with liver-specific ablation (L-ARNT KO) using ARNT IoxP mice and adenoviral-mediated delivery of Cre. L-ARNT KO mice had normal blood glucose but increased fed insulin levels. These mice also exhibited features of type 2 diabetes with increased hepatic gluconeogenesis, increased lipogenic gene expression, and low serum beta-hydroxybutyrate. These effects appear to be secondary to increased expression of CCAAT/enhancer-binding protein alpha (C/EBP alpha), farnesoid X receptor (FXR), and sterol response element-binding protein 1 c (SREBP-1c) and a reduction in phosphorylation of AMPK without changes in the expression of enzymes in ketogenesis, fatty acid oxidation, or FGF21. These results demonstrate that a deficiency of ARNT action in the liver, coupled with that in beta cells, could contribute to the metabolic phenotype of human type 2 diabetes.
C1 [Wang, Xiaohui L.; Suzuki, Ryo; Lee, Kevin; Tran, Thien; Gunton, Jenny E.; Patti, Mary-Elizabeth; Goldfine, Allison; Kahn, C. Ronald] Harvard Univ, Joslin Diabet Ctr, Sch Med, Boston, MA 02215 USA.
[Saha, Asish K.; Ruderman, Neil B.] Boston Med Ctr, Diabet Unit, Endocrinol Sect, Boston, MA 02118 USA.
[Saha, Asish K.; Ruderman, Neil B.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Saha, Asish K.; Ruderman, Neil B.] Boston Univ, Sch Med, Dept Physiol, Boston, MA 02118 USA.
[Gonzalez, Frank J.] NCI, Lab Metab, Bethesda, MD 20892 USA.
[Gunton, Jenny E.] Garvan Inst Med Res, Sydney, NSW, Australia.
RP Kahn, CR (reprint author), Harvard Univ, Joslin Diabet Ctr, Sch Med, Boston, MA 02215 USA.
EM c.ronald.kahn@joslin.harvard.edu
OI Saha, Asish/0000-0003-1001-5110; Ruderman, Neil/0000-0002-6589-6587
FU Intramural NIH HHS [Z01 BC005708-17]; NHLBI NIH HHS [P01 HL068758,
P01HL68758]; NIDDK NIH HHS [R01 DK067509, DK-067509, R01 DK060837,
DK-060837]
NR 33
TC 42
Z9 42
U1 1
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD MAY 6
PY 2009
VL 9
IS 5
BP 428
EP 439
DI 10.1016/j.cmet.2009.04.001
PG 12
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 442LC
UT WOS:000265841700007
PM 19416713
ER
PT J
AU Zhang, DL
Hughes, RI
Ollivierre-Wilson, H
Ghosh, MC
Rouault, TA
AF Zhang, De-Liang
Hughes, Robert Im.
Ollivierre-Wilson, Hayden
Ghosh, Manik C.
Rouault, Tracey A.
TI A Ferroportin Transcript that Lacks an Iron-Responsive Element Enables
Duodenal and Erythroid Precursor Cells to Evade Translational Repression
SO CELL METABOLISM
LA English
DT Article
ID REGULATORY PROTEINS; GENE-EXPRESSION; POLYCYTHEMIA MICE; FACTOR GATA-1;
HOMEOSTASIS; METABOLISM; HEPCIDIN; TRANSPORTER; ERYTHROPOIESIS;
HEMATOPOIESIS
AB Ferroportin (FPN1), the sole characterized mammalian iron exporter, has an iron-responsive element (IRE) in its 5' untranslated region, which ensures that its translation is repressed by iron regulatory proteins (IRPs) in iron-deficient conditions to maintain cellular iron content. However, here we demonstrate that duodenal epithelial and erythroid precursor cells utilize an alternative upstream promoter to express a FPN1 transcript, FPN1 13, which lacks the IRE and is not repressed in iron-deficient conditions. The FPN1 B transcript encodes ferroportin with an identical open reading frame and contributes significantly to ferroportin protein expression in erythroid precursors and likely also in the duodenum of iron-starved animals. The identification of FPN1B reveals how FPN1 expression can bypass IRP-dependent repression in intestinal iron uptake, even when cells throughout the body are iron deficient. In erythroid precursor cells, we hypothesize that FPN1 B expression enhances real-time sensing of systemic iron status and facilitates restriction of erythropoiesis in response to low systemic iron.
C1 [Zhang, De-Liang; Hughes, Robert Im.; Ollivierre-Wilson, Hayden; Ghosh, Manik C.; Rouault, Tracey A.] NICHHD, Program Mol Med, Bethesda, MD 20892 USA.
RP Rouault, TA (reprint author), NICHHD, Program Mol Med, Bethesda, MD 20892 USA.
EM rouault@mail.nih.gov
RI Zhang, Deliang/F-7848-2013;
OI Zhang, Deliang/0000-0001-9478-5344
FU Intramural NIH HHS [Z01 HD001602-23]
NR 40
TC 130
Z9 132
U1 0
U2 10
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD MAY 6
PY 2009
VL 9
IS 5
BP 461
EP 473
DI 10.1016/j.cmet.2009.03.006
PG 13
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 442LC
UT WOS:000265841700010
PM 19416716
ER
PT J
AU Abdelmohsen, K
Srikantan, S
Yang, XL
Lal, A
Kim, HH
Kuwano, Y
Galban, S
Becker, KG
Kamara, D
de Cabo, R
Gorospe, M
AF Abdelmohsen, Kotb
Srikantan, Subramanya
Yang, Xiaoling
Lal, Ashish
Kim, Hyeon Ho
Kuwano, Yuki
Galban, Stefanie
Becker, Kevin G.
Kamara, Davida
de Cabo, Rafael
Gorospe, Myriam
TI Ubiquitin-mediated proteolysis of HuR by heat shock
SO EMBO JOURNAL
LA English
DT Article
DE post-transcriptional gene regulation; proteasome; protein stability;
ribonucleoprotein complex; ubiquitination
ID MESSENGER-RNA STABILITY; BINDING PROTEIN HUR; TRANSLATIONAL CONTROL;
NUCLEAR IMPORT; STABILIZATION; TURNOVER; EXPRESSION; STRESS;
PHOSPHORYLATION; KINASE
AB The RNA-binding protein HuR regulates the stability and translation of numerous mRNAs encoding stress-response and proliferative proteins. Although its post-transcriptional influence has been linked primarily to its cytoplasmic translocation, here we report that moderate heat shock (HS) potently reduces HuR levels, thereby altering the expression of HuR target mRNAs. HS did not change HuR mRNA levels or de novo translation, but instead reduced HuR protein stability. Supporting the involvement of the ubiquitin-proteasome system in this process were results showing that (1) HuR was ubiquitinated in vitro and in intact cells, (2) proteasome inhibition increased HuR abundance after HS, and (3) the HuR kinase checkpoint kinase 2 protected against the loss of HuR by HS. Within a central, HS-labile similar to 110-amino-acid region, K182 was found to be essential for HuR ubiquitination and proteolysis as mutant HuR(K182R) was left virtually un-ubiquitinated and was refractory to HS-triggered degradation. Our findings reveal that HS transiently lowers HuR by proteolysis linked to K182 ubiquitination and that HuR reduction enhances cell survival following HS. The EMBO Journal (2009) 28, 1271-1282. doi: 10.1038/emboj.2009.67; Published online 26 March 2009
C1 [Abdelmohsen, Kotb; Srikantan, Subramanya; Yang, Xiaoling; Lal, Ashish; Kim, Hyeon Ho; Kuwano, Yuki; Galban, Stefanie; Gorospe, Myriam] NIA, Cellular & Mol Biol Lab, IRP, NIH, Baltimore, MD 21224 USA.
[Abdelmohsen, Kotb; Becker, Kevin G.] NIA, Res Resources Branch, IRP, NIH, Baltimore, MD 21224 USA.
[Kamara, Davida; de Cabo, Rafael] NIA, Lab Expt Gerontol, IRP, NIH, Baltimore, MD 21224 USA.
[Lal, Ashish] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[Lal, Ashish] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
RP Abdelmohsen, K (reprint author), NIA, Cellular & Mol Biol Lab, IRP, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM abdelmohsenk@grc.nia.nih.gov; myriam-gorospe@nih.gov
RI de Cabo, Rafael/J-5230-2016;
OI de Cabo, Rafael/0000-0002-3354-2442; srikantan,
subramanya/0000-0003-1810-6519; abdelmohsen, Kotb/0000-0001-6240-5810;
Becker, Kevin/0000-0002-6794-6656; , rafael/0000-0003-2830-5693
FU NIA-IRP Program [Z01-AG000511-10]; NIA-IRP, NIH
FX We thank MJ Pazin, V Dixit, WH Wood 3rd, B Frank, S Subaran, and FE
Indig for their assistance with these studies. HCT116 cells were kindly
provided by F Bunz. This research was supported entirely by the NIA-IRP
Program Z01-AG000511-10 and by set-aside funds of the NIA-IRP, NIH.
NR 55
TC 68
Z9 69
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0261-4189
J9 EMBO J
JI Embo J.
PD MAY 6
PY 2009
VL 28
IS 9
BP 1271
EP 1282
DI 10.1038/emboj.2009.67
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 443BK
UT WOS:000265885000009
PM 19322201
ER
PT J
AU Kayagil, TA
Bai, O
Henriquez, CS
Lin, P
Furlani, SJ
Vorbach, S
Hallett, M
AF Kayagil, Turan A.
Bai, Ou
Henriquez, Craig S.
Lin, Peter
Furlani, Stephen J.
Vorbach, Sherry
Hallett, Mark
TI A binary method for simple and accurate two-dimensional cursor control
from EEG with minimal subject training
SO JOURNAL OF NEUROENGINEERING AND REHABILITATION
LA English
DT Article
ID BRAIN-COMPUTER-INTERFACE; MENTAL PROSTHESIS; COMMUNICATION; PERFORMANCE;
POTENTIALS
AB Background: Brain-computer interfaces (BCI) use electroencephalography (EEG) to interpret user intention and control an output device accordingly. We describe a novel BCI method to use a signal from five EEG channels (comprising one primary channel with four additional channels used to calculate its Laplacian derivation) to provide two-dimensional (2-D) control of a cursor on a computer screen, with simple threshold-based binary classification of band power readings taken over pre-defined time windows during subject hand movement.
Methods: We tested the paradigm with four healthy subjects, none of whom had prior BCI experience. Each subject played a game wherein he or she attempted to move a cursor to a target within a grid while avoiding a trap. We also present supplementary results including one healthy subject using motor imagery, one primary lateral sclerosis (PLS) patient, and one healthy subject using a single EEG channel without Laplacian derivation.
Results: For the four healthy subjects using real hand movement, the system provided accurate cursor control with little or no required user training. The average accuracy of the cursor movement was 86.1% (SD 9.8%), which is significantly better than chance (p = 0.0015). The best subject achieved a control accuracy of 96%, with only one incorrect bit classification out of 47. The supplementary results showed that control can be achieved under the respective experimental conditions, but with reduced accuracy.
Conclusion: The binary method provides naive subjects with real-time control of a cursor in 2-D using dichotomous classification of synchronous EEG band power readings from a small number of channels during hand movement. The primary strengths of our method are simplicity of hardware and software, and high accuracy when used by untrained subjects.
C1 [Kayagil, Turan A.; Bai, Ou; Lin, Peter; Furlani, Stephen J.; Vorbach, Sherry; Hallett, Mark] NINDS, Bethesda, MD 20892 USA.
[Kayagil, Turan A.; Henriquez, Craig S.] Duke Univ, Dept Biomed Engn, Durham, NC 27708 USA.
[Kayagil, Turan A.] Georgetown Univ, Sch Med, Washington, DC 20057 USA.
[Bai, Ou] Virginia Commonwealth Univ, Dept Biomed Engn, Richmond, VA 23284 USA.
RP Bai, O (reprint author), NINDS, Bethesda, MD 20892 USA.
EM tkayagil@gmail.com; obai@vcu.edu; ch@duke.edu; linpe@ninds.nih.gov;
sfur777@hotmail.com; vorbachs@ninds.nih.gov; hallettm@ninds.nih.gov
FU Intramural Research Program of the NIH (National Institute of
Neurological Disorders and Stroke)
FX This research was supported by the Intramural Research Program of the
NIH (National Institute of Neurological Disorders and Stroke). We thank
Dr. Robert Lutz and the National Institutes of Health Biomedical
Engineering Summer Internship Program, which is supported by the
National Institute of Biomedical Imaging and Bioengineering. We thank
Dr. Mary Kay Floeter for her collaboration on the PLS study.
NR 26
TC 12
Z9 12
U1 0
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1743-0003
J9 J NEUROENG REHABIL
JI J. NeuroEng. Rehabil.
PD MAY 6
PY 2009
VL 6
AR 14
DI 10.1186/1743-0003-6-14
PG 16
WC Engineering, Biomedical; Neurosciences; Rehabilitation
SC Engineering; Neurosciences & Neurology; Rehabilitation
GA 455HB
UT WOS:000266748100001
PM 19419576
ER
PT J
AU Robak, LA
Venkatesh, K
Lee, H
Raiker, SJ
Duan, Y
Lee-Osbourne, J
Hofer, T
Mage, RG
Rader, C
Giger, RJ
AF Robak, Laurie A.
Venkatesh, Karthik
Lee, Hakjoo
Raiker, Stephen J.
Duan, Yuntao
Lee-Osbourne, Jane
Hofer, Thomas
Mage, Rose G.
Rader, Christoph
Giger, Roman J.
TI Molecular Basis of the Interactions of the Nogo-66 Receptor and Its
Homolog NgR2 with Myelin-Associated Glycoprotein: Development of
NgR(OMNI)-Fc, a Novel Antagonist of CNS Myelin Inhibition
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID NEURITE OUTGROWTH INHIBITION; CENTRAL-NERVOUS-SYSTEM;
SPINAL-CORD-INJURY; ACID BINDING-SITE; AXON REGENERATION; WHITE-MATTER;
IB-ALPHA; GROWTH; RECOVERY; DISTINCT
AB Myelin-associated glycoprotein (MAG) is a sialic acid-binding Ig-family lectin that functions in neuronal growth inhibition and stabilization of axon-glia interactions. The ectodomain of MAG is comprised of five Ig-like domains and uses neuronal cell-type-specific mechanisms to signal growth inhibition. We show that the first three Ig-like domains of MAG bind with high affinity and in a sialic acid-dependent manner to the Nogo-66 receptor-1 (NgR1) and its homolog NgR2. Domains Ig3-Ig5 of MAG are sufficient to inhibit neurite outgrowth but fail to associate with NgR1 or NgR2. Nogo receptors are sialoglycoproteins comprised of 8.5 canonical leucine-rich repeats (LRR) flanked by LRR N-terminal (NT) and C-terminal (CT)-cap domains. The LRR cluster is connected through a stalk region to a membrane lipid anchor. The CT-cap domain and stalk region of NgR2, but not NgR1, are sufficient for MAG binding, and when expressed in neurons, exhibit constitutive growth inhibitory activity. The LRR cluster of NgR1 supports binding of Nogo-66, OMgp, and MAG. Deletion of disulfide loop Cys(309)-Cys(336) of NgR1 selectively increases its affinity for Nogo-66 and OMgp. A chimeric Nogo receptor variant (NgR(OMNI)) in which Cys(309)-Cys(336) is deleted and followed by a 13 aa MAG-binding motif of the NgR2 stalk, shows superior binding of OMgp, Nogo-66, and MAG compared with wild-type NgR1 or NgR2. Soluble NgR(OMNI) (NgR(OMNI)-Fc) binds strongly to membrane-bound inhibitors and promotes neurite outgrowth on both MAG and CNS myelin substrates. Thus, NgR(OMNI)-Fc may offer therapeutic opportunities following nervous system injury or disease where myelin inhibits neuronal regeneration.
C1 [Raiker, Stephen J.; Duan, Yuntao; Giger, Roman J.] Univ Michigan, Sch Med, Dept Cell & Dev Biol, Ann Arbor, MI 48109 USA.
[Venkatesh, Karthik; Raiker, Stephen J.; Duan, Yuntao; Giger, Roman J.] Univ Michigan, Sch Med, Dept Neurol, Ann Arbor, MI 48109 USA.
[Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Mage, Rose G.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Robak, Laurie A.; Lee, Hakjoo; Raiker, Stephen J.; Lee-Osbourne, Jane; Giger, Roman J.] Univ Rochester, Sch Med & Dent, Dept Biomed Genet, Rochester, NY 14642 USA.
RP Giger, RJ (reprint author), Univ Michigan, Sch Med, Dept Cell & Dev Biol, 109 Zina Pitcher Pl,3065 BSRB, Ann Arbor, MI 48109 USA.
EM rgiger@umich.edu
FU National Institutes of Health [T32 NS07489]; National Research Service
Award Ruth Kirschstein Fellowship [F31NS049870]; New York State Spinal
Cord Injury Research Program; Christopher Reeve and Sam Schmidt
Paralysis Foundation; Ellison Medical Foundation; National Alliance for
Research on Schizophrenia and Depression; Miriam and Sheldon G. Adelson
Medical Foundation; National Institute of Neurological Disorders and
Stroke [NS047333]
FX This work was supported by National Institutes of Health Training Grant
T32 NS07489 (L. R. and K. V.), National Research Service Award Ruth
Kirschstein Fellowship F31NS049870 (K. V.), the New York State Spinal
Cord Injury Research Program (R. J. G. and C. R.), the Christopher Reeve
and Sam Schmidt Paralysis Foundation, the Ellison Medical Foundation,
the National Alliance for Research on Schizophrenia and Depression, the
Dr. Miriam and Sheldon G. Adelson Medical Foundation's Adelson Program
in Neural Repair and Rehabilitation, and National Institute of
Neurological Disorders and Stroke Grant NS047333 (R. J. G.). We thank R.
Geary, B. Carlin, and J. J. Winters for excellent technical assistance,
R. Schnaar for Galgt1 mouse brain tissue, and R. Quarles for anti-MAG
B11F7.
NR 55
TC 33
Z9 33
U1 1
U2 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD MAY 6
PY 2009
VL 29
IS 18
BP 5768
EP 5783
DI 10.1523/JNEUROSCI.4935-08.2009
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 442GC
UT WOS:000265827900008
PM 19420245
ER
PT J
AU Goldstein, RZ
Tomasi, D
Alia-Klein, N
Carrillo, JH
Maloney, T
Woicik, PA
Wang, RL
Telang, F
Volkow, ND
AF Goldstein, Rita Z.
Tomasi, Dardo
Alia-Klein, Nelly
Carrillo, Jean Honorio
Maloney, Thomas
Woicik, Patricia A.
Wang, Ruiliang
Telang, Frank
Volkow, Nora D.
TI Dopaminergic Response to Drug Words in Cocaine Addiction
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID VENTRAL TEGMENTAL AREA; ANTERIOR CINGULATE; GLUTAMATE; CORTEX; CUES;
SENSITIVITY; ACTIVATION; STRIATUM; SIGNALS; SEEKING
AB When exposed to drug conditioned cues (stimuli associated with the drug), addicted individuals experience an intense desire for the drug, which is associated with increased dopamine cell firing. We hypothesized that drug-related words can trigger activation in the mesencephalon, where dopaminergic cells are located. During functional magnetic resonance imaging (fMRI), 15 individuals with cocaine use disorders and 15 demographically matched healthy control subjects pressed buttons for color of drug-related versus neutral words. Results showed that the drug words, but not neutral words, activated the mesencephalon in the cocaine users only. Further, in the cocaine users only, these increased drug-related mesencephalic responses were associated with enhanced verbal fluency specifically for drug words. Our results for the first time demonstrate fMRI response to drug words in cocaine-addicted individuals in mesencephalic regions as possibly associated with dopaminergic mechanisms and with conditioning to language (in this case drug words). The correlation between the brief verbal fluency test, which can be easily administered (crucial for clinical studies), and fMRI cue reactivity could be used as a biomarker of neurobiological changes in addiction.
C1 [Goldstein, Rita Z.; Tomasi, Dardo; Alia-Klein, Nelly; Carrillo, Jean Honorio; Maloney, Thomas; Woicik, Patricia A.; Wang, Ruiliang; Telang, Frank] Brookhaven Natl Lab, Dept Med Res, Ctr Translat Neuroimaging, Upton, NY 11973 USA.
[Carrillo, Jean Honorio] SUNY Stony Brook, Stony Brook, NY 11794 USA.
[Telang, Frank; Volkow, Nora D.] NIAAA, Rockville, MD 20857 USA.
[Volkow, Nora D.] Natl Inst Drug Abuse, Bethesda, MD 20892 USA.
RP Goldstein, RZ (reprint author), Brookhaven Natl Lab, Dept Med Res, Ctr Translat Neuroimaging, POB 5000, Upton, NY 11973 USA.
EM rgoldstein@bnl.gov
RI Tomasi, Dardo/J-2127-2015
FU National Institute on Drug Abuse [1R01DA023579, R21DA02062]; General
Clinical Research Center [5-MO1-RR-10710]
FX This study was supported by grants from the National Institute on Drug
Abuse (Grants 1R01DA023579 and R21DA02062 to R. Z. G.) and the General
Clinical Research Center (Grant 5-MO1-RR-10710). WethankMuhammadA.
Parvaz for help with task administration, Alex Panagopoulos and Dimitris
Samaras for help with early data analyses, and Gene-JackWangfor help
with medical screens. Wealso thank Sahib S. Khalsa and Steve Berry for
help with word selection, matching, and ratings and Suparna Rajaram for
help with early task design.
NR 44
TC 43
Z9 47
U1 1
U2 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD MAY 6
PY 2009
VL 29
IS 18
BP 6001
EP 6006
DI 10.1523/JNEUROSCI.4247-08.2009
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 442GC
UT WOS:000265827900029
PM 19420266
ER
PT J
AU Ye, WJ
Sangaiah, R
Degen, DE
Gold, A
Jayaraj, K
Koshlap, KM
Boysen, G
Williams, J
Tomer, KB
Mocanu, V
Dicheva, N
Parker, CE
Schaaper, RM
Ball, LM
AF Ye, Wenjie
Sangaiah, R.
Degen, Diana E.
Gold, Avram
Jayaraj, K.
Koshlap, Karl M.
Boysen, Gunnar
Williams, Jason
Tomer, Kenneth B.
Mocanu, Viorel
Dicheva, Nedyalka
Parker, Carol E.
Schaaper, Roel M.
Ball, Louise M.
TI Iminohydantoin Lesion Induced in DNA by Peracids and Other Epoxidizing
Oxidants
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID MITOCHONDRIAL-DNA; GUANINE OXIDATION; PURINE NUCLEOSIDES; TANDEM
LESIONS; SIDE REACTIONS; MAJOR PRODUCT; ONE-ELECTRON; DAMAGE;
SPIROIMINODIHYDANTOIN; MECHANISM
AB The oxidation of guanine to 5-carboxamido-5-formamido-2-iminohydantoin (2-1h) is shown to be a major transformation in the oxidation of the single-stranded DNA 5-mer d(TTGTT) by m-chloroperbenzoic acid (m-CPBA) and dimethyldioxirane (DMDO) as a model for peracid oxidants and in the oxidation of the 5-base pair duplex d[(TTGTT) center dot (AACAA)] with DMDO. 2-1h has not been reported as an oxidative lesion at the level of single/double-stranded DNA or at the nucleoside/nucleotide level. The lesion is stable to DNA digestion and chromatographic purification, suggesting that 2-1h may be a stable biomarker in vivo. The oxidation products have been structurally characterized and the reaction mechanism has been probed by oxidation of the monomeric species dGuo, dGMP, and dGTP. DMDC) selectively oxidizes the guanine moiety of dGuo, dGMP, and dGTP to 2-1h, and both peracetic and m-chloroperbenzoic acids exhibit the same selectivity. The presence of the glycosidic bond results in the stereoselective induction of an asymmetric center at the Spiro carbon to give a mixture of diastereomers, with each diastereomer in equilibrium with a minor conformer through rotation about the formamido C-N bond. Labeling studies with [O-18(2)]-m-CPBA and (H2O)-O-18 to determine the source of the added oxygen atoms have established initial epoxidation of the guanine 4-5 bond with pyrimidine ring contraction by an acyl 1,2-migration of guanine carbonyl C6 to form a transient dehydrodeoxyspiroiminodihydantoin followed by hydrolytic ring-opening of the imidazolone ring. Consistent with the proposed mechanism, no 8-oxoguanine was detected as a product of the oxidations of the oligonucleotides or monomeric species mediated by DMDO or the peracids. The 2-1h base thus appears to be a pathway-specific lesion generated by peracids and possibly other epoxidizing agents and holds promise as a potential biomarker.
C1 [Ye, Wenjie; Sangaiah, R.; Degen, Diana E.; Gold, Avram; Jayaraj, K.; Boysen, Gunnar; Ball, Louise M.] Univ N Carolina, Dept Environm Sci & Engn, Chapel Hill, NC 27599 USA.
[Koshlap, Karl M.] Univ N Carolina, Sch Pharm, Chapel Hill, NC 27599 USA.
[Mocanu, Viorel; Dicheva, Nedyalka; Parker, Carol E.] Univ N Carolina, UNC Duke Prote Ctr, Program Mol Biol & Biotechnol, Chapel Hill, NC 27599 USA.
[Williams, Jason; Tomer, Kenneth B.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Schaaper, Roel M.] NIEHS, Genet Mol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Gold, A (reprint author), Univ N Carolina, Dept Environm Sci & Engn, CB7431, Chapel Hill, NC 27599 USA.
EM golda@email.unc.edu
RI Tomer, Kenneth/E-8018-2013;
OI Boysen, Gunnar/0000-0001-8364-9881
FU PHS [P42-ES005948]; NIEHS [ESR30262]; Intramural Research Program of the
NIEHS/NIH [Z01 ES050171]; UNC-Duke Proteomics Center
FX This work was supported in part by PHS Grant P42-ES005948 and NIEHS
Contract ESR30262. K.B.T and J.W. thank the Intramural Research Program
of the NIEHS/NIH (Grant Z01 ES050171) for support. The UNC-Duke
Proteomics Center was partially funded by a gift from an anonymous donor
in honor of Michael Hooker.
NR 42
TC 18
Z9 18
U1 0
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD MAY 6
PY 2009
VL 131
IS 17
BP 6114
EP 6123
DI 10.1021/ja8090752
PG 10
WC Chemistry, Multidisciplinary
SC Chemistry
GA 441FX
UT WOS:000265755800035
PM 19354244
ER
PT J
AU Turjanski, AG
Hummer, G
Gutkind, JS
AF Gustavo Turjanski, Adrian
Hummer, Gerhard
Gutkind, J. Silvio
TI How Mitogen-Activated Protein Kinases Recognize and Phosphorylate Their
Targets: A QM/MM Study
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID CYCLIN-DEPENDENT KINASE; MAP KINASES; AB-INITIO; MOLECULAR-DYNAMICS;
CRYSTAL-STRUCTURE; ERK2; MECHANISM; PATHWAY; CONFORMATION; BINDING
AB Mitogen-activated protein kinase (MAPK) signaling pathways play an essential role in the transduction of environmental stimuli to the nucleus, thereby regulating a variety of cellular processes, including cell proliferation, differentiation, and programmed cell death. The components of the MAPK extracellular activated protein kinase (ERK) cascade represent attractive targets for cancer therapy, as their aberrant activation is a frequent event among highly prevalent human cancers. To understand how MAPKs recognize and phosphorylate their targets is key to unravel their function. However, these events are still poorly understood because of the lack of complex structures of MAPKs with their bound targets in the active site. Here we have modeled the interaction of ERK with a target peptide and analyzed the specificity toward Ser/Thr-Pro motifs. By using a quantum mechanics/molecular mechanics (QM/MM) approach, we propose a mechanism for the phosphoryl transfer catalyzed by ERK that offers new insights into MAPK function. Our results suggest that (1) the proline residue has a role in both specificity and phospho transfer efficiency, (2) the reaction occurs in one step, with ERK2 Asp(147) acting as the catalytic base, (3) a conserved Lys in the kinase superfamily that is usually mutated to check kinase activity strongly stabilizes the transition state, and (4) the reaction mechanism is similar with either one or two Mg(2+) ions in the active site. Taken together, our results provide a detailed description of the molecular events involved in the phosphorylation reaction catalyzed by MAPK and contribute to the general understanding of kinase activity.
C1 [Gustavo Turjanski, Adrian; Gutkind, J. Silvio] Natl Inst Dental & Craniofacial Res, Oral & Pharyngeal Canc Branch, Bethesda, MD 20892 USA.
[Hummer, Gerhard] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Turjanski, AG (reprint author), Univ Buenos Aires, Fac Ciencias Exactas & Nat, Dept Quim Inorgan Analit & Quim Fis, Buenos Aires, DF, Argentina.
EM adrian@qi.fcen.uba.ar
RI Gutkind, J. Silvio/A-1053-2009; Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
FU PEW Latin American Fellow; Intramural Research Programs of NIDCR, NIH;
NIDDK, NIH
FX Adrian Turjanski was supported as a PEW Latin American Fellow. The
authors acknowledge support by the Intramural Research Programs of
NIDCR, NIH (A.G.T. and J.S.G.) and NIDDK, NIH (G.H.).
NR 55
TC 24
Z9 24
U1 0
U2 9
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD MAY 6
PY 2009
VL 131
IS 17
BP 6141
EP 6148
DI 10.1021/ja8071995
PG 8
WC Chemistry, Multidisciplinary
SC Chemistry
GA 441FX
UT WOS:000265755800038
PM 19361221
ER
PT J
AU Ballard-Barbash, R
Hunsberger, S
Alciati, MH
Blair, SN
Goodwin, PJ
McTiernan, A
Wing, R
Schatzkin, A
AF Ballard-Barbash, Rachel
Hunsberger, Sally
Alciati, Marianne H.
Blair, Steven N.
Goodwin, Pamela J.
McTiernan, Anne
Wing, Rena
Schatzkin, Arthur
TI Physical Activity, Weight Control, and Breast Cancer Risk and Survival:
Clinical Trial Rationale and Design Considerations
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID CORONARY HEART-DISEASE; BODY-MASS INDEX; DIABETES-PREVENTION-PROGRAM;
LIFE-STYLE INTERVENTIONS; HEALTHY FOOD CHOICES; ALL-CAUSE MORTALITY;
RANDOMIZED-TRIAL; FOLLOW-UP; CARDIORESPIRATORY FITNESS; RECRUITMENT
METHODS
AB Substantial observational epidemiological evidence exists that physical activity and weight control are associated with decreased risk of postmenopausal breast cancer. Uncertainty remains regarding several aspects of these associations, including the effect of possible confounding factors on these associations. We present the rationale and design for two randomized controlled trials that can help resolve this uncertainty. In a 5-year prevention trial conducted among women at high risk of breast cancer, the primary endpoint would be breast cancer incidence. For a comparable survivorship trial, the primary endpoint would be the disease-free interval and secondary endpoints would be breast cancer recurrence-free interval, second primary breast cancer, and total invasive plus in situ breast cancer. A set of inclusion and exclusion criteria is proposed for both trials. Intervention goals are the same for both trials. Goals for the weight control intervention would be, for women whose body mass index (BMI) is greater than 25 kg/m(2), to lose 10% of body weight and, for women whose BMI is less than or equal to 25 kg/m(2), to avoid weight gain. The goal for the physical activity intervention would be to achieve and maintain regular participation in a moderate-intensity physical activity program for a total of 150-225 minutes over at least 5 days per week. Sample size calculations are based on alternative assumptions about hazard ratio, adherence, follow-up duration, and power and are presented for the primary prevention and survivorship trials. Although both studies could enhance our understanding of breast cancer etiology and benefit public health, practical considerations, including smaller sample size, ease of recruitment, and reduced likelihood of early termination, favor the survivorship trial at this time.
C1 [Ballard-Barbash, Rachel] NCI, Appl Res Program, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Hunsberger, Sally] NCI, Biometr Res Branch, Div Canc Treatment, NIH, Bethesda, MD 20892 USA.
[Schatzkin, Arthur] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Alciati, Marianne H.] Susan G Komen Cure, Sci Operat, Dallas, TX USA.
[Blair, Steven N.] Univ S Carolina, Dept Exercise Sci, Columbia, SC 29208 USA.
[Goodwin, Pamela J.] Univ Toronto, Mt Sinai Hosp, Dept Med, Toronto, CA USA.
[McTiernan, Anne] Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA 98104 USA.
[Wing, Rena] Miriam Hosp, Ctr Behav Med, Providence, RI 02906 USA.
[Wing, Rena] Miriam Hosp, Ctr Prevent Med, Providence, RI 02906 USA.
[Wing, Rena] Brown Univ, Providence, RI 02912 USA.
RP Ballard-Barbash, R (reprint author), NCI, Appl Res Program, Div Canc Control & Populat Sci, NIH, EPN 4005,Execut Blvd, Bethesda, MD 20892 USA.
EM barbashr@mail.nih.gov
RI Goodwin, Pamela/K-1477-2013;
OI Alciati, Marianne/0000-0001-6294-1090
NR 81
TC 51
Z9 51
U1 1
U2 13
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD MAY 6
PY 2009
VL 101
IS 9
BP 630
EP 643
DI 10.1093/jnci/djp068
PG 14
WC Oncology
SC Oncology
GA 444AR
UT WOS:000265952700007
PM 19401543
ER
PT J
AU Anderson, WF
Sherman, ME
Carreon, JD
Brinton, LA
AF Anderson, William F.
Sherman, Mark E.
Carreon, J. Daniel
Brinton, Louise A.
TI Response: Re: Recent Trends in Breast Cancer Among Younger Women in the
United States
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
ID RATES
C1 [Anderson, William F.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Sherman, Mark E.; Carreon, J. Daniel; Brinton, Louise A.] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
RP Anderson, WF (reprint author), NCI, Biostat Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Rm 8036, Rockville, MD 20852 USA.
EM wanderso@mail.nih.gov
RI Brinton, Louise/G-7486-2015
OI Brinton, Louise/0000-0003-3853-8562
NR 7
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD MAY 6
PY 2009
VL 101
IS 9
BP 692
EP 693
DI 10.1093/jnci/djp027
PG 2
WC Oncology
SC Oncology
GA 444AR
UT WOS:000265952700016
ER
PT J
AU Hong, SY
Saavedra, JE
Keefer, LK
Chakrapani, H
AF Hong, Sam Y.
Saavedra, Joseph E.
Keefer, Larry K.
Chakrapani, Harinath
TI Improved synthesis of V-PYRRO/NO, a liver-selective nitric oxide
prodrug, and analogues
SO TETRAHEDRON LETTERS
LA English
DT Article
ID INDUCED HEPATOTOXICITY; SECONDARY-AMINES; DONOR; MICE; PROTECTS;
APOPTOSIS; TOXICITY; CHEMISTRY
AB The reported synthesis of O(2)-vinyl 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate(V-PYRRO/NO), a hepatoprotective agent, was cumbersome and limited by a poor overall yield of 4% from sodium 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (PYRRO/No). We report an improved synthesis of V-PYRRO/NO in two steps with a significantly higher overall yield of 40% from PYRRO/NO. Using this protocol, a number of structural analogues of V-PYRRO/NO were prepared in good yields. Published by Elsevier Ltd.
C1 [Hong, Sam Y.; Keefer, Larry K.; Chakrapani, Harinath] NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
[Saavedra, Joseph E.] NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA.
RP Chakrapani, H (reprint author), NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
EM chakrah@ncifcrf.gov
RI Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU Intramural Research Program of the NIH; National Cancer Institute
[N01-CO2008-00001]; Center for Cancer Research
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research, as
well as National Cancer Institute contract N01-CO2008-00001 to SAIC.
NR 27
TC 6
Z9 6
U1 0
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0040-4039
J9 TETRAHEDRON LETT
JI Tetrahedron Lett.
PD MAY 6
PY 2009
VL 50
IS 18
BP 2069
EP 2071
DI 10.1016/j.tetlet.2009.02.103
PG 3
WC Chemistry, Organic
SC Chemistry
GA 431HS
UT WOS:000265052800010
ER
PT J
AU Wu, HT
Kaur, G
Griffiths, GL
AF Wu, Haitao
Kaur, Gurpreet
Griffiths, Gary L.
TI An improved synthesis of a fluorescent gabapentin-choline conjugate for
single molecule detection
SO TETRAHEDRON LETTERS
LA English
DT Article
DE Calcium ion channel; Gabapentin; Single molecule detection; Fluorescence
imaging
ID ACETYLCHOLINE; PHARMACOLOGY
AB Voltage-gated calcium ion channels comprise pore-forming alpha(1) and auxiliary alpha(2)delta, beta, and gamma subunits. They are important molecular devices involved in a variety of cell functions. Fluorescently labeled acylcholine analogues are important in studies such as ion channel regulation. Cy3-3-acetylcholine has recently been synthesized for single molecule detection studies; albeit in an extremely low overall yield (0.06%). In this Work, an alternative route to that used in the previous Cy3-3-acetylcholine synthesis was developed with a 90% yield at a significantly lower material cost. Published by Elsevier Ltd.
C1 [Wu, Haitao; Kaur, Gurpreet; Griffiths, Gary L.] NHLBI, Imaging Probe Dev Ctr, NIH, Rockville, MD 20850 USA.
RP Griffiths, GL (reprint author), NHLBI, Imaging Probe Dev Ctr, NIH, 9800 Med Ctr Dr, Rockville, MD 20850 USA.
EM griffithsgl@mail.nih.gov
FU NIH Roadmap for Medical Research Initiative
FX This work was supported by the NIH Roadmap for Medical Research
Initiative through its establishment of the imaging Probe Development
Center, administered by the National Heart, Lung, and Blood Institute.
NR 11
TC 8
Z9 8
U1 0
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0040-4039
J9 TETRAHEDRON LETT
JI Tetrahedron Lett.
PD MAY 6
PY 2009
VL 50
IS 18
BP 2100
EP 2102
DI 10.1016/j.tetlet.2009.02.125
PG 3
WC Chemistry, Organic
SC Chemistry
GA 431HS
UT WOS:000265052800019
PM 20161233
ER
PT J
AU Levey, AS
Stevens, LA
Schmid, CH
Zhang, YP
Castro, AF
Feldman, HI
Kusek, JW
Eggers, P
Van Lente, F
Greene, T
Coresh, J
AF Levey, Andrew S.
Stevens, Lesley A.
Schmid, Christopher H.
Zhang, Yaping (Lucy)
Castro, Alejandro F., III
Feldman, Harold I.
Kusek, John W.
Eggers, Paul
Van Lente, Frederick
Greene, Tom
Coresh, Josef
CA Chronic Kidney Dis Epidemiology Co
TI A New Equation to Estimate Glomerular Filtration Rate
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; COCKCROFT-GAULT EQUATIONS; RENIN-ANGIOTENSIN
SYSTEM; SERUM CREATININE VALUES; RENAL-DISEASE; DIABETIC-NEPHROPATHY;
PREDICTIVE PERFORMANCE; NATIONAL-HEALTH; DUAL BLOCKADE; CYSTATIN-C
AB Background: Equations to estimate glomerular filtration rate (GFR) are routinely used to assess kidney function. Current equations have limited precision and systematically underestimate measured GFR at higher values.
Objective: To develop a new estimating equation for GFR: the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation.
Design: Cross-sectional analysis with separate pooled data sets for equation development and validation and a representative sample of the U. S. population for prevalence estimates.
Setting: Research studies and clinical populations ("studies") with measured GFR and NHANES (National Health and Nutrition Examination Survey), 1999 to 2006.
Participants: 8254 participants in 10 studies (equation development data set) and 3896 participants in 16 studies (validation data set). Prevalence estimates were based on 16 032 participants in NHANES.
Measurements: GFR, measured as the clearance of exogenous filtration markers (iothalamate in the development data set; iothalamate and other markers in the validation data set), and linear regression to estimate the logarithm of measured GFR from standardized creatinine levels, sex, race, and age.
Results: In the validation data set, the CKD-EPI equation performed better than the Modification of Diet in Renal Disease Study equation, especially at higher GFR (P < 0.001 for all subsequent comparisons), with less bias (median difference between measured and estimated GFR, 2.5 vs. 5.5 mL/min per 1.73 m(2)), improved precision (interquartile range [IQR] of the differences, 16.6 vs. 18.3 mL/min per 1.73 m(2)), and greater accuracy (percentage of estimated GFR within 30% of measured GFR, 84.1% vs. 80.6%). In NHANES, the median estimated GFR was 94.5 mL/min per 1.73 m(2) ( IQR, 79.7 to 108.1) vs. 85.0 (IQR, 72.9 to 98.5) mL/min per 1.73 m(2), and the prevalence of chronic kidney disease was 11.5% (95% CI, 10.6% to 12.4%) versus 13.1% (CI, 12.1% to 14.0%).
Limitation: The sample contained a limited number of elderly people and racial and ethnic minorities with measured GFR.
Conclusion: The CKD-EPI creatinine equation is more accurate than the Modification of Diet in Renal Disease Study equation and could replace it for routine clinical use.
Primary Funding Source: National Institute of Diabetes and Digestive and Kidney Diseases.
C1 [Levey, Andrew S.; Stevens, Lesley A.; Schmid, Christopher H.; Zhang, Yaping (Lucy)] Tufts Med Ctr, Div Nephrol, Boston, MA 02111 USA.
[Castro, Alejandro F., III; Coresh, Josef] Johns Hopkins Univ, Baltimore, MD USA.
[Feldman, Harold I.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Kusek, John W.; Eggers, Paul] NIH, Bethesda, MD 20892 USA.
[Van Lente, Frederick] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Greene, Tom] Univ Utah, Salt Lake City, UT USA.
RP Levey, AS (reprint author), Tufts Med Ctr, Div Nephrol, 800 Washington St,Box 391, Boston, MA 02111 USA.
RI Nelson, Robert/B-1470-2012;
OI Schmid, Christopher/0000-0002-0855-5313
FU National Institute of Diabetes and Digestive and Kidney Diseases [UO1 DK
053869, UO1 DK 067651, UO1 DK 35073]
FX By grants UO1 DK 053869, UO1 DK 067651, and UO1 DK 35073 as part of a
cooperative agreement with the National Institute of Diabetes and
Digestive and Kidney Diseases.
NR 50
TC 4953
Z9 5157
U1 27
U2 150
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
EI 1539-3704
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD MAY 5
PY 2009
VL 150
IS 9
BP 604
EP 612
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 443IQ
UT WOS:000265903800004
PM 19414839
ER
PT J
AU O'Brien, EP
Brooks, BR
Thirumalai, D
AF O'Brien, Edward P.
Brooks, Bernard R.
Thirumalai, D.
TI Molecular Origin of Constant m-Values, Denatured State Collapse, and
Residue-Dependent Transition Midpoints in Globular Proteins
SO BIOCHEMISTRY
LA English
DT Article
ID AQUEOUS UREA SOLUTIONS; FREE-ENERGY CHANGES; TRANSFER MODEL; AMINO-ACID;
GUANIDINE-HYDROCHLORIDE; LINEAR EXTRAPOLATION; ALPHA-CHYMOTRYPSIN;
DYNAMICS METHOD; LATTICE MODELS; SIDE-CHAINS
AB Experiments show that for many two-state folders the free energy of the native state, Delta G(ND)([C]) changes linearly as the denaturant concentration, [C], is varied. The slope {m = [d Delta G(ND)([C])]/(d[C])}, is nearly constant. According to the transfer model, the m-value is associated with the difference in the 2 surface area between the native (N) and denatured (D) state, which should be a function of Delta R-g(2), the difference in the square of the radius of gyration between the D and N states. Single-molecule experiments show that the R-g of the structurally heterogeneous denatured state undergoes an equilibrium collapse transition as [C] decreases, which implies m also should be [C]-dependent. We resolve the conundrum between constant m-values and [C]-dependent changes in R-g using molecular simulations of a coarse-grained representation of protein L, and the molecular transfer model, for which the equilibrium folding can be accurately calculated as a function of denaturant (urea) concentration. In agreement with experiment, we find that over a large range of denaturant concentration (>3 M) the m-value is a constant, whereas under strongly renaturing conditions (<3 M), it depends on [C]. The m-value is a constant above [C] > 3 M because the [C]-dependent changes in the surface area of the backbone groups, which make the largest contribution to m, are relatively narrow in the denatured state. The burial of the backbone and hydrophobic side chains gives rise to substantial surface area changes below [C] < 3 M, leading to collapse in the denatured state of protein L. Dissection of the contribution of various amino acids to the total surface area change with [C] shows that both the sequence context and residual structure are important. There are [C]-dependent variations in the surface area for chemically identical groups such as the backbone or Ala. Consequently, the midpoints of transition of individual residues vary significantly (which we call the Holtzer effect) even though global folding can be described as an all-or-none transition. The collapse is specific in nature, resulting in the formation of compact structures with appreciable populations of nativelike secondary structural elements. The collapse transition is driven by the loss of favorable residue-solvent interactions and a concomitant increase in the strength of intrapeptide interactions with a decreasing [C]. The strength of these interactions is nonuniformly distributed throughout the structure of protein L. Certain secondary structure elements have stronger [C]-dependent interactions than others in the denatured state.
C1 [O'Brien, Edward P.; Thirumalai, D.] Univ Maryland, Inst Phys Sci & Technol, Biophys Program, College Pk, MD 20742 USA.
[O'Brien, Edward P.; Thirumalai, D.] Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA.
[O'Brien, Edward P.; Brooks, Bernard R.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Thirumalai, D (reprint author), Univ Maryland, Inst Phys Sci & Technol, Biophys Program, College Pk, MD 20742 USA.
EM thirum@umd.edu
RI O'Brien, Edward/C-3587-2015
FU National Science Foundation [05-14056]; Air Force Office of Scientific
Research [FA9550-07-1-0098]; National Institutes of Health; National
Heart, Lung and Blood Institute
FX This work was supported in part by a grant from the National Science
Foundation (05-14056) and the Air Force Office of Scientific Research
(FA9550-07-1-0098) to D.T., by a National Institutes of Health GPP
Biophysics Fellowship to E.P.O., and by the Intramural Research Program
of the National Heart, Lung and Blood Institute.
NR 65
TC 25
Z9 25
U1 2
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD MAY 5
PY 2009
VL 48
IS 17
BP 3743
EP 3754
DI 10.1021/bi8021119
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 438AR
UT WOS:000265528800006
PM 19278261
ER
PT J
AU Gohlke, JM
Thomas, R
Zhang, YQ
Rosenstein, MC
Davis, AP
Murphy, C
Becker, KG
Mattingly, CJ
Portier, CJ
AF Gohlke, Julia M.
Thomas, Reuben
Zhang, Yonqing
Rosenstein, Michael C.
Davis, Allan P.
Murphy, Cynthia
Becker, Kevin G.
Mattingly, Carolyn J.
Portier, Christopher J.
TI Genetic and environmental pathways to complex diseases
SO BMC SYSTEMS BIOLOGY
LA English
DT Article
ID INFLAMMATION-RELATED GENES; EXPRESSION PROFILES; SYSTEMATIC
METAANALYSES; INTERACTION NETWORKS; RETINOIC ACID; PPAR-GAMMA; GENOME;
OBESITY; DATABASE; RISK
AB Background: Pathogenesis of complex diseases involves the integration of genetic and environmental factors over time, making it particularly difficult to tease apart relationships between phenotype, genotype, and environmental factors using traditional experimental approaches.
Results: Using gene-centered databases, we have developed a network of complex diseases and environmental factors through the identification of key molecular pathways associated with both genetic and environmental contributions. Comparison with known chemical disease relationships and analysis of transcriptional regulation from gene expression datasets for several environmental factors and phenotypes clustered in a metabolic syndrome and neuropsychiatric subnetwork supports our network hypotheses. This analysis identifies natural and synthetic retinoids, antipsychotic medications, Omega 3 fatty acids, and pyrethroid pesticides as potential environmental modulators of metabolic syndrome phenotypes through PPAR and adipocytokine signaling and organophosphate pesticides as potential environmental modulators of neuropsychiatric phenotypes.
Conclusion: Identification of key regulatory pathways that integrate genetic and environmental modulators define disease associated targets that will allow for efficient screening of large numbers of environmental factors, screening that could set priorities for further research and guide public health decisions.
C1 [Gohlke, Julia M.; Thomas, Reuben; Portier, Christopher J.] Natl Inst Environm Hlth Sci, Environm Syst Biol Grp, Mol Toxicol Lab, Res Triangle Pk, NC 27709 USA.
[Zhang, Yonqing; Becker, Kevin G.] NIA, Gene Express & Genom Unit, NIH, Baltimore, MD 21224 USA.
[Rosenstein, Michael C.; Davis, Allan P.; Murphy, Cynthia; Mattingly, Carolyn J.] Mt Desert Isl Biol Lab, Dept Bioinformat, Salsbury Cove, ME 04672 USA.
RP Portier, CJ (reprint author), Natl Inst Environm Hlth Sci, Environm Syst Biol Grp, Mol Toxicol Lab, Res Triangle Pk, NC 27709 USA.
EM gohlkej@niehs.nih.gov; thomasr3@niehs.nih.gov; zhangyon@grc.nia.nih.gov;
mcr@mdibl.org; apdavis@mdibl.org; cmurphy@mdibl.org;
beckerk@grc.nia.nih.gov; cmattin@mdibl.org; portier@niehs.nih.gov
RI Portier, Christopher/A-3160-2010;
OI Portier, Christopher/0000-0002-0954-0279; Gohlke,
Julia/0000-0002-6984-2893; Becker, Kevin/0000-0002-6794-6656
FU NIH, National Institute of Environmental Health Sciences; National
Institute of Aging; NIEHS [5R01ES014065-02]
FX This research was supported in part by the Intramural Research Program
of the NIH, National Institute of Environmental Health Sciences (J.G.,
R.T., C.P.) and National Institute of Aging (Y.Z., K.B.) as well as
NIEHS extramural funding under grant 5R01ES014065-02 ( M. R., A.D., C.M.
and C.J.M.).
NR 78
TC 40
Z9 40
U1 1
U2 12
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1752-0509
J9 BMC SYST BIOL
JI BMC Syst. Biol.
PD MAY 5
PY 2009
VL 3
AR 46
DI 10.1186/1752-0509-3-46
PG 15
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 444TA
UT WOS:000266002100001
PM 19416532
ER
PT J
AU Miao, CL
Chen, SG
Macedo, R
Lai, SH
Liu, K
Li, DB
Wasserman, BA
Vogel-Clausen, J
Lima, JAC
Bluemke, DA
AF Miao, Cuilian
Chen, Shaoguang
Macedo, Robson
Lai, Shenghan
Liu, Kiang
Li, Debiao
Wasserman, Bruce A.
Vogel-Clausen, Jens
Lima, Joao A. C.
Bluemke, David A.
TI Positive Remodeling of the Coronary Arteries Detected by Magnetic
Resonance Imaging in an Asymptomatic Population MESA (Multi-Ethnic Study
of Atherosclerosis)
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE subclinical atherosclerosis; magnetic resonance imaging; coronary artery
disease; plaque
ID VESSEL WALL; IN-VIVO; INTRAVASCULAR ULTRASOUND; COMPENSATORY
ENLARGEMENT; COMPUTED-TOMOGRAPHY; PLAQUE; MRI; INDIVIDUALS; ENDOTHELIUM;
THERAPY
AB Objectives The purpose of this study was to assess coronary arterial remodeling as a marker of subclinical atherosclerosis using coronary wall magnetic resonance imaging (MRI) in an asymptomatic population-based cohort.
Background In early atherosclerosis, compensatory enlargement of both the outer wall of the vessel as well as the lumen, termed compensatory enlargement or positive remodeling, occurs before luminal narrowing.
Methods One hundred seventy-nine participants in the MESA (Multi-Ethnic Study of Atherosclerosis) trial were evaluated using black-blood coronary wall MRI. Coronary cross-sectional area (vessel size), lumen area, and mean wall thickness of the proximal coronary arteries were measured.
Results Men had a greater vessel size, lumen area, and mean wall thickness than women (38.3 +/- 11.3 mm(2) vs. 32.6 +/- 9.4 mm(2), 6.7 +/- 3.2 mm(2) vs. 5.3 +/- 2.4 mm(2), and 2.0 +/- 0.3 mm vs. 1.9 +/- 0.3 mm, respectively, p < 0.05). No significant coronary artery narrowing was present by magnetic resonance angiography. Overall, coronary vessel size increased 25.9 mm(2) per millimeter increase in coronary wall thickness, whereas lumen area increased only slightly at 3.1 mm(2) for every millimeter increase in wall thickness (difference in slopes, p < 0.0001). Adjusting for age and sex, participants with an Agatston score > 0 were more likely to have wall thickness > 2.0 mm (odds ratio: 2.0, 95% confidence interval: 1.01 to 3.84).
Conclusions Coronary wall MRI detected positive arterial remodeling in asymptomatic men and women with subclinical atherosclerosis. (J Am Coll Cardiol 2009; 53: 1708-15) (C) 2009 by the American College of Cardiology Foundation
C1 [Miao, Cuilian; Macedo, Robson; Wasserman, Bruce A.; Vogel-Clausen, Jens; Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, Baltimore, MD USA.
[Chen, Shaoguang; Lai, Shenghan] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Liu, Kiang] Northwestern Univ, Sch Med, Dept Prevent Med, Chicago, IL USA.
[Li, Debiao] Northwestern Univ, Sch Med, Dept Radiol, Chicago, IL 60611 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
RP Bluemke, DA (reprint author), Johns Hopkins Univ Hosp, MRI Room 143 Nelson Basement,600 N Wolfe St, Baltimore, MD 21287 USA.
EM dbluemke@jhmi.edu
RI Li, Debiao/B-7622-2009;
OI Bluemke, David/0000-0002-8323-8086
FU National Heart, Lung, and Blood Institute [R01 HL78909, N01-HC95159,
N01-HC-95169]
FX This research was supported by R01 HL78909 and contracts N01-HC95159
through N01-HC-95169 from the National Heart, Lung, and Blood Institute.
Paul Schoenhagen, MD, served as Guest Editor for this article.
NR 27
TC 66
Z9 71
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD MAY 5
PY 2009
VL 53
IS 18
BP 1708
EP 1715
DI 10.1016/j.jacc.2008.12.063
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 439LL
UT WOS:000265628500012
PM 19406347
ER
PT J
AU Copenhaver, BR
Shin, J
Warach, S
Butman, JA
Saver, JL
Kidwell, CS
AF Copenhaver, B. R.
Shin, J.
Warach, S.
Butman, J. A.
Saver, J. L.
Kidwell, C. S.
TI Gradient echo MRI Implementation of a training tutorial for intracranial
hemorrhage diagnosis
SO NEUROLOGY
LA English
DT Article
ID ACUTE STROKE; THROMBOLYTIC THERAPY; COMPUTED-TOMOGRAPHY;
ISCHEMIC-STROKE; CT; DISEASE; HEME
AB Background: Recent studies have demonstrated that gradient echo (GRE) MRI sequences are as accurate as CT for the detection of intracerebral hemorrhage (ICH) in the context of acute stroke. However, many physicians who currently read acute stroke imaging studies may be unfamiliar with interpretation of GRE images.
Methods: An NIH Web-based training program was developed including a pretest, tutorial, and posttest. Physicians involved in the care of acute stroke patients were encouraged to participate. The tutorial covered acute, chronic, and mimic hemorrhages as they appear on CT, diffusion-weighted imaging, and GRE sequences. Ability of users to identify ICH presence, type, and age on GRE was compared from the pretest to posttest timepoint.
Results: A total of 104 users completed the tutorial. Specialties represented included general radiology (42%), general neurology (16%), neuroradiology (15%), stroke neurology (14%), emergency medicine (1%), and other (12%). Median overall score improved pretest to posttest from 66.7% to 83.3%, p < 0.001. Improvement by category was as follows: acute ICH, 66.7%-100%, p < 0.001; chronic ICH, 33.3%-66.7%, p < 0.001; ICH negatives/mimics, 100%-100%, p = 0.787. Sensitivity for identification of acute hemorrhage improved from 68.2% to 96.4%.
Conclusions: Physicians involved in acute stroke care achieved significant improvement in gradient echo ( GRE) hemorrhage interpretation after completing the NIH GRE MRI tutorial. This indicates that a Web-based tutorial may be a viable option for the widespread education of physicians to achieve an acceptable level of diagnostic accuracy at reading GRE MRI, thus enabling confident acute stroke treatment decisions. Neurology (R) 2009;72:1576-1581
C1 [Copenhaver, B. R.; Kidwell, C. S.] Georgetown Univ, Dept Neurol, Washington, DC USA.
[Shin, J.; Saver, J. L.] Univ Calif Los Angeles, Los Angeles, CA 90024 USA.
[Warach, S.] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD USA.
[Butman, J. A.] NIH, Ctr Clin, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
RP Kidwell, CS (reprint author), 4000 Reservoir Rd,Bldg D,Suite 150, Washington, DC 20007 USA.
EM ck256@georgetown.edu
RI Butman, John/A-2694-2008;
OI Butman, John/0000-0002-1547-9195; Saver, Jeffrey/0000-0001-9141-2251
FU Intramural NIH HHS; NINDS NIH HHS [P50 NS044378, P50 NS044378-069011]
NR 12
TC 2
Z9 2
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD MAY 5
PY 2009
VL 72
IS 18
BP 1576
EP 1581
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 441PZ
UT WOS:000265782600008
PM 19414724
ER
PT J
AU Wolf, YI
Novichkov, PS
Karev, GP
Koonin, EV
Lipman, DJ
AF Wolf, Yuri I.
Novichkov, Pavel S.
Karev, Georgy P.
Koonin, Eugene V.
Lipman, David J.
TI The universal distribution of evolutionary rates of genes and distinct
characteristics of eukaryotic genes of different apparent ages
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gene age; gene expression; genome evolution; intron density
ID PROTEIN EVOLUTION; INVERSE RELATIONSHIP; SEQUENCE EVOLUTION; MAMMALIAN
GENES; PSI-BLAST; GENOME; DATABASE; DISPENSABILITY; DIVERGENCE;
EXPRESSION
AB The evolutionary rates of protein-coding genes in an organism span, approximately, 3 orders of magnitude and show a universal, approximately log-normal distribution in a broad variety of species from prokaryotes to mammals. This universal distribution implies a steady-state process, with identical distributions of evolutionary rates among genes that are gained and genes that are lost. A mathematical model of such process is developed under the single assumption of the constancy of the distributions of the propensities for gene loss (PGL). This model predicts that genes of different ages, that is, genes with homologs detectable at different phylogenetic depths, substantially differ in those variables that correlate with PGL. We computationally partition protein-coding genes from humans, flies, and Aspergillus fungus into age classes, and show that genes of different ages retain the universal log-normal distribution of evolutionary rates, with a shift toward higher rates in "younger'' classes but also with a substantial overlap. The only exception involves human primate-specific genes that show a heavy tail of rapidly evolving genes, probably owing to gene annotation artifacts. As predicted, the gene age classes differ in characteristics correlated with PGL. Compared with "young'' genes (e.g., mammal-specific human ones), "old'' genes (e.g., eukaryote-specific), on average, are longer, are expressed at a higher level, possess a higher intron density, evolve slower on the short time scale, and are subject to stronger purifying selection. Thus, genome evolution fits a simple model with approximately uniform rates of gene gain and loss, without major bursts of genomic innovation.
C1 [Wolf, Yuri I.; Karev, Georgy P.; Koonin, Eugene V.; Lipman, David J.] NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
[Novichkov, Pavel S.] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA.
RP Lipman, DJ (reprint author), NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
EM lipman@ncbi.nlm.nih.gov
FU Department of Health and Human Services (National Library of Medicine,
National Institutes of Health)
FX We thank Liran Carmel for valuable help with the expression data and
useful discussions of the statistical analysis and Josh Cherry for
critical reading of the manuscript. This work was supported by the
Department of Health and Human Services (National Library of Medicine,
National Institutes of Health).
NR 64
TC 98
Z9 100
U1 0
U2 14
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 5
PY 2009
VL 106
IS 18
BP 7273
EP 7280
DI 10.1073/pnas.0901808106
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441QI
UT WOS:000265783600004
PM 19351897
ER
PT J
AU Dikeakos, JD
Di Lello, P
Lacombe, MJ
Ghirlando, R
Legault, P
Reudelhuber, TL
Omichinski, JG
AF Dikeakos, Jimmy D.
Di Lello, Paola
Lacombe, Marie-Josee
Ghirlando, Rodolfo
Legault, Pascale
Reudelhuber, Timothy L.
Omichinski, James G.
TI Functional and structural characterization of a dense core secretory
granule sorting domain from the PC1/3 protease
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE NMR; prohormone convertases
ID C-13-LABELED PROTEINS; IMPROVED SENSITIVITY; REGULATED PATHWAY; NMR
EXPERIMENTS; ALPHA-HELIX; J COUPLINGS; SPECTROSCOPY; PROPROTEIN;
SEQUENCE; SYSTEM
AB Several peptide hormones are initially synthesized as inactive precursors. It is only on entry of these prohormones and their processing proteases into dense core secretory granules (DCSGs) that the precursors are cleaved to generate their active forms. Prohormone convertase (PC)1/3 is a processing protease that is targeted to DCSGs. The signal for targeting PC1/3 to DCSGs resides in its carboxy-terminal tail (PC1/3(617-753)), where 3 regions (PC1/3(617-625), PC1/3(665-682), and PC1/3(711-753)) are known to aid in sorting and membrane association. In this article, we have determined a high-resolution structure of the extreme carboxy-terminal sorting domain, PC1/3(711-753) in micelles by NMR spectroscopy. PC1/3(711-753) contains 2 alpha helices located between residues 722-728 and 738-750. Functional assays demonstrate that the second helix (PC1/3(738-750)) is necessary and sufficient to target a constitutively secreted protein to granules, and that L(745) anchors a hydrophobic patch that is critical for sorting. Also, we demonstrate that calcium binding by the second helix of PC1/3(711-753) promotes aggregation of the domain via the hydrophobic patch centered on L(745). These results provide a structure-function analysis of a DCSG-sorting domain, and reveal the importance of a hydrophobic patch and calcium binding in controlling the sorting of proteins containing alpha helices to DCSGs.
C1 [Dikeakos, Jimmy D.; Lacombe, Marie-Josee; Reudelhuber, Timothy L.] Clin Res Inst Montreal, Lab Mol Biochem Hypertens, Montreal, PQ H2W 1R7, Canada.
[Di Lello, Paola; Legault, Pascale; Omichinski, James G.] Univ Montreal, Dept Biochem, Montreal, PQ H3C 3J7, Canada.
[Ghirlando, Rodolfo] NIDDK, Mol Biol Lab, Bethesda, MD 20892 USA.
RP Reudelhuber, TL (reprint author), Clin Res Inst Montreal, Lab Mol Biochem Hypertens, 110 Pine Ave W, Montreal, PQ H2W 1R7, Canada.
EM reudelt@ircm.qc.ca; jg.omichinski@umontreal.ca
RI Ghirlando, Rodolfo/A-8880-2009; di lello, paola/C-8605-2013
FU National Institutes of Health; National Institute of Diabetes and
Digestive and Kidney Diseases
FX The 800 MHz NMR experiments were recorded at the Quebec/Eastern Canada
High Field NMR Facility, supported by grants from the Canada Foundation
for Innovation and the Quebec Ministere de la Recherche en Science et
Technologie. This work was supported by the Canadian Institutes of
Health Research (CIHR) Grants MOP-135604 (to J.G.O.) and MOP-53177 ( to
T. L. R.). J.D.D. is a recipient of a studentship from the Fonds de la
Recherche en Sante du Quebec, and P. D. L. of a fellowship from the
CIHR. P. L. is a Canadian Research Chair in Structural Biology of RNA.
This work was also supported in part by the Intramural Research Program
of the National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases (R. G.).
NR 39
TC 21
Z9 21
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 5
PY 2009
VL 106
IS 18
BP 7408
EP 7413
DI 10.1073/pnas.0809576106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441QI
UT WOS:000265783600028
PM 19376969
ER
PT J
AU Pedersen, MG
Sherman, A
AF Pedersen, Morten Gram
Sherman, Arthur
TI Newcomer insulin secretory granules as a highly calcium-sensitive pool
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE beta-cells; biphasic secretion; exocytosis; pancreatic islets; vesicles
ID PANCREATIC BETA-CELLS; ADRENAL CHROMAFFIN CELLS; PROTEIN-KINASE-C;
CA2+-SENSITIVE POOL; CA2+ SENSORS; MOLECULAR-MECHANISMS; TARGET
MEMBRANE; FAST EXOCYTOSIS; VESICLE FUSION; INS-1 CELLS
AB Insulin secretion is biphasic in response to a step in glucose stimulation. Recent experiments suggest that 2 different mechanisms operate during the 2 phases, with transient first-phase secretion due to exocytosis of docked granules but the second sustained phase due largely to newcomer granules. Another line of research has shown that there exist 2 pools of releasable granules with different Ca(2+) sensitivities. An immediately releasable pool (IRP) is located in the vicinity of Ca(2+) channels, whereas a highly Ca(2+)-sensitive pool (HCSP) resides mainly away from Ca(2+) channels. We extend a previous model of exocytosis and insulin release by adding an HCSP and show that the inclusion of this pool naturally leads to insulin secretion mainly from newcomer granules during the second phase of secretion. We show that the model is compatible with data from single cells on the HCSP and from stimulation of islets by glucose, including L- and R-type Ca(2+) channel knockouts, as well as from Syntaxin-1A-deficient cells. We also use the model to investigate the relative contribution of calcium signaling and pool depletion in controlling biphasic secretion.
C1 [Pedersen, Morten Gram] Univ Padua, Dept Informat Engn, I-35131 Padua, Italy.
[Sherman, Arthur] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
RP Pedersen, MG (reprint author), Univ Padua, Dept Informat Engn, Via Gradenigo 6-A, I-35131 Padua, Italy.
EM pedersen@dei.unipd.it
RI Pedersen, Morten/F-4134-2012
OI Pedersen, Morten/0000-0002-2639-2394
FU Intramural NIH HHS
NR 61
TC 46
Z9 46
U1 0
U2 6
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 5
PY 2009
VL 106
IS 18
BP 7432
EP 7436
DI 10.1073/pnas.0901202106
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441QI
UT WOS:000265783600032
PM 19372374
ER
PT J
AU Paravastu, AK
Qahwash, I
Leapman, RD
Meredith, SC
Tycko, R
AF Paravastu, Anant K.
Qahwash, Isam
Leapman, Richard D.
Meredith, Stephen C.
Tycko, Robert
TI Seeded growth of beta-amyloid fibrils from Alzheimer's brain-derived
fibrils produces a distinct fibril structure
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Alzheimer's disease; electron microscopy; solid-state nuclear magnetic
resonance
ID NUCLEAR-MAGNETIC-RESONANCE; SOLID-STATE NMR; EXPERIMENTAL CONSTRAINTS;
DISTANCE MEASUREMENTS; DISEASE; PROTEIN; PEPTIDE; CONFORMATION;
ORGANIZATION; POLYMORPHISM
AB Studies by solid-state nuclear magnetic resonance (NMR) of amyloid fibrils prepared in vitro from synthetic 40-residue beta-amyloid (A beta(1-40)) peptides have shown that the molecular structure of A beta(1-40) fibrils is not uniquely determined by amino acid sequence. Instead, the fibril structure depends on the precise details of growth conditions. The molecular structures of beta-amyloid fibrils that develop in Alzheimer's disease (AD) are therefore uncertain. We demonstrate through thioflavin T fluorescence and electron microscopy that fibrils extracted from brain tissue of deceased AD patients can be used to seed the growth of synthetic A beta(1-40) fibrils, allowing preparation of fibrils with isotopic labeling and in sufficient quantities for solid-state NMR and other measurements. Because amyloid structures propagate themselves in seeded growth, as shown in previous studies, the molecular structures of brain-seeded synthetic A beta(1-40) fibrils most likely reflect structures that are present in AD brain. Solid-state (13)C NMR spectra of fibril samples seeded with brain material from two AD patients were found to be nearly identical, indicating the same molecular structures. Spectra of an unseeded control sample indicate greater structural heterogeneity. (13)C chemical shifts and other NMR data indicate that the predominant molecular structure in brain-seeded fibrils differs from the structures of purely synthetic A beta(1-40) fibrils that have been characterized in detail previously. These results demonstrate a new approach to detailed structural characterization of amyloid fibrils that develop in human tissue, and to investigations of possible correlations between fibril structure and the degree of cognitive impairment and neurodegeneration in AD.
C1 [Paravastu, Anant K.; Tycko, Robert] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Qahwash, Isam; Meredith, Stephen C.] Univ Chicago, Dept Biochem & Mol Biol, Chicago, IL 60637 USA.
[Qahwash, Isam; Meredith, Stephen C.] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
[Leapman, Richard D.] Natl Inst Biomed Imaging & Bioengn, Lab Bioengn & Phys Sci, NIH, Bethesda, MD 20892 USA.
RP Tycko, R (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM robertty@mail.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Institutes of Health [NS042852]; Alzheimer's Association
[IIRG-06-27794]
FX This work was supported by the Intramural Research Programs of the
National Institute of Diabetes and Digestive and Kidney Diseases (to A.
K. P. and R. T.); by the National Institute of Biomedical Imaging and
Bioengineering of the National Institutes of Health (to R. D. L.); and
by the National Institutes of Health (grant NS042852, to S. C. M.); and
by the Alzheimer's Association (grant IIRG-06-27794, to S. C. M.).
NR 39
TC 156
Z9 156
U1 3
U2 49
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 5
PY 2009
VL 106
IS 18
BP 7443
EP 7448
DI 10.1073/pnas.0812033106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441QI
UT WOS:000265783600034
PM 19376973
ER
PT J
AU Zheng, P
Dean, J
AF Zheng, Ping
Dean, Jurrien
TI Role of Filia, a maternal effect gene, in maintaining euploidy during
cleavage-stage mouse embryogenesis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE aneuploidy; mitotic kinases; spindle assembly checkpoint
ID EARLY EMBRYONIC-DEVELOPMENT; AURORA-A KINASE; LIM PROTEIN; RHO-GTPASES;
HELA-CELLS; SPINDLE; OOCYTES; ACTIVATION; TRANSITION; CENTROSOME
AB During oogenesis, mammalian eggs accumulate proteins required for early embryogenesis. Although limited data suggest a vital role of these maternal factors in chromatin reprogramming and embryonic genome activation, the full range of their functions in preimplantation development remains largely unknown. Here we report a role for maternal proteins in maintaining chromosome stability and euploidy in early-cleavage mouse embryogenesis. Filia, expressed in growing oocytes, encodes a protein that binds to MATER and participates in a subcortical maternal complex essential for cleavage-stage embryogenesis. The depletion of maternal stores of Filia impairs preimplantation embryo development with a high incidence of aneuploidy that results from abnormal spindle assembly, chromosome misalignment, and spindle assembly checkpoint (SAC) inactivation. In helping to ensure normal spindle morphogenesis, Filia regulates the proper allocation of the key spindle assembly regulators (i.e., AURKA, PLK1, and gamma-tubulin) to the microtubule-organizing center via the RhoA signaling pathway. Concurrently, Filia is required for the placement of MAD2, an essential component of the SAC, to kinetochores to enable SAC function. Thus, Filia is central to integrating the spatiotemporal localization of regulators that helps ensure euploidy and high-quality cell cycle progression in preimplantation mouse development. Defects in the well-conserved human homologue could play a similar role and account for recurrent human fetal wastage.
C1 [Zheng, Ping; Dean, Jurrien] NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Dean, J (reprint author), NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
EM jurrien@helix.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health. We express our sincere appreciation to
Drs. Chuxia Deng and Cuiling Li for establishing mutant mouse lines and
to Dr. Boris Baibakov for his insightful assistance with confocal
microscopy.
NR 47
TC 66
Z9 68
U1 1
U2 8
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 5
PY 2009
VL 106
IS 18
BP 7473
EP 7478
DI 10.1073/pnas.0900519106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441QI
UT WOS:000265783600039
PM 19376971
ER
PT J
AU Zhang, ML
Yao, ZS
Dubois, S
Ju, W
Muller, JR
Waldmann, TA
AF Zhang, Meili
Yao, Zhengsheng
Dubois, Sigrid
Ju, Wei
Mueller, Juergen R.
Waldmann, Thomas A.
TI Interleukin-15 combined with an anti-CD40 antibody provides enhanced
therapeutic efficacy for murine models of colon cancer
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE animal model; cancer immunotherapy; IL-15 receptor-alpha
ID REGULATORY T-CELLS; DENDRITIC CELLS; NATURAL-KILLER; NK CELLS; LYMPHOID
HOMEOSTASIS; GROWTH-FACTOR; BETA-CHAIN; IL-15; RECEPTOR; ANTITUMOR
AB IL-15 has potential as an immunotherapeutic agent for cancer treatment because it is a critical factor for the proliferation and activation of natural killer (NK) and CD8(+) T cells. Administration of anti-CD40 antibodies has shown anti-tumor effects in vivo through a variety of mechanisms. Furthermore, activation of CD40 led to increased expression of IL-15 receptor-alpha by dendritic cells, an action that is critical for trans- presentation of IL-15 to NK and CD8(+) T cells. In this study, we investigated the therapeutic efficacy of the combination regimen of murine IL-15 (mIL-15) with an agonistic anti-CD40 antibody (FGK4.5) in murine lung metastasis models involving CT26 and MC38, which are murine colon cancer cell lines syngeneic to BALB/c and C57BL/6 mice, respectively. Treatment with mIL-15 or the anti-CD40 antibody alone significantly prolonged survival of both CT26 and MC38 tumor-bearing mice compared with the mice in the PBS solution control group (P < 0.01). Furthermore, combination therapy with both mIL-15 and the anti-CD40 antibody provided greater therapeutic efficacy as demonstrated by prolonged survival of the mice compared with either mIL-15 or the anti-CD40 antibody-alone groups (P < 0.001). We found that NK cells isolated from the mice that received the combination regimen expressed increased levels of intracellular granzyme B and showed stronger cytotoxic activity on the target cells. The findings from this study provide the scientific basis for clinical trials using the combination regimen of IL-15 with an anti-CD40 antibody for the treatment of patients with cancer.
C1 [Zhang, Meili; Yao, Zhengsheng; Dubois, Sigrid; Ju, Wei; Mueller, Juergen R.; Waldmann, Thomas A.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Zhang, Meili] NCI, Lab Anim Sci Program, Sci Applicat Int Corp, Frederick, MD 21702 USA.
RP Waldmann, TA (reprint author), NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM tawald@helix.nih.gov
FU National Institutes of Health (NIH) [N01-CO-12400]; NCl, Center for
Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health (NIH), NCl, Center for Cancer Research.
This project has been funded in whole or in part with federal funds from
the NCl, NIH, under contract N01-CO-12400. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the US
Government.
NR 48
TC 64
Z9 65
U1 1
U2 4
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 5
PY 2009
VL 106
IS 18
BP 7513
EP 7518
DI 10.1073/pnas.0902637106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441QI
UT WOS:000265783600046
PM 19383782
ER
PT J
AU Zhang, P
Zhong, LL
Struble, EB
Watanabe, H
Kachko, A
Mihalik, K
Virata-Theimer, ML
Alter, HJ
Feinstone, S
Major, M
AF Zhang, Pei
Zhong, Lilin
Struble, Evi Budo
Watanabe, Hisayoshi
Kachko, Alla
Mihalik, Kathleen
Virata-Theimer, Maria Luisa
Alter, Harvey J.
Feinstone, Stephen
Major, Marian
TI Depletion of interfering antibodies in chronic hepatitis C patients and
vaccinated chimpanzees reveals broad cross-genotype neutralizing
activity
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID VIRUS-LIKE PARTICLES; CD81 BINDING; E2; GLYCOPROTEIN; INFECTION;
IDENTIFICATION; REPLICATION; PROTEIN; PLASMA; AP33
AB Using human immune globulins made from antihepatitis C virus (HCV)-positive plasma, we recently identified two antibody epitopes in the E2 protein at residues 412-426 (epitope I) and 434-446 (epitope II). Whereas epitope I is highly conserved among genotypes, epitope II varies. We discovered that epitope I was implicated in HCV neutralization whereas the binding of non-neutralizing antibody to epitope II disrupted virus neutralization mediated by antibody binding at epitope I. These findings suggested that, if this interfering mechanism operates in vivo during HCV infection, a neutralizing antibody against epitope I can be restrained by an interfering antibody, which may account for the persistence of HCV even in the presence of an abundance of neutralizing antibodies. We tested this hypothesis by affinity depletion and peptide-blocking of epitope-II-specific antibodies in plasma of a chronically HCV-infected patient and recombinant E1E2 vaccinated chimpanzees. We demonstrate that, by removing the restraints imposed by the interfering antibodies to epitope-II, neutralizing activity can be revealed in plasma that previously failed to neutralize viral stock in cell culture. Further, cross-genotype neutralization could be generated from monospecific plasma. Our studies contribute to understanding the mechanisms of anti-body-mediated neutralization and interference and provide a practical approach to the development of more potent and broadly reactive hepatitis C immune globulins.
C1 [Zhang, Pei; Zhong, Lilin; Struble, Evi Budo; Virata-Theimer, Maria Luisa] US FDA, Div Hematol, Bethesda, MD 20892 USA.
[Watanabe, Hisayoshi; Kachko, Alla; Mihalik, Kathleen; Feinstone, Stephen; Major, Marian] US FDA, Div Viral Prod, Bethesda, MD 20892 USA.
[Watanabe, Hisayoshi; Kachko, Alla; Mihalik, Kathleen; Feinstone, Stephen; Major, Marian] US FDA, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
[Alter, Harvey J.] NIH, Dept Transfus Med, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Zhang, P (reprint author), US FDA, Div Hematol, Bethesda, MD 20892 USA.
EM pei.zhang@fda.hhs.gov; halter@mail.nih.gov; marian.major@fda.hhs.gov
NR 22
TC 86
Z9 88
U1 0
U2 4
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 5
PY 2009
VL 106
IS 18
BP 7537
EP 7541
DI 10.1073/pnas.0902749106
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 441QI
UT WOS:000265783600050
PM 19380744
ER
PT J
AU Bernard, MA
Blanchette, PL
Brummel-Smith, K
AF Bernard, Marie A.
Blanchette, Patricia L.
Brummel-Smith, Kenneth
TI Strength and Influence of Geriatrics Departments in Academic Health
Centers
SO ACADEMIC MEDICINE
LA English
DT Article
ID INTERNAL-MEDICINE; CARE; PHYSICIANS; STUDENTS
AB The United States is establishing new medical schools and increasing class size by 30% in response to the predicted increased needs of the baby boom generation, which will retire soon and live longer than prior generations. Society in general and the medical profession in particular are ill equipped to care for the special needs of the elderly. Since the early 1980s, departments of geriatric medicine have been developed in the United States. However, the prevailing U.S. system for the training of physicians in geriatrics is through sections, divisions, or institutes. This article reviews the advantages and disadvantages of departments of geriatrics, using case examples from three (University of Oklahoma College of Medicine, Florida State University College of Medicine, and University of Hawaii at Manoa John A. Burns School of Medicine) of the extant 11 medical schools in the United States with departments of geriatrics. Commonalities among the three departments include a seat at the planning table in academic life, equal treatment and collaboration with other departments in academic and research program development, and direct access to key decision makers and opportunities for negotiation for funds. Each department has outreach to all undergraduate medical students through its training program. All three departments were launched through the investment of significant resources obtained both internally and externally. The challenge for the future will be to definitively demonstrate the efficacy of the department model versus the more prevalent section, division, and institute approach to training physicians to care for the elderly.
C1 [Bernard, Marie A.] Univ Oklahoma, Coll Med, Reynolds Dept Geriatr, Oklahoma City, OK 73190 USA.
[Blanchette, Patricia L.] Univ Hawaii Manoa, Dept Geriatr Med, John A Burns Sch Med, Honolulu, HI 96822 USA.
[Brummel-Smith, Kenneth] Florida State Univ, Dept Geriatr, Coll Med, Tallahassee, FL 32306 USA.
RP Bernard, MA (reprint author), NIA, NIH, Dept Hlth & Human Serv, Bldg 31,5C35,31 Ctr Dr MSC-2992, Bethesda, MD 20892 USA.
EM mbernard@nia.nih.gov
NR 21
TC 5
Z9 5
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD MAY
PY 2009
VL 84
IS 5
BP 627
EP 632
PG 6
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA 466IR
UT WOS:000267655300018
PM 19704196
ER
PT J
AU Lie, D
Bereknyei, S
Braddock, CH
Encinas, J
Ahearn, S
Boker, JR
AF Lie, Desiree
Bereknyei, Sylvia
Braddock, Clarence H., III
Encinas, Jennifer
Ahearn, Susan
Boker, John R.
TI Assessing Medical Students' Skills in Working With Interpreters During
Patient Encounters: A Validation Study of the Interpreter Scale
SO ACADEMIC MEDICINE
LA English
DT Article
ID CLINICIAN COMMUNICATION-SKILLS; INFORMED DECISION-MAKING; HEALTH-CARE;
EMERGENCY-DEPARTMENT; LANGUAGE CONCORDANCE; ENGLISH PROFICIENCY;
OUTPATIENT PRACTICE; QUALITY; SERVICES; IMPACT
AB Purpose
Interpreted patient encounters require distinct communication skills. The absence of available reliable, valid, and practical measures hinders the assessment of these skills; therefore, the authors aimed to construct and validate the Interpreter Scale (IS).
Method
The authors constructed the IS based on expert consensus and prior studies. They administered the IS to two classes (n = 182) in an interpreted standardized patient (SP) case setting. Standardized interpreters in the examination room assessed, using the IS, students' communication skills. Concurrently, SIPS, using the validated Patient-Physician interaction scale (PPI) and the Interpreter Impact Rating Scale (IIRS), also assessed students' skills. Trained observers watched DVDs and used the Faculty Observer Rating Scale (FORS) to assess student performance. A prior study documented the qualities of the IIRS and FORS. The authors determined the internal consistency reliability and examined construct validity of IS scores through factor analysis and concordance with other measures' scores.
Results
IS reliability analysis yielded Cronbach alpha = 0.77. Factor analysis demonstrated two IS dimensions. Nine items, "managing the encounter," and four items, "setting the stage," explained 76% and 15% of score variance, respectively. IS and FORS scores significantly correlated (r = 0.385; P < .0001). IS factor 1 scores significantly correlated (all P < .0001) with FORS (r = 0.402), IIRS (r = 0.277), and PPI (r = 0.332) scores.
Conclusions
The IS has reasonable internal consistency reliability and construct validity to warrant use for formatively measuring student communication skills in interpreted SP encounters, and it needs testing in actual patient encounters.
C1 [Lie, Desiree; Encinas, Jennifer] Univ Calif Irvine, Sch Med, Dept Family Med, Irvine, CA 92717 USA.
[Ahearn, Susan] Univ Calif Irvine, Sch Med, Clin Skills Training Ctr, Irvine, CA 92717 USA.
[Bereknyei, Sylvia; Braddock, Clarence H., III] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Bereknyei, Sylvia] NHLBI, NIH, Natl Consortium Multicultural Educ Hlth Profess, Stanford, CA USA.
[Boker, John R.] Geisinger Hlth Syst, Danville, PA USA.
RP Lie, D (reprint author), Dept Family Med, 101 City Dr S,Bldg 200,Rm 512, Orange, CA 92868 USA.
EM dalie@uci.edu
OI Bereknyei Merrell, Sylvia /0000-0002-5525-0379
FU National Institutes of Health (NIH); National Heart, Blood, and Lung
Institute [K07 HL079256-01, K07 HL079330-04]
FX This project was supported in part by a grant from the National
Institutes of Health (NIH), National Heart, Blood, and Lung Institute,
award #K07 HL079256-01, entitled "An Integrative, Evidence-Based Model
of Cultural Competency Training in Latino Health Across the Continuum of
Medical Education" (2004-2009), and award #K07 HL079330-04, entitled
"Integrated Immersive Approaches to Cultural Competence." The contents
are solely the responsibility of the authors and do not necessarily
represent the official views of the NIH.
NR 42
TC 8
Z9 8
U1 3
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD MAY
PY 2009
VL 84
IS 5
BP 643
EP 650
PG 8
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA 466IR
UT WOS:000267655300020
PM 19704202
ER
PT J
AU Sherrill, JT
Sommers, DI
Nierenberg, AA
Leon, AC
Arndt, S
Bandeen-Roche, K
Greenhouse, J
Guthrie, D
Normand, SL
Phillips, KA
Shear, MK
Woolson, R
AF Sherrill, Joel T.
Sommers, David I.
Nierenberg, Andrew A.
Leon, Andrew C.
Arndt, Stephan
Bandeen-Roche, Karen
Greenhouse, Joel
Guthrie, Donald
Normand, Sharon-Lise
Phillips, Katharine A.
Shear, M. Katherine
Woolson, Robert
TI Integrating Statistical and Clinical Research Elements in
Intervention-Related Grant Applications: Summary From an NIMH Workshop
SO ACADEMIC PSYCHIATRY
LA English
DT Article
ID MISSING DATA; TRIALS; POWER; CAUTION; ISSUES; SIZE
AB Objective: The authors summarize points for consideration generated in a National Institute of Mental Health (NIMH) workshop convened to provide an opportunity for reviewers from different disciplines-specifically clinical researchers and statisticians-to discuss how their differing and complementary expertise can be well integrated in the review of intervention-related grant applications.
Methods: A 1-day workshop was convened in October, 2004. The workshop featured panel presentations on key topics followed by interactive discussion. This article summarizes the workshop and subsequent discussions, which centered on topics including weighting the statistics/data analysis elements of an application in the assessment of the application's overall merit; the level of statistical sophistication appropriate to different stages of research and for different funding mechanisms; some key considerations in the design and analysis portions of applications; appropriate statistical methods for addressing essential questions posed by an application; and the role of the statistician in the application's development, study conduct, and interpretation and dissemination of results.
Results: A number of key elements crucial to the construction and review of grant applications were identified. It was acknowledged that intervention-related studies unavoidably involve trade-offs. Reviewers are helped when applications acknowledge such trade-offs and provide good rationale for their choices. Clear linkage among the design, aims, hypotheses, and data analysis plan and avoidance of disconnections among these elements also strengthens applications.
Conclusion: The authors identify multiple points to consider when constructing intervention-related grant applications. The points are presented here as questions and do not reflect institute policy or comprise a list of best practices, but rather represent points for consideration.
C1 [Sommers, David I.] NIMH, Div Extramural Activ, Bethesda, MD 20892 USA.
[Sherrill, Joel T.] NIMH, DSIR, Bethesda, MD 20892 USA.
[Leon, Andrew C.] Cornell Univ, Dept Psychiat, Weill Med Coll, Ithaca, NY 14853 USA.
[Arndt, Stephan] Univ Iowa Hosp & Clin, Iowa Consortium Subst Abuse Res, Iowa City, IA 52242 USA.
[Greenhouse, Joel] Carnegie Mellon, Dept Stat, Pittsburgh, PA USA.
[Guthrie, Donald] Univ Calif Los Angeles, Los Angeles, CA 90024 USA.
[Normand, Sharon-Lise] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Phillips, Katharine A.] Brown Univ, Dept Psychiat & Human Behav, Providence, RI 02912 USA.
[Shear, M. Katherine] Columbia Univ, Sch Social Work, New York, NY 10027 USA.
[Woolson, Robert] Med Univ S Carolina, Dept Psychiat Biostat, Charleston, SC USA.
RP Sommers, DI (reprint author), NIMH, Div Extramural Activ, 6001 Execut Blvd,Room 6144, Bethesda, MD 20892 USA.
EM dsommers@mail.nih.gov
OI Arndt, Stephan/0000-0003-0783-8204
FU Intramural NIH HHS [Z99 MH999999]; NIMH NIH HHS [K24 MH063975]
NR 22
TC 6
Z9 6
U1 0
U2 1
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1042-9670
J9 ACAD PSYCHIATR
JI Acad. Psych.
PD MAY-JUN
PY 2009
VL 33
IS 3
BP 221
EP 228
PG 8
WC Education & Educational Research; Psychiatry
SC Education & Educational Research; Psychiatry
GA 467CI
UT WOS:000267713700009
PM 19574520
ER
PT J
AU Solomon, D
Papillo, JL
Davey, DD
AF Solomon, Diane
Papillo, Jacalyn L.
Davey, Diane D.
CA Consortium, CE&T
TI Statement on HPV DNA Test Utilization
SO ACTA CYTOLOGICA
LA English
DT Editorial Material
DE cervical cancer; cervix neoplasms; human papillomavirus
ID CANCER
C1 [Solomon, Diane] NCI, Canc Prevent Div, Dept Hlth & Human Serv, NIH, Rockville, MD 20852 USA.
Fletcher Allen Hlth Care, Dept Anat Pathol, Burlington, VT USA.
Univ Cent Florida, Coll Med, Orlando, FL 32816 USA.
RP Solomon, D (reprint author), NCI, Canc Prevent Div, Dept Hlth & Human Serv, NIH, Execut Plaza N,Room 2130,6130 Executive Blvd, Rockville, MD 20852 USA.
EM ds87v@nih.gov
NR 3
TC 5
Z9 5
U1 0
U2 0
PU SCI PRINTERS & PUBL INC
PI ST LOUIS
PA PO DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 USA
SN 0001-5547
J9 ACTA CYTOL
JI Acta Cytol.
PD MAY-JUN
PY 2009
VL 53
IS 3
BP 247
EP 248
DI 10.1159/000325302
PG 2
WC Pathology
SC Pathology
GA 449NG
UT WOS:000266336700002
PM 19534262
ER
PT J
AU Cox, JT
Moriarty, AT
Castle, PE
AF Cox, J. Thomas
Moriarty, Ann T.
Castle, Philip E.
TI Statement on HPV DNA Test Utilization Commentary
SO ACTA CYTOLOGICA
LA English
DT Article
DE cervical cancer; cervix neoplasms; human papillomavirus
ID CANCER-SOCIETY GUIDELINE; HUMAN-PAPILLOMAVIRUS; CERVICAL-CANCER;
SCREENING-TESTS; NEOPLASIA; COHORT; WOMEN; AMERICAN; RISK; METAANALYSIS
AB Michaela had a Pap test at age 17, less than 3 months after her first intercourse. The Pap was interpreted as atypical squamous cells of undetermined significance (ASC-US), and the laboratory automatically "reflexed" this to human papillomavirus (HPV) testing. Michaela tested positive for high-risk, (carcinogenic) HPV, had colposcopy and biopsy, and cryotherapy for cervical intraepithelial neoplasia, grade 1 (CIN 1). Her 4-month postcrotherapy Pap was ASC-US HPV positive.
C1 [Cox, J. Thomas] Univ Calif Santa Barbara, Gynecol & Colposcopy Clin, Student Hlth Serv, Santa Barbara, CA 93106 USA.
[Moriarty, Ann T.] AmeriPath Indiana, Indianapolis, IN USA.
[Castle, Philip E.] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RP Cox, JT (reprint author), Univ Calif Santa Barbara, Gynecol & Colposcopy Clin, Student Hlth Serv, Santa Barbara, CA 93106 USA.
EM cox-t@sa.ucsb.edu
NR 21
TC 0
Z9 0
U1 0
U2 0
PU SCI PRINTERS & PUBL INC
PI ST LOUIS
PA PO DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 USA
SN 0001-5547
J9 ACTA CYTOL
JI Acta Cytol.
PD MAY-JUN
PY 2009
VL 53
IS 3
BP 249
EP 252
PG 4
WC Pathology
SC Pathology
GA 449NG
UT WOS:000266336700003
ER
PT J
AU Kurup, S
Lew, J
Byrnes, G
Yeh, S
Nussenblatt, R
Levy-Clarke, G
AF Kurup, Shree
Lew, Julie
Byrnes, Gordon
Yeh, Steven
Nussenblatt, Robert
Levy-Clarke, Grace
TI Therapeutic efficacy of intravitreal bevacizumab on posterior uveitis
complicated by neovascularization
SO ACTA OPHTHALMOLOGICA
LA English
DT Article
DE anti-VEGF; bevacizumab; lupus retinopathy; neovascularization;
proliferative retinopathy; sarcoidosis
ID ENDOTHELIAL GROWTH-FACTOR; SARCOIDOSIS
AB To evaluate the therapeutic effect of intravitreal bevacizumab in patients with uveitis-associated choroidal/retinal neovascularization.
Two female patients (40 years, 15 years) with posterior uveitis, (one presumed ocular sarcoidosis, one lupus) were evaluated for neovascularization of the posterior segment. Both patients were given a single dose of 1.25 mg intravitreal bevacizumab.
Significant anatomical and functional recovery was evident in both patients within a few weeks.
In selected uveitic patients, bevacizumab may be an option for managing neovascularization.
C1 [Kurup, Shree] Wake Forest Univ, Dept Ophthalmol, Ctr Eye, Winston Salem, NC 27101 USA.
[Lew, Julie; Yeh, Steven; Nussenblatt, Robert; Levy-Clarke, Grace] NEI, NIH, Bethesda, MD 20892 USA.
[Byrnes, Gordon] Retina Grp Washington, Chevy Chase, MD USA.
RP Kurup, S (reprint author), Wake Forest Univ, Dept Ophthalmol, Ctr Eye, Winston Salem, NC 27101 USA.
EM skurup@wfubmc.edu
FU Intramural NIH HHS [ZIE EY000482-01]
NR 7
TC 21
Z9 22
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1755-375X
J9 ACTA OPHTHALMOL
JI Acta Ophthalmol.
PD MAY
PY 2009
VL 87
IS 3
BP 349
EP 352
DI 10.1111/j.1755-3768.2008.01208.x
PG 4
WC Ophthalmology
SC Ophthalmology
GA 434BY
UT WOS:000265251400021
PM 18513266
ER
PT J
AU Semba, RD
Ferrucci, L
Sun, K
Patel, KV
Guralnik, JM
Fried, LP
AF Semba, Richard D.
Ferrucci, Luigi
Sun, Kai
Patel, Kushang V.
Guralnik, Jack M.
Fried, Linda P.
TI Elevated serum advanced glycation end products and their circulating
receptors are associated with anaemia in older community-dwelling women
SO AGE AND AGEING
LA English
DT Article
DE advanced glycation end products; anaemia; haemoglobin; women; elderly
ID DIABETIC-NEPHROPATHY; SOLUBLE RECEPTOR; OXIDATIVE STRESS; GLYCOTOXINS;
LINK; N-EPSILON-(CARBOXYMETHYL)LYSINE; ATHEROSCLEROSIS; ERYTHROCYTES;
INFLAMMATION; ENDPRODUCTS
AB Objective: to determine whether serum carboxymethyl-lysine, a dominant advanced glycation end product (AGE), and circulating total receptor for AGEs (sRAGE) and endogenous secretory receptor for AGEs (esRAGE) are associated with anaemia.
Design: cross-sectional analysis.
Setting: moderately severely disabled women, >= 65 years, living in the community in Baltimore, MD (the Women's Health and Aging Study I).
Participants: 519 women with and without anaemia.
Main outcome measure: haemoglobin and anaemia (haemoglobin < 12 g/dL).
Results: of 519 women, 128 (24.7%) had anaemia. All odds ratios (OR) were expressed per one standard deviation. Serum CML was associated with anaemia [OR 1.47, 95% confidence interval (CI) 1.11-1.95, P = 0.008] in a multivariate logistic regression model adjusting for age, race, smoking, education and chronic diseases. Serum sRAGE (ng/mL) and esRAGE (ng/mL) were associated with anaemia (OR 1.52, 95% CI 1.21-1.92, P = 0.0004; OR 1.49, 95% CI 1.18-1.87, P = 0.0006, respectively) in separate multivariate logistic regression models, adjusting for the same covariates mentioned above. Serum CML (P = 0.004), sRAGE (P < 0.0001) and esRAGE (P < 0.0001) were inversely and independently associated with haemoglobin concentrations.
Conclusion: AGEs and circulating RAGE are independently associated with haemoglobin and anaemia in older women. AGEs are amenable to interventions, as serum AGEs can be lowered by a change in dietary pattern and pharmacological treatment.
C1 [Semba, Richard D.; Sun, Kai; Fried, Linda P.] Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA.
[Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Patel, Kushang V.; Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Fried, Linda P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
RP Semba, RD (reprint author), Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA.
EM rdsemba@jhmi.edu
FU National Institute on Aging [R01 AG029148, R01 AG027012, R37 AG19905];
Intramural Research Program; National Institute on Aging; NIH
FX This work was supported by National Institute on Aging Grant R01
AG029148, R01 AG027012, R37 AG19905, and the Intramural Research
Program, National Institute on Aging, NIH.
NR 30
TC 5
Z9 6
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0002-0729
J9 AGE AGEING
JI Age Ageing
PD MAY
PY 2009
VL 38
IS 3
BP 283
EP 289
DI 10.1093/ageing/afp011
PG 7
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 434HV
UT WOS:000265266700009
PM 19252206
ER
PT J
AU Keyes, KM
Geier, T
Grant, BF
Hasin, DS
AF Keyes, Katherine M.
Geier, Timothy
Grant, Bridget F.
Hasin, Deborah S.
TI Influence of a Drinking Quantity and Frequency Measure on the Prevalence
and Demographic Correlates of DSM-IV Alcohol Dependence
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE At-Risk Drinking; Binge Drinking; Diagnostic and Statistical Manual of
Mental and Behavior Disorders V; Alcohol Dependence; Epidemiology
ID SUBSTANCE USE DISORDERS; NATIONAL EPIDEMIOLOGIC SURVEY; INTERVIEW
SCHEDULE AUDADIS; GENERAL-POPULATION SAMPLE; ITEM RESPONSE THEORY;
UNITED-STATES; DRUG-USE; METHODOLOGICAL ISSUES; SERVICE UTILIZATION;
BREAST-CANCER
AB Recent research suggests that adding a quantity/frequency alcohol consumption measure to diagnoses of alcohol use disorders may improve construct validity of the diagnoses for Diagnostic and Statistical Manual of Mental and Behavior Disorders (DSM-V). This study explores the epidemiological impact of including weekly at-risk drinking (WAD) in the DMS-IV diagnostic definition of alcohol dependence via 3 hypothetical reformulations of the current criteria.
The sample was the National Epidemiologic Survey on Alcohol and Related Conditions, a nationally representative sample with 43,093 adults aged > 18 in the U.S interviewed with the Alcohol Use Disorder and Associated Disabilities Interview Schedule IV. The current (DSM-IV) definition of alcohol dependence was compared with 4 hypothetical alcohol dependence reformulations that included WAD: (1) WAD added as an eighth criteria; (2) WAD required for a diagnosis; (3) adding abuse and dependence criteria together, and including WAD with a 3 of 12 symptom threshold; (4) adding abuse and dependence criteria together, and including WAD with a 5 of 12 symptom threshold.
The inclusion of at-risk drinking as an eighth criterion of alcohol dependence has a minimal impact on the sociodemographic correlates of alcohol dependence but substantially increases the prevalence of dependence (from 3.8% to 5.0%). At-risk drinking as a required criterion or as part of a diagnosis that combines abuse with dependence criteria with a higher threshold (5+ criteria) decreases prevalence and has a larger impact on sociodemographic correlates. Blacks, Hispanics, and women are less likely to be included in diagnostic reformulations that include WAD, whereas individuals with low-income and education are more likely to remain diagnosed.
Including WAD as either a requirement of diagnosis or as an additional criterion would have a large impact on the prevalence of alcohol dependence in the general population. The inclusion of a quantity/frequency requirement may eliminate false positives from studies of alcohol disorder etiology and improve phenotype definition for genetic association studies by reducing heterogeneity in the diagnosis, but may also reduce eligibility for treatment services among women and racial/ethnic minorities compared.
C1 [Keyes, Katherine M.; Geier, Timothy; Hasin, Deborah S.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Keyes, Katherine M.; Hasin, Deborah S.] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
[Grant, Bridget F.] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, Dept Hlth & Human Serv,NIH, Bethesda, MD USA.
[Hasin, Deborah S.] Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY USA.
RP Hasin, DS (reprint author), New York State Psychiat Inst & Hosp, 1051 Riverside Dr 123, New York, NY 10032 USA.
EM dsh2@columbia.edu
FU National Institute on Alcoholism and Alcohol Abuse [K05 AA014223];
National Institute on Drug Abuse [RO1 DA018652]; National Institute of
Mental Health [T32 MH013043-36]
FX This research was supported in part by grants from the National
Institute on Alcoholism and Alcohol Abuse (K05 AA014223, Hasin), the
National Institute on Drug Abuse (RO1 DA018652, Hasin), a fellowship
from the National Institute of Mental Health (T32 MH013043-36, Keyes),
and support from New York State Psychiatric Institute. A version of this
paper was presented at the 2008 meeting of the Research Society on
Alcoholism in Washington, DC, where it received the Enoch Gordis prize
for student psychosocial research. The authors wish to thank Sarah
Braunstein and Ann Madsen for helpful comments on previous drafts of
this manuscript.
NR 84
TC 28
Z9 28
U1 1
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2009
VL 33
IS 5
BP 761
EP 771
DI 10.1111/j.1530-0277.2009.00894.x
PG 11
WC Substance Abuse
SC Substance Abuse
GA 432PG
UT WOS:000265145600002
PM 19298332
ER
PT J
AU Hingson, RW
Edwards, EM
Heeren, T
Rosenbloom, D
AF Hingson, Ralph W.
Edwards, Erika M.
Heeren, Timothy
Rosenbloom, David
TI Age of Drinking Onset and Injuries, Motor Vehicle Crashes, and Physical
Fights After Drinking and When Not Drinking
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Drinking Onset; Injuries; Fights; Traffic Crashes; Alcohol Dependence
ID DATING VIOLENCE VICTIMIZATION; IV ALCOHOL-ABUSE; HIGH-SCHOOL-STUDENTS;
RISK BEHAVIORS; EPIDEMIOLOGIC SURVEY; COLLEGE DRINKING; DEPENDENCE;
INVOLVEMENT; ASSOCIATION; ADOLESCENTS
AB Earlier age of drinking onset has been associated with greater odds of involvement in motor vehicle crashes, unintentional injuries, and physical fights after drinking. This study explores whether early drinkers take more risks even when sober by comparing potential associations between age of drinking onset and these outcomes after drinking relative to when respondents have not been drinking.
From a national sample, 4,021 ever-drinkers ages 18 to 39 were asked age of drinking onset, not counting tastes or sips. They were also asked if they were ever in motor vehicle crashes, unintentionally injured, or in physical fights after drinking and when not drinking. GEE logistic regression models for repeated measures dichotomous outcomes compared whether odds ratios between age of onset and these adverse outcomes significantly differed when they occurred after drinking versus when not drinking, controlling for respondents' demographic characteristics, cigarette and marijuana use, family history of alcoholism, ever experiencing alcohol dependence, and frequency of binge drinking.
Compared with persons who started drinking at age 21+, those who started at ages < 14, 14 to 15, 16 to 17, and 18 to 20 had, after drinking, respectively greater odds: 6.3 (2.6, 15.3), 5.2 (2.2, 12.3), 3.3 (1.5, 7.3), and 2.2 (0.9, 5.1) of having been in a motor vehicle crash; 6.0 (3.4, 10.5), 4.9 (3.0, 8.6), 3.7 (2.4, 5.6), and 1.9 (1.2, 2.9) of ever being in a fight; and 4.6 (2.4, 8.7), 4.7 (2.6, 8.6), 3.2 (1.9, 5.6), and 2.3 (1.3, 4.0) of ever being accidentally injured. The odds of experiencing motor vehicle accidents or injuries when not drinking were not significantly elevated among early onset drinkers. The odds of earlier onset drinkers being in fights were also significantly greater when respondents had been drinking than not drinking.
Starting to drink at an earlier age is associated with greater odds of experiencing motor vehicle crash involvement, unintentional injuries, and physical fights when respondents were drinking, but less so when respondents had not been drinking. These findings reinforce the need for programs and policies to delay drinking onset.
C1 [Hingson, Ralph W.] NIAAA, Div Epidemiol & Prevent Res, Bethesda, MD 20892 USA.
[Edwards, Erika M.; Heeren, Timothy; Rosenbloom, David] Boston Univ, Sch Publ Hlth, Youth Alcohol Prevent Ctr, Boston, MA USA.
RP Hingson, RW (reprint author), NIAAA, Div Epidemiol & Prevent Res, 5635 Fishers Lane,Room 2077, Bethesda, MD 20892 USA.
EM rhingson@mail.nih.gov
OI Heeren, Timothy/0000-0001-5643-3559
FU National Institute on Alcohol Abuse and Alcoholism [P60-AA013759]
FX This research was supported by grant P60-AA013759 from the National
Institute on Alcohol Abuse and Alcoholism.
NR 35
TC 73
Z9 74
U1 1
U2 14
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2009
VL 33
IS 5
BP 783
EP 790
DI 10.1111/j.1530-0277.2009.00896.x
PG 8
WC Substance Abuse
SC Substance Abuse
GA 432PG
UT WOS:000265145600004
PM 19298330
ER
PT J
AU Harford, TC
Yi, HY
Faden, VB
Chen, CM
AF Harford, Thomas C.
Yi, Hsiao-ye
Faden, Vivian B.
Chen, Chiung M.
TI The Dimensionality of DSM-IV Alcohol Use Disorders Among Adolescent and
Adult Drinkers and Symptom Patterns by Age, Gender, and Race/Ethnicity
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Adolescents; Adults; DSM-IV Alcohol Use Disorders; Item Response Theory;
Symptom Patterns
ID ITEM RESPONSE THEORY; NATIONAL EPIDEMIOLOGIC SURVEY; UNITED-STATES;
12-MONTH PREVALENCE; DEPENDENCE SYMPTOM; ABUSE; VALIDITY; CRITERIA;
MODEL; CONSUMPTION
AB There is limited information on the validity of Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) alcohol use disorders (AUD) symptom criteria among adolescents in the general population. The purpose of this study is to assess the DSM-IV AUD symptom criteria as reported by adolescent and adult drinkers in a single representative sample of the U.S. population aged 12 years and older. This design avoids potential confounding due to differences in survey methodology when comparing adolescents and adults from different surveys.
A total of 133,231 current drinkers (had at least 1 drink in the past year) aged 12 years and older were drawn from respondents to the 2002 to 2005 National Surveys on Drug Use and Health. DSM-IV AUD criteria were assessed by questions related to specific symptoms occurring during the past 12 months. Factor analytic and item response theory models were applied to the 11 AUD symptom criteria to assess the probabilities of symptom item endorsements across different values of the underlying trait.
A 1-factor model provided an adequate and parsimonious interpretation for the 11 AUD criteria for the total sample and for each of the gender-age groups. The MIMIC model exhibited significant indication for item bias among some criteria by gender, age, and race/ethnicity. Symptom criteria for "tolerance,""time spent," and "hazardous use" had lower item thresholds (i.e., lower severity) and low item discrimination, and they were well separated from the other symptoms, especially in the 2 younger age groups (12 to 17 and 18 to 25). "Larger amounts,""cut down,""withdrawal," and "legal problems" had higher item thresholds but generally lower item discrimination, and they tend to exhibit greater dispersion at higher AUD severity, particularly in the youngest age group (12 to 17).
Findings from the present study do not provide support for the 2 separate DSM-IV diagnoses of alcohol abuse and dependence among either adolescents or adults. Variations in criteria severity for both abuse and dependence offer support for a dimensional approach to diagnosis which should be considered in the ongoing development of DSM-V.
C1 [Harford, Thomas C.; Yi, Hsiao-ye; Chen, Chiung M.] NIAAA, NIH, CSR Inc, Arlington, VA 22201 USA.
[Faden, Vivian B.] NIAAA, NIH, Bethesda, MD USA.
RP Yi, HY (reprint author), NIAAA, NIH, CSR Inc, 2107 Wilson Blvd,Suite 1000, Arlington, VA 22201 USA.
EM hyi@csrincorporated.com
FU Alcohol Epidemiologic Data System (AEDS) [N0AA32007]; Division of
Epidemiology and Prevention Research; National Institute on Alcohol
Abuse and Alcoholism
FX This study was conducted for the Alcohol Epidemiologic Data System
(AEDS) under Contract No. N0AA32007 for the Division of Epidemiology and
Prevention Research, National Institute on Alcohol Abuse and Alcoholism.
NR 33
TC 39
Z9 39
U1 6
U2 10
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2009
VL 33
IS 5
BP 868
EP 878
DI 10.1111/j.1530-0277.2009.00910.x
PG 11
WC Substance Abuse
SC Substance Abuse
GA 432PG
UT WOS:000265145600014
PM 19320629
ER
PT J
AU Ramchandani, VA
Plawecki, M
Li, TK
O'Connor, S
AF Ramchandani, Vijay A.
Plawecki, Martin
Li, Ting-Kai
O'Connor, Sean
TI Intravenous Ethanol Infusions Can Mimic the Time Course of Breath
Alcohol Concentrations Following Oral Alcohol Administration in Healthy
Volunteers
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Clamp; Route of Administration; Physiologically-Based
Pharmacokinetic Model; Pharmacokinetic Variability; Healthy Social
Drinkers; Breath Alcohol Concentration
ID FAMILY-HISTORY; RECENT DRINKING; MG-PERCENT; ELIMINATION; METABOLISM;
GENDER; CLAMP; POLYMORPHISMS; RELIABILITY; RESPONSES
AB Our previous studies have used intravenous (IV) clamping methods to demonstrate that family history positive (FHP) subjects exhibit a greater initial response to alcohol than family history negative (FHN) subjects. These results differ from other studies of family history of alcoholism (FHA) influences, most of which have used an oral alcohol challenge, suggesting that the route of administration may influence both the response to alcohol and FHA-related differences in response. To examine this possibility, one approach would be to directly compare responses following oral and IV alcohol administration in the same subjects. There is, however, a 3- to 4-fold variance, between- and within-subjects, in the breath alcohol concentrations (BrACs) following oral alcohol administration. Thus, our objective was to characterize the between-subject variability in the time course of BrACs following oral alcohol administration in healthy volunteers and to develop an IV infusion method to mimic the BrAC-time course attained following oral alcohol in the same subject.
This was a 2-session study in young adult, healthy, nondependent drinkers. In the first session, subjects ingested an oral dose of alcohol, based on total body water, to achieve a target peak BrAC of 80 mg%. In the second session, subjects received an IV infusion of ethanol designed to achieve the same BrAC time course as that achieved in the first session. The individualized infusion-rate profile was precomputed using a physiologically-based pharmacokinetic (PBPK) model for alcohol with model parameters adjusted to the individual's physiology. The peak BrACs (C(max)), times of peak BrAC (T(max)), and the areas under the BrAC vs. time curve (AUC) were compared between sessions to assess how closely the BrAC exposure during the IV infusion session mimicked the exposure following oral alcohol.
The time course of BrACs following oral alcohol administration showed a high degree of between-subject variability. Mean C(max), T(max), and AUC did not differ by gender, indicating that calculation of oral doses based on total body water results in comparable BrAC-time courses, on average, for females and males. The IV infusion driven BrAC-time profiles demonstrated good fidelity to the BrAC-time curves resulting from oral alcohol: the mean %difference in C(max) and AUC were both 11%, while the mean %difference for T(max) was 27%. This degree of variability is less than half that seen across individuals following oral alcohol administration, which was substantial [coefficient of variation (%CV) ranging from 22 to 52%].
Despite the use of standardized doses and controlled experimental conditions, there was substantial between-subject variability in the BrAC time course following oral administration of alcohol. The PBPK-model-based infusion method can mimic the BrACs attained with oral alcohol for individual subjects. This method provides a platform to evaluate effects attributable to the route of administration on the response to alcohol, as well as the influence of determinants such as family history of alcoholism on the alcohol response.
C1 [Ramchandani, Vijay A.] NIAAA, Unit Human Physiol & Pharmacokinet, Lab Clin & Translat Studies, Bethesda, MD 20892 USA.
[Plawecki, Martin; O'Connor, Sean] Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA.
[O'Connor, Sean] RL Roudeboush VA Med Ctr, Indianapolis, IN USA.
RP Ramchandani, VA (reprint author), NIAAA, Unit Human Physiol & Pharmacokinet, Lab Clin & Translat Studies, 10 Ctr Dr,Bldg 10 CRC,Rm 2-2352,MSC 1540, Bethesda, MD 20892 USA.
EM vijayr@mail.nih.gov
FU PHS [P50 AA 07611, R37 AA 02342, M01 RR 750]; NIAAA Division of
Intramural Clinical and Biological Research
FX Supported by PHS Grants P50 AA 07611, R37 AA 02342, and M01 RR 750 and
the NIAAA Division of Intramural Clinical and Biological Research.
NR 27
TC 26
Z9 26
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2009
VL 33
IS 5
BP 938
EP 944
DI 10.1111/j.1530-0277.2009.00906.x
PG 7
WC Substance Abuse
SC Substance Abuse
GA 432PG
UT WOS:000265145600022
PM 19320632
ER
PT J
AU Carrillo, MC
Sanders, CA
Katz, RG
AF Carrillo, Maria C.
Sanders, Charles A.
Katz, Russell G.
TI Maximizing the Alzheimer's Disease Neuroimaging Initiative II
SO ALZHEIMERS & DEMENTIA
LA English
DT Article
DE Alzheimer's disease; Biomarkers; Neuroimaging; Early defection;
Longitudinal study; Natural history study; Mild cognitive impairment
ID PROGRESSION; MRI; AD
AB The Alzheimer's Disease Neuroimaging Initiative is the largest public-private partnership on brain research underway at the National Institutes of Health. This 6-year Study tracks cognitive and brain changes in normal subjects, those with mild cognitive impairment, and individuals with Alzheimer's disease. It was designed to provide better tools for performing effective clinical trials, and is slated to run until 2010. While data are being generated and analyzed, researchers involved in the study are developing an extension, i.e., the Alzheimer's Disease Neuroimaging Initiative U. The Foundation for the National Institutes of Health and the Alzheimer's Association convened a meeting to review the progress, evaluate future directions, and obtain the United States Food and Drug Administration's perspective on how the Alzheimer's Disease Neuroimaging Initiative could affect the drug-approval process. (C) 2009 The Alzheimer's Association. All rights reserved.
C1 [Carrillo, Maria C.] Alzheimers Assoc, Chicago, IL USA.
[Sanders, Charles A.] Fdn Natl Inst Hlth, Bethesda, MD USA.
[Katz, Russell G.] US FDA, Washington, DC 20204 USA.
RP Carrillo, MC (reprint author), Alzheimers Assoc, Chicago, IL USA.
EM Maria.Carrillo@alz.org
NR 9
TC 10
Z9 10
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1552-5260
J9 ALZHEIMERS DEMENT
JI Alzheimers. Dement.
PD MAY
PY 2009
VL 5
IS 3
BP 271
EP 275
DI 10.1016/j.jalz.2009.02.005
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA 445HW
UT WOS:000266042900006
PM 19362888
ER
PT J
AU Duggan, PS
Siegel, AW
Blass, DM
Bok, H
Coyle, JT
Faden, R
Finkel, J
Gearhart, JD
Greely, HT
Hillis, A
Hoke, A
Johnson, R
Johnston, M
Kahn, J
Kerr, D
King, P
Kurtzberg, J
Liao, SM
McDonald, JW
McKhann, G
Nelson, KB
Rao, M
Regenberg, A
Smith, K
Solter, D
Song, H
Sugarman, J
Traystman, RJ
Vescovi, A
Yanofski, J
Young, W
Mathews, DJH
AF Duggan, P. S.
Siegel, A. W.
Blass, D. M.
Bok, H.
Coyle, J. T.
Faden, R.
Finkel, J.
Gearhart, J. D.
Greely, H. T.
Hillis, A.
Hoke, A.
Johnson, R.
Johnston, M.
Kahn, J.
Kerr, D.
King, P.
Kurtzberg, J.
Liao, S. M.
McDonald, J. W.
McKhann, G.
Nelson, K. B.
Rao, M.
Regenberg, A.
Smith, K.
Solter, D.
Song, H.
Sugarman, J.
Traystman, R. J.
Vescovi, A.
Yanofski, J.
Young, W.
Mathews, D. J. H.
TI Unintended Changes in Cognition, Mood, and Behavior Arising from
Cell-Based Interventions for Neurological Conditions: Ethical Challenges
SO AMERICAN JOURNAL OF BIOETHICS
LA English
DT Article
DE CNS; personal identity; risks; stem cells
ID DEEP-BRAIN-STIMULATION; UMBILICAL-CORD BLOOD; STEM-CELLS;
PARKINSONS-DISEASE; ELECTROCONVULSIVE-THERAPY; DISORDERS;
TRANSPLANTATION; DEPRESSION; CHIMERAS; ISSUES
AB The prospect of using cell-based interventions (CBIs) to treat neurological conditions raises several important ethical and policy questions. In this target article, we focus on issues related to the unique constellation of traits that characterize CBIs targeted at the central nervous system. In particular, there is at least a theoretical prospect that these cells will alter the recipients' cognition, mood, and behavior-brain functions that are central to our concept of the self. The potential for such changes, although perhaps remote, is cause for concern and careful ethical analysis. Both to enable better informed consent in the future and as an end in itself, we argue that early human trials of CBIs for neurological conditions must monitor subjects for changes in cognition, mood, and behavior; further, we recommend concrete steps for that monitoring. Such steps will help better characterize the potential risks and benefits of CBIs as they are tested and potentially used for treatment.
C1 [Duggan, P. S.; Siegel, A. W.; Blass, D. M.; Bok, H.; Faden, R.; Finkel, J.; Gearhart, J. D.; Hillis, A.; Hoke, A.; Johnson, R.; Kerr, D.; McKhann, G.; Regenberg, A.; Smith, K.; Song, H.; Sugarman, J.; Mathews, D. J. H.] Johns Hopkins Univ, Baltimore, MD 21205 USA.
[Blass, D. M.] Abarbanel Mental Hlth Ctr, Bat Yam, Israel.
[Coyle, J. T.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Greely, H. T.] Stanford Univ, Stanford, CA 94305 USA.
[Kahn, J.] Univ Minnesota, Minneapolis, MN 55455 USA.
[King, P.] Georgetown Univ, Washington, DC 20057 USA.
[Kurtzberg, J.] Duke Univ, Durham, NC 27706 USA.
[Liao, S. M.] Univ Oxford, Oxford OX1 2JD, England.
[Nelson, K. B.] NIH, Bethesda, MD USA.
[Rao, M.] Invitrogen Corp, Carlsbad, CA USA.
[Solter, D.] Duke Natl Univ Singapore, Singapore, Singapore.
[Traystman, R. J.] Univ Colorado, Boulder, CO 80309 USA.
[Vescovi, A.] Univ Milano Bicocca, Milan, Italy.
[Yanofski, J.] Univ Texas SW Med Ctr Dallas, Dallas, TX USA.
[Young, W.] Rutgers State Univ, Piscataway, NJ 08855 USA.
RP Mathews, DJH (reprint author), Johns Hopkins Univ, 624 N Broadway,Hampton House 352, Baltimore, MD 21205 USA.
EM dmathews@jhmi.edu
OI Hoke, Ahmet/0000-0003-1215-3373
NR 43
TC 14
Z9 14
U1 0
U2 6
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1526-5161
J9 AM J BIOETHICS
JI Am. J. Bioeth.
PD MAY
PY 2009
VL 9
IS 5
BP 31
EP 36
DI 10.1080/15265160902788645
PG 6
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 446TU
UT WOS:000266144900012
PM 19396681
ER
PT J
AU Gottlieb, SS
Kop, WJ
Ellis, SJ
Binkley, P
Howlett, J
O'Connor, C
Blumenthal, JA
Fletcher, G
Swank, AM
Cooper, L
AF Gottlieb, Stephen S.
Kop, Willem J.
Ellis, Stephen J.
Binkley, Philip
Howlett, Jonathan
O'Connor, Christopher
Blumenthal, James A.
Fletcher, Gerald
Swank, Ann M.
Cooper, Lawton
CA HF-ACTION Investigators
TI Relation of Depression to Severity of Illness in Heart Failure (from
Heart Failure And a Controlled Trial Investigating Outcomes of Exercise
Training [HF-ACTION])
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; CARDIOVASCULAR-DISEASE; SYMPTOMS
AB Depression is common in patients with heart failure (HF), prognostic for adverse outcomes and. purportedly related to disease severity. Psychological and physiologic factors relevant to HF were assessed in HF-ACTION, a large randomized study of aerobic exercise training in patients with systolic HF. The relation of objective and subjective parameters was compared with scores on the Beck Depression Inventory (BDI) to examine the hypothesis that depressive symptoms are better associated with perception of disease severity than with objective markers of HF severity. At baseline, 2,322 of 2,331 subjects entered into HF-ACTION completed questionnaires to assess depression (BDI) and quality of life (Kansas City Cardiomyopathy Questionnaire [KCCQ]). Objective markers of HF severity included ejection fraction, B-type natriuretic peptide, and peak oxygen consumption (using cardiopulmonary exercise testing, with evaluation of duration and respiratory exchange ratio also performed). Measures more likely to be affected by perceived functional status included New York Heart Association (NYHA) classification and the 6-minute walk test. Objective assessments of disease severity were slightly related (peak oxygen consumption) or not related (B-type natriuretic peptide and ejection fraction) to BDI scores. Using multivariate analysis (KCCQ not included), only age, gender, cardiopulmonary exercise testing duration, NYHA class, 6-minute walk distance, and peak respiratory exchange ratio independently correlated with BDI scores. In conclusion, depression was minimally related to objective assessments of severity of disease in patients with HF, but was associated with patient (and clinician) perceptions of disease severity. Addressing depression might improve symptoms in patients with HF. (C) 2009 Published by Elsevier Inc. (Am J Cardiol 2009;103:1285-1289)
C1 [Gottlieb, Stephen S.; Kop, Willem J.] Univ Maryland, Baltimore, MD 21201 USA.
[Ellis, Stephen J.; O'Connor, Christopher; Blumenthal, James A.] Duke Univ, Med Ctr, Durham, NC USA.
[Binkley, Philip] Ohio State Univ, Columbus, OH 43210 USA.
[Howlett, Jonathan] Halifax Univ, Halifax, NS, Canada.
[Fletcher, Gerald] Mayo Clin Florida, Jacksonville, FL USA.
[Swank, Ann M.] Univ Louisville, Louisville, KY 40292 USA.
[Cooper, Lawton] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Gottlieb, SS (reprint author), Univ Maryland, Baltimore, MD 21201 USA.
EM sgottlie@medicine.umaryland.edu
FU National Heart, Lung, and Blood Institute, National Institutes of
Health, Bethesda, Maryland [5 U01 HL063747-06]
FX The HF-ACTION study was supported by Grant No. 5 U01 HL063747-06 from
the National Heart, Lung, and Blood Institute, National Institutes of
Health, Bethesda, Maryland.
NR 17
TC 52
Z9 55
U1 1
U2 4
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD MAY 1
PY 2009
VL 103
IS 9
BP 1285
EP 1289
DI 10.1016/j.amjcard.2009.01.025
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 442TK
UT WOS:000265863300018
PM 19406273
ER
PT J
AU Chen, LW
Appel, LJ
Loria, C
Lin, PH
Champagne, CM
Elmer, PJ
Ard, JD
Mitchell, D
Batch, BC
Svetkey, LP
Caballero, B
AF Chen, Liwei
Appel, Lawrence J.
Loria, Catherine
Lin, Pao-Hwa
Champagne, Catherine M.
Elmer, Patricia J.
Ard, Jamy D.
Mitchell, Diane
Batch, Bryan C.
Svetkey, Laura P.
Caballero, Benjamin
TI Reduction in consumption of sugar-sweetened beverages is associated with
weight loss: the PREMIER trial
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID INSULIN-RESISTANCE SYNDROME; LIFE-STYLE MODIFICATION; BODY-MASS INDEX;
BLOOD-PRESSURE; ENERGY-INTAKE; PHYSICAL-ACTIVITY; NUTRIENT INTAKE;
DAIRY-PRODUCTS; CLINICAL-TRIAL; DIETARY-INTAKE
AB Background: Consumption of liquid calories from beverages has increased in parallel with the obesity epidemic in the US population, but their causal relation remains unclear.
Objective: The objective of this study was to examine how changes in beverage consumption affect weight change among adults.
Design: This was a prospective study of 810 adults participating in the PREMIER trial, an 18-mo randomized, controlled, behavioral intervention trial. Measurements (weight, height, and 24-h dietary recall) were made at baseline, 6 mo, and 18 mo.
Results: Baseline mean intake of liquid calories was 356 kcal/d (19% of total energy intake). After potential confounders and intervention assignment were controlled for, a reduction in liquid calorie intake of 100 kcal/d was associated with a weight loss of 0.25 kg (95% CI: 0.11, 0.39; P < 0.001) at 6 mo and of 0.24 kg (95% CI: 0.06, 0.41; P = 0.008) at 18 mo. A reduction in liquid calorie intake had a stronger effect than did a reduction in solid calorie intake on weight loss. Of the individual beverages, only intake of sugar-sweetened beverages (SSBs) was significantly associated with weight change. A reduction in SSB intake of 1 serving/d was associated with a weight loss of 0.49 kg (95% CI: 0.11, 0.82; P = 0.006) at 6 mo and of 0.65 kg (95% CI: 0.22, 1.09; P = 0.003) at 18 mo.
Conclusions: These data support recommendations to limit liquid calorie intake among adults and to reduce SSB consumption as a means to accomplish weight loss or avoid excess weight gain. This trial was registered at clinicaltrials.gov as NCT00000616. Am J Clin Nutr 2009;89:1299-306.
C1 [Chen, Liwei; Caballero, Benjamin] Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Human Nutr, Baltimore, MD 21205 USA.
[Appel, Lawrence J.] Johns Hopkins Sch Med, Dept Internal Med, Baltimore, MD USA.
[Loria, Catherine] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Lin, Pao-Hwa] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Champagne, Catherine M.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Elmer, Patricia J.] Kaiser Permanente Ctr Hlth Res, Portland, OR USA.
[Ard, Jamy D.] Univ Alabama, Div Clin Nutr & Dietet, Birmingham, AL USA.
[Mitchell, Diane] Penn State Univ, Diet Assessment Ctr, University Pk, PA 16802 USA.
[Batch, Bryan C.; Svetkey, Laura P.] Duke Univ, Duke Hypertens Ctr, Durham, NC USA.
RP Caballero, B (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Human Nutr, 615 N Wolfe St,Room 2041, Baltimore, MD 21205 USA.
EM caballero@jhu.edu
FU National Heart, Lung, and Blood Institute; NIH [UO1 HL60570, UO1
HL60571, UO1 HL60573, UO1 HL60574, UO1 HL62828]; Center for Human
Nutrition; Johns Hopkins Bloomberg School of Public Health; Eunice
Kennedy Shriver National Institute of Child Health & Human Development
FX Supported by the National Heart, Lung, and Blood Institute; NIH grants
UO1 HL60570, UO1 HL60571, UO1 HL60573, UO1 HL60574, and UO1 HL62828; the
Center for Human Nutrition, Johns Hopkins Bloomberg School of Public
Health; and the Eunice Kennedy Shriver National Institute of Child
Health & Human Development.
NR 46
TC 99
Z9 103
U1 0
U2 15
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY 1
PY 2009
VL 89
IS 5
BP 1299
EP 1306
DI 10.3945/ajcn.2008.27240
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 436EB
UT WOS:000265394300005
PM 19339405
ER
PT J
AU Qi, L
Cornelis, MC
Zhang, CL
van Dam, RM
Hu, FB
AF Qi, Lu
Cornelis, Marilyn C.
Zhang, Cuilin
van Dam, Rob M.
Hu, Frank B.
TI Genetic predisposition, Western dietary pattern, and the risk of type 2
diabetes in men
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; PLASMA ADIPONECTIN CONCENTRATION; BODY IRON
STORES; MEAT INTAKE; WOMEN; CONSUMPTION; INSULIN; DISEASE; VARIANT; LOCI
AB Background: A widely held hypothesis is that interactions between genetic predisposition and Western-type lifestyle contribute to the epidemic of type 2 diabetes (T2D). No study has tested this hypothesis.
Objective: The objective was to assess whether established genetic variants, mainly from genomewide association studies, modify dietary patterns in predicting diabetes risk.
Design: We determined 10 polymorphisms in a prospective, nested, case-control study of 1196 diabetic and 1337 nondiabetic men. A genetic risk score (GRS) was generated by using an allele counting method. Baseline dietary intakes were collected by using a semi-quantitative food-frequency questionnaire. We used factor analysis to derive Western and "Prudent'' dietary patterns from 40 food groups.
Results: A significant interaction (P = 0.02) was observed between the GRS and Western dietary pattern. The multivariable odds ratios (ORs) of T2D across increasing quartiles for the Western dietary pattern were 1.00, 1.23 (95% CI: 0.88, 1.73), 1.49 (1.06,2.09), and 2.06 (1.48, 2.88) among men with a high GRS (>= 12 risk alleles; P for trend 0.01). The Western dietary pattern was not associated with diabetes risk among those with a lower GRS. In addition, we found that intakes of processed meat, red meat, and heme iron, which characterized the Western dietary pattern, showed significant interactions with GRS in relation to diabetes risk (P for interaction 0.029, 0.02, and 0.0004, respectively). The diet-diabetes associations were more evident among men with a high GRS (>= 12) than in those with a low GRS.
Conclusion: Genetic predisposition may synergistically interact with a Western dietary pattern in determining diabetes risk in men. Am J Clin Nutr 2009;89:1453-8.
C1 [Qi, Lu; Cornelis, Marilyn C.; van Dam, Rob M.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Qi, Lu; van Dam, Rob M.; Hu, Frank B.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Qi, Lu; van Dam, Rob M.; Hu, Frank B.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Zhang, Cuilin] NICHHD, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Rockville, MD USA.
RP Qi, L (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA.
EM nhlqi@channing.harvard.edu
RI van Dam, Rob/F-9674-2010
OI van Dam, Rob/0000-0002-7354-8734
FU NIH [DK58845, CA87969, HL071981]; AHA Scientist Development [0730094N];
Boston Obesity Nutrition Research Center [DK46200]
FX Supported by NIH grants DK58845 and CA87969. LQ was supported by NIH
grant HL071981, AHA Scientist Development Grant award 0730094N, and the
Boston Obesity Nutrition Research Center (DK46200).
NR 27
TC 49
Z9 56
U1 1
U2 7
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY 1
PY 2009
VL 89
IS 5
BP 1453
EP 1458
DI 10.3945/ajcn.2008.27249
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 436EB
UT WOS:000265394300024
PM 19279076
ER
PT J
AU Jiao, L
Silverman, DT
Schairer, C
Thiebaut, ACM
Hollenbeck, AR
Leitzmann, MF
Schatzkin, A
Stolzenberg-Solomon, RZ
AF Jiao, Li
Silverman, Debra T.
Schairer, Catherine
Thiebaut, Anne C. M.
Hollenbeck, Albert R.
Leitzmann, Michael F.
Schatzkin, Arthur
Stolzenberg-Solomon, Rachael Z.
TI Alcohol Use and Risk of Pancreatic Cancer
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article; Proceedings Paper
CT 98th Annual Meeting of the American-Association-for-Cancer-Research
CY APR 14-18, 2007
CL Los Angeles, CA
SP Amer Assoc Canc Res
DE alcohol drinking; cohort studies; pancreatic neoplasms; risk; smoking
ID HEALTH-AMERICAN-ASSOCIATION; POPULATION-BASED COHORT; RETIRED-PERSONS
DIET; UNITED-STATES; CIGARETTE-SMOKING; MEDICAL HISTORY; BEVERAGE
CONSUMPTION; NATIONAL-INSTITUTES; COFFEE CONSUMPTION; DRINKING HABITS
AB The epidemiologic evidence for the role of alcohol use in pancreatic cancer development is equivocal. The authors prospectively examined the relation between alcohol use and risk of pancreatic cancer among 470,681 participants who were aged 50-71 years in 1995-1996 in the US National Institutes of Health-AARP Diet and Health Study. The authors identified 1,149 eligible exocrine pancreatic cancer cases through December 2003. Multivariate Cox proportional hazards regression models were used to calculate relative risks and 95% confidence intervals with the referent group being light drinkers (< 1 drink/day). The relative risks of developing pancreatic cancer were 1.45 (95% confidence interval (CI): 1.17, 1.80; P(trend) = 0.002) for heavy total alcohol use (>= 3 drinks/day, similar to 40 g of alcohol/day) and 1.62 (95% CI: 1.24, 2.10; P(trend) = 0.001) for heavy liquor use, compared with the respective referent group. The increased risk with heavy total alcohol use was seen in never smokers (relative risk = 1.35, 95% CI: 0.79, 2.30) and participants who quit smoking 10 or more years ago before baseline (relative risk = 1.41, 95% CI: 1.01, 2.00). These findings suggest a moderately increased pancreatic cancer risk with heavy alcohol use, particularly liquor; however, residual confounding by cigarette smoking cannot be completely excluded.
C1 [Jiao, Li; Thiebaut, Anne C. M.; Leitzmann, Michael F.; Schatzkin, Arthur; Stolzenberg-Solomon, Rachael Z.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Silverman, Debra T.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Schairer, Catherine] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Jiao, L (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 3032, Rockville, MD 20852 USA.
EM jiaol@mail.nih.gov
FU Intramural NIH HHS
NR 63
TC 38
Z9 39
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD MAY 1
PY 2009
VL 169
IS 9
BP 1043
EP 1051
DI 10.1093/aje/kwp034
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 434HZ
UT WOS:000265267100001
PM 19299403
ER
PT J
AU Chen, HL
Mosley, TH
Alonso, A
Huang, XM
AF Chen, Honglei
Mosley, Thomas H.
Alonso, Alvaro
Huang, Xuemei
TI Plasma Urate and Parkinson's Disease in the Atherosclerosis Risk in
Communities (ARIC) Study
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE cohort studies; Parkinson disease; uric acid
ID URIC-ACID LEVELS; OXIDATIVE STRESS; ASSOCIATION; COHORT; GOUT
AB Higher plasma urate concentration has been linked to lower risk of Parkinson's disease in men, but data are lacking on women and African Americans. The authors examined plasma urate in relation to Parkinson's disease in the biracial, population-based Atherosclerosis Risk in Communities (ARIC) cohort. Between 1987 and 1989, 15,792 participants, aged 45-64 years, were recruited from 4 US communities and have since been followed with 3 triennial visits and annual surveillance. Plasma urate was measured at visits 1 and 2, and the concentrations were highly correlated. From visit 1 through 2004, 95 potential cases of Parkinson's disease were identified from multiple sources. Odds ratios and 95% confidence intervals were calculated from multivariate logistic regression models. Plasma urate concentration was inversely associated with Parkinson's disease occurrence. The odds ratios between extreme quartiles of plasma urate were 0.4 (95% confidence interval: 0.2, 0.8) in the overall analysis, 0.3 (95% confidence interval: 0.1, 0.7) for men, and 0.4 (95% confidence interval: 0.2, 1.0) for Caucasians. Such an association was also suggested among women and African Americans but was not statistically significant because of small sample sizes. These data support the previous finding that urate may be a protective factor against Parkinson's disease.
C1 [Chen, Honglei] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Mosley, Thomas H.] Univ Mississippi, Med Ctr, Div Geriatr Med, Jackson, MS 39216 USA.
[Alonso, Alvaro] Univ Minnesota, Dept Epidemiol, Minneapolis, MN USA.
[Huang, Xuemei] Penn State Univ, Milton S Hershey Med Ctr, Dept Neurol, Hershey, PA 17033 USA.
[Huang, Xuemei] Penn State Univ, Milton S Hershey Med Ctr, Dept Radiol, Hershey, PA 17033 USA.
[Huang, Xuemei] Penn State Univ, Milton S Hershey Med Ctr, Dept Neurosurg, Hershey, PA 17033 USA.
[Huang, Xuemei] Penn State Univ, Milton S Hershey Med Ctr, Dept Pharmacol, Hershey, PA 17033 USA.
[Huang, Xuemei] Penn State Univ, Milton S Hershey Med Ctr, Dept Kinesiol & Bioengn, Hershey, PA 17033 USA.
[Huang, Xuemei] Penn State Univ, Milton S Hershey Med Ctr, Hershey Brain Anal Res Lab Neurodegenerat Disorde, Hershey, PA 17033 USA.
RP Chen, HL (reprint author), NIEHS, Epidemiol Branch, 111 TW Alexander Dr,POB 12233,Mail Drop A3-05, Res Triangle Pk, NC 27709 USA.
EM chenh2@niehs.nih.gov
RI Alonso, Alvaro/A-4917-2010;
OI Alonso, Alvaro/0000-0002-2225-8323; Chen, Honglei/0000-0003-3446-7779
FU National Institutes of Health; National Institute of Environmental
Health Sciences [Z01ES101986]; National Heart, Lung, and Blood Institute
[N01-HC-55015, N01-HC-55016, N01HC- 55018, N01-HC-55019, N01-HC-55020,
N01-HC55021, N01-HC-55022]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences (grant Z01ES101986). The ARIC Study is carried out as a
collaborative study supported by National Heart, Lung, and Blood
Institute contracts N01-HC-55015, N01-HC-55016, N01HC- 55018,
N01-HC-55019, N01-HC-55020, N01-HC55021, and N01-HC-55022.
NR 26
TC 60
Z9 65
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD MAY 1
PY 2009
VL 169
IS 9
BP 1064
EP 1069
DI 10.1093/aje/kwp033
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 434HZ
UT WOS:000265267100003
PM 19299404
ER
PT J
AU Whitehead, T
Metayer, C
Ward, MH
Nishioka, MG
Gunier, R
Colt, JS
Reynolds, P
Selvin, S
Buffler, P
Rappaport, SM
AF Whitehead, Todd
Metayer, Catherine
Ward, Mary H.
Nishioka, Marcia G.
Gunier, Robert
Colt, Joanne S.
Reynolds, Peggy
Selvin, Steve
Buffler, Patricia
Rappaport, Stephen M.
TI Is House-Dust Nicotine a Good Surrogate for Household Smoking?
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE child; dust; environmental exposure; infant; leukemia; linear models;
nicotine; smoking
ID ENVIRONMENTAL TOBACCO-SMOKE; CHILDRENS-CANCER-GROUP; SELF-REPORTED
SMOKING; PARENTAL SMOKING; CIGARETTE-SMOKING; CHILDHOOD-CANCER;
ALCOHOL-CONSUMPTION; GENETIC POLYMORPHISMS; MYELOID-LEUKEMIA; URINARY
COTININE
AB The literature is inconsistent regarding associations between parental smoking and childhood leukemia, possibly because previous studies used self-reported smoking habits as surrogates for children's true exposures to cigarette smoke. Here, the authors investigated the use of nicotine concentrations in house dust as measures of children's exposure to cigarette smoke in 469 households from the Northern California Childhood Leukemia Study (1999-2007). House dust was collected by using high-volume surface samplers and household vacuum cleaners and was analyzed for nicotine via gas chromatography-mass spectrometry. Using multivariable linear regression, the authors evaluated the effects of self-reported parental smoking, parental demographics, house characteristics, and other covariates on house-dust nicotine concentrations. They observed that nicotine concentrations in house dust were associated with self-reported smoking for periods of months and years before dust collection. Furthermore, the authors found that the relation between nicotine dust levels and self-reported smoking varied by parental age and socioeconomic status. These findings suggest that house-dust nicotine concentrations reflect long-term exposures to cigarette smoke in the home and that they may be less biased surrogates for children's exposures to cigarette smoke than self-reported smoking habits.
C1 [Whitehead, Todd; Metayer, Catherine; Selvin, Steve; Buffler, Patricia; Rappaport, Stephen M.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Ward, Mary H.; Colt, Joanne S.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Nishioka, Marcia G.] Battelle Mem Inst, Columbus, OH 43201 USA.
[Gunier, Robert; Reynolds, Peggy] No Calif Canc Ctr, Berkeley, CA USA.
RP Whitehead, T (reprint author), Univ Calif Berkeley, Sch Publ Hlth, 50 Univ Hall,MC 7360, Berkeley, CA 94720 USA.
EM toddpwhitehead@berkeley.edu
OI Gunier, Robert/0000-0001-5485-9919
FU National Institute of Environmental Health Sciences [R01ES009137,
P-42-ES-04705-18]; National Cancer Institute, National Institute of
Health [7590-S-04, 7590-S-01]; National Cancer Institute [N02-CP-11015]
FX This work was supported by the National Institute of Environmental
Health Sciences (grants R01ES009137, P-42-ES-04705-18), the Intramural
Research Program of the National Cancer Institute, National Institute of
Health (subcontracts 7590-S-04, 7590-S-01); and the National Cancer
Institute (contract N02-CP-11015).
NR 32
TC 27
Z9 27
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD MAY 1
PY 2009
VL 169
IS 9
BP 1113
EP 1123
DI 10.1093/aje/kwp021
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 434HZ
UT WOS:000265267100009
PM 19299402
ER
PT J
AU Ferrucci, LM
Sinha, R
Graubard, BI
Mayne, ST
Ma, XM
Schatzkin, A
Schoenfeld, PS
Cash, BD
Flood, A
Cross, AJ
AF Ferrucci, Leah M.
Sinha, Rashmi
Graubard, Barry I.
Mayne, Susan T.
Ma, Xiaomei
Schatzkin, Arthur
Schoenfeld, Philip S.
Cash, Brooks D.
Flood, Andrew
Cross, Amanda J.
TI Dietary Meat Intake in Relation to Colorectal Adenoma in Asymptomatic
Women
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID HETEROCYCLIC AMINE CONTENT; N-NITROSO COMPOUNDS; BODY IRON STORES;
NON-HEME IRON; RED MEAT; COLON-CANCER; ALCOHOL-CONSUMPTION; VARYING
DEGREES; AVERAGE-RISK; COOKED FOOD
AB OBJECTIVES: No previous study has concurrently assessed the associations between meat intake, meat-cooking methods and doneness levels, meat mutagens (heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons), heme iron, and nitrite from meat and colorectal adenoma in asymptomatic women undergoing colonoscopy.
METHODS: Of the 807 eligible women in a cross-sectional multicenter colonoscopy screening study, 158 prevalent colorectal adenoma cases and 649 controls satisfactorily completed the validated food frequency and meat questionnaires. Using an established meat mutagen database and new heme iron and nitrite databases, we comprehensively investigated the components of meat that may be involved in carcinogenesis. Using logistic regression, we estimated odds ratios (ORs) and 95% confidence intervals (CIs) within quartiles of meat-related variables.
RESULTS: Red meat was associated positively with colorectal adenoma (OR fourth vs. first quartile = 2.02; 95% CI = 1.06-3.83; P trend = 0.38). Intake of pan-fried meat (OR = 1.72; 95% CI = 0.96-3.07; P trend = 0.01) and the HCA: 2-amino-3,8-dimethylimidazo[4,5-f] quinoxaline (MeIQx) (OR = 1.90; 95% CI = 1.05-3.42; P trend = 0.07) were also associated with an increased risk of colorectal adenoma. The new databases yielded lower estimates of heme iron and nitrite than previous assessment methods, although the two methods were highly correlated for both exposures. Although not statistically significant, there were positive associations between iron and heme iron from meat and colorectal adenoma.
CONCLUSIONS: In asymptomatic women undergoing colonoscopy, colorectal adenomas were associated with high intake of red meat, pan-fried meat, and the HCA MeIQx. Other meat-related exposures require further investigation.
C1 [Ferrucci, Leah M.; Sinha, Rashmi; Graubard, Barry I.; Schatzkin, Arthur; Cross, Amanda J.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Ferrucci, Leah M.; Mayne, Susan T.; Ma, Xiaomei] Yale Sch Publ Hlth, New Haven, CT USA.
[Schoenfeld, Philip S.] Univ Michigan, Sch Med, Div Gastroenterol, Ann Arbor, MI USA.
[Schoenfeld, Philip S.] Vet Affairs Ctr Excellence Hlth Serv Res, Ann Arbor, MI USA.
[Schoenfeld, Philip S.; Cash, Brooks D.] Uniformed Serv Univ Hlth Sci, Div Gastroenterol, Bethesda, MD 20814 USA.
[Flood, Andrew] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Flood, Andrew] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN USA.
RP Ferrucci, LM (reprint author), NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
EM ferruccil@mail.nih.gov
RI Sinha, Rashmi/G-7446-2015
OI Sinha, Rashmi/0000-0002-2466-7462
FU National Institutes of Health, National Cancer Institute; National
Cancer Institute [TU2 CA105666]
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute, and by
Grant TU2 CA105666 from the National Cancer Institute.
NR 58
TC 37
Z9 38
U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD MAY
PY 2009
VL 104
IS 5
BP 1231
EP 1240
DI 10.1038/ajg.2009.102
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 447VB
UT WOS:000266219000021
PM 19367270
ER
PT J
AU Furia, AC
Lee, RE
Strother, ML
Huang, TTK
AF Furia, Andrea C.
Lee, Rebecca E.
Strother, Myra L.
Huang, Terry T-K
TI College Students' Motivation to Achieve and Maintain a Healthy Weight
SO AMERICAN JOURNAL OF HEALTH BEHAVIOR
LA English
DT Article
DE weight maintenance; obesity; overweight; motivation; college students
ID PHYSICAL-ACTIVITY; UNITED-STATES; HIGH-SCHOOL; OBESITY; EXERCISE;
OVERWEIGHT; PREDICTORS; BEHAVIORS; FRESHMAN; DISEASE
AB Objectives: To develop and refine a scale of motivational factors related to healthy weight achievement and maintenance and to examine differences by gender and weight status. Methods: A cross-sectional survey of 300,university students aged 18-24 years. Results: Factor analysis yielded 6 factors - Intrinsic (Cronbach's alpha=0.73): affective motivation, self-efficacy/interest; Extrinsic (Cronbach's alpha=0.68): social reward, peer pressure, lack of choice, and authority influence. Males and normal-weight students showed higher affective motivation and overall intrinsic motivation compared to females and overweight students, (P<.001). Conclusion: Intrinsic motivational factors and gender differences should be considered in developing obesity prevention interventions in this age-group.
C1 [Huang, Terry T-K] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
[Furia, Andrea C.] US FDA, Off Special Hlth Issues, Rockville, MD 20857 USA.
[Lee, Rebecca E.] Univ Houston, Dept Hlth & Human Performance, Houston, TX USA.
[Strother, Myra L.] Univ Kansas, Watkins Mem Hlth Ctr, Lawrence, KS 66045 USA.
RP Huang, TTK (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, 6100 Execut Blvd,4B11, Bethesda, MD 20892 USA.
EM huangter@mail.nih.gov
NR 26
TC 12
Z9 12
U1 4
U2 8
PU PNG PUBLICATIONS
PI STAR CITY
PA PO BOX 4593, STAR CITY, WV 26504-4593 USA
SN 1087-3244
J9 AM J HEALTH BEHAV
JI Am. J. Health Behav.
PD MAY-JUN
PY 2009
VL 33
IS 3
BP 256
EP 263
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 439WE
UT WOS:000265657400004
PM 19063647
ER
PT J
AU Kilfoy, BA
Zheng, TZ
Lan, Q
Han, XS
Qin, Q
Rothman, N
Holford, T
Zhang, YW
AF Kilfoy, Briseis A.
Zheng, Tongzhang
Lan, Qing
Han, Xuesong
Qin, Qin
Rothman, Nathaniel
Holford, Theodore
Zhang, Yawei
TI Genetic polymorphisms in glutathione S-transferases and cytochrome
P450s, tobacco smoking, and risk of non-Hodgkin lymphoma
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID B-CELL LYMPHOMA; CIGARETTE-SMOKING; POOLED ANALYSIS; UNITED-STATES;
SUBTYPES; CANCER; WOMEN; P1-1; CONJUGATION; CONSORTIUM
AB We investigated variation in glutathione S-transferases (GSTs) and cytochrome P450s (CYPs), and smoking in a population-based case-control study of NHL including 1,115 women. Although risk of NHL was not altered by variant polymorphisms in GSTs or CYPs, it was significantly changed for DLBCL when considered in conjunction with smoking behavior, though only in nonsmokers. An increased risk of DLBCL in nonsmokers was associated with the variant G allele for GSTP1 (OR = 1.6, 95% CI 1.0-2.3) and CYP1A1 (OR = 2.4; 95% CI 1.0-5.7), but a decreased risk for the variant G allele for CYP1B1 (OR = 0.6, 95% CI 0.4-1.0). Our results confer support investigation of the gene-environment interaction in a larger study population of DLBCL. Am. J. Hematol. 84:279-282, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Kilfoy, Briseis A.; Zheng, Tongzhang; Han, Xuesong; Holford, Theodore; Zhang, Yawei] Yale Univ, Sch Epidemiol & Publ Hlth, Dept Environm Hlth Sci, New Haven, CT 06520 USA.
[Kilfoy, Briseis A.; Lan, Qing; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Rockville, MD USA.
[Qin, Qin] Univ So Maine, Ctr Toxicol & Environm Hlth, Portland, ME 04103 USA.
RP Zhang, YW (reprint author), Yale Univ, Sch Publ Hlth, 60 Coll St,LEPH 440,POB 208034, New Haven, CT 06520 USA.
EM yawei.zhang@yale.edu
RI Aschebrook-Kilfoy, Briseis/A-2537-2012
FU National Institutes of Health [CA62006, 1D43TW007864-01]; National
Center for Research Resources [UL1 RR0241139]; NIH
FX Contract grant sponsor: National Institutes of Health; Contract grant
numbers: CA62006, 1D43TW007864-01; Contract grant sponsor: National
Center for Research Resources; Contract grant number: UL1 RR0241139;
Contract grant sponsor: Intramural Research Program of the NIH.
NR 31
TC 6
Z9 6
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD MAY
PY 2009
VL 84
IS 5
BP 279
EP 282
DI 10.1002/ajh.21386
PG 4
WC Hematology
SC Hematology
GA 440ZR
UT WOS:000265738900005
PM 19338043
ER
PT J
AU Soloway, LE
Demerath, EW
Ochs, N
James, GD
Little, MA
Bindon, JR
Garruto, RM
AF Soloway, Laura E.
Demerath, Ellen W.
Ochs, Natalie
James, Gary D.
Little, Michael A.
Bindon, James R.
Garruto, Ralph M.
TI Blood Pressure and Lifestyle on Saba, Netherlands Antilles
SO AMERICAN JOURNAL OF HUMAN BIOLOGY
LA English
DT Article
ID CARDIOVASCULAR RISK-FACTORS; ENVIRONMENTAL CONTRIBUTIONS; HYPERTENSION;
HERITABILITY; FAMILY; MODERNIZATION; MIGRATION; COMMUNITY; DISEASE;
TRAITS
AB During the 20th century, infectious disease morbidity and mortality generally waned whereas chronic degenerative diseases posed a growing burden at the global level. The population on Saba, Netherlands Antilles has recently experienced such an epidemiologic transition, and hypertension was reported to be extraordinarily high, although no prevalences have been reported and relationships with lifestyle factors associated with rapid modernization have not been explored. In this study, a medical and demographic questionnaires, as well as body composition and blood pressure measures were collected from 278 Saban men and women aged 18-91 years. When age and sex adjusted, 48% of the population was hypertensive. Age, BMI, and Afro-Caribbean descent were all associated with higher blood pressures. In a second phase, 124 individuals of the 278 were invited to receive a longer questionnaire on individual exposure to modernizing influences such as travel and education. Higher blood pressure was associated with having lived in fewer different places in the past; those who stayed only on Saba or Statia had higher blood pressures than those who had also lived in more modernized areas. However, this was no longer statistically significant after adjustment for age and BMI. Lifestyle incongruity was positively associated with higher blood pressure in that those with more discord between material wealth and income were more likely to be hypertensive, and this remained statistically significant after adjustment for age and adiposity. In summary, hypertension is highly prevalent on Saba and tended to be associated with greater age, adiposity, Afro-Caribbean ancestry, and lifestyle incongruity. Am. J. Hum. Biol. 21:319-325, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Soloway, Laura E.; Demerath, Ellen W.] Univ Minnesota, Div Epidemiol & Community Hlth, Sch Publ Hlth, Minneapolis, MN 55455 USA.
[Ochs, Natalie] NIAID, NIH, Bethesda, MD 20892 USA.
[James, Gary D.; Little, Michael A.; Garruto, Ralph M.] SUNY Binghamton, Dept Anthropol, Binghamton, NY USA.
[James, Gary D.] SUNY Binghamton, Decker Sch Nursing, Binghamton, NY USA.
[Bindon, James R.] Univ Alabama, Dept Anthropol, Tuscaloosa, AL USA.
RP Soloway, LE (reprint author), Univ Minnesota, Div Epidemiol & Community Hlth, Sch Publ Hlth, 1300 S 2nd St,Suite 300, Minneapolis, MN 55455 USA.
EM solow002@umn.edu
FU NHLBI NIH HHS [T32 HL007779-15, T32 HL007779]
NR 32
TC 4
Z9 4
U1 0
U2 4
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1042-0533
J9 AM J HUM BIOL
JI Am. J. Hum. Biol.
PD MAY-JUN
PY 2009
VL 21
IS 3
BP 319
EP 325
DI 10.1002/ajhb.20862
PG 7
WC Anthropology; Biology
SC Anthropology; Life Sciences & Biomedicine - Other Topics
GA 435IS
UT WOS:000265338200006
PM 19189411
ER
PT J
AU Franceschini, N
North, KE
Arnett, D
Pankow, JS
Chung, JH
Baird, L
Leppert, MF
Eckfeldt, JH
Boerwinkle, E
Gu, CC
Lewis, CE
Myers, RH
Turner, ST
Weder, A
Kao, WHL
Mosley, TH
Chakravarti, A
Kramer, H
Zhang, J
Hunt, SC
AF Franceschini, Nora
North, Kari E.
Arnett, Donna
Pankow, James S.
Chung, Jay H.
Baird, Lisa
Leppert, Mark F.
Eckfeldt, John H.
Boerwinkle, Eric
Gu, C. Charles
Lewis, Cora E.
Myers, Richard H.
Turner, Stephen T.
Weder, Alan
Kao, W. H. Linda
Mosley, Thomas H.
Chakravarti, Aravinda
Kramer, Holly
Zhang, Jinghui
Hunt, Steven C.
TI The Association of Cell Cycle Checkpoint 2 Variants and Kidney Function:
Findings of the Family Blood Pressure Program and the Atherosclerosis
Risk in Communities Study
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
ID STAGE RENAL-DISEASE; URINARY ALBUMIN EXCRETION; GENOTYPE-PHENOTYPE
ASSOCIATIONS; GLOMERULAR-FILTRATION-RATE; CARNOSINASE GENE CNDP1;
DNA-DAMAGE CHECKPOINTS; LINKAGE ANALYSIS; ANGIOTENSIN-II; HYPERTENSIVE
FAMILIES; DIABETIC-NEPHROPATHY
AB BACKGROUND
Recent experimental evidence suggests that DNA damage and cell cycle regulatory proteins are involved in kidney injury and apoptosis. The checkpoint 2 gene (CHEK2) is an important transducer in DNA damage signaling pathways in response to injury, and therefore, CHEK2 variants may affect susceptibility to kidney disease.
METHODS
We used tag-single-nucleotide polymorphisms (tag-SNPs) to evaluate the association of the CHEK2 with kidney function (estimated glomerular filtration rate, eGFR) in 1,549 African-American and 1,423 white Hypertension Genetic Epidemiology Network (HyperGEN) participants. We performed replication analyses in the Genetic Epidemiology Network of Arteriopathy (GENOA) participants (1,746 African Americans and 1,418 whites), GenNet participants (706 whites), and Atherosclerosis Risk in Communities (ARIC) study participants (3,783 African Americans and 10,936 whites). All analyses were race-stratified and used additive genetic models with adjustments for covariates and for family structure, if needed.
RESULTS
One tag-SNP, rs5762764, was associated with eGFR in HyperGEN (P = 0.003) and GENOA white participants (P = 0.009), and it was significantly associated with eGFR in meta-analyses (P = 0.002). The associations were independent of type 2 diabetes.
CONCLUSIONS
These results suggest that CHEK2 variants may influence eGFR in the context of hypertension.
C1 [Franceschini, Nora; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Arnett, Donna] Univ Alabama, Dept Epidemiol, Birmingham, AL USA.
[Pankow, James S.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Chung, Jay H.] NHLBI, Lab Biochem Genet, Bethesda, MD 20892 USA.
[Baird, Lisa; Leppert, Mark F.] Univ Utah, Dept Human Genet, Salt Lake City, UT USA.
[Baird, Lisa; Leppert, Mark F.] Univ Utah, Eccles Inst Human Genet, Salt Lake City, UT USA.
[Eckfeldt, John H.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Ctr Human Genet, Houston, TX USA.
[Gu, C. Charles] Washington Univ, Sch Med, Div Biostat, St Louis, MO 63110 USA.
[Lewis, Cora E.] Univ Alabama, Dept Med, Div Prevent Med, Birmingham, AL 35294 USA.
[Myers, Richard H.] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Turner, Stephen T.] Mayo Clin & Mayo Fdn, Div Nephrol & Hypertens, Dept Internal Med, Rochester, MN USA.
[Weder, Alan] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Kao, W. H. Linda] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Mosley, Thomas H.] Univ Mississippi, Med Ctr, Dept Geriatr Med, Jackson, MS 39216 USA.
[Chakravarti, Aravinda] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
[Kramer, Holly] Loyola Univ, Dept Prevent Med & Med, Maywood, IL 60153 USA.
[Zhang, Jinghui] NCI, Ctr Biomed Informat & Informat Technol, Rockville, MD USA.
[Hunt, Steven C.] Univ Utah, Sch Med, Div Cardiovasc Genet, Salt Lake City, UT USA.
RP Franceschini, N (reprint author), Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
EM noraf@unc.edu
RI Gu, Charles/A-7934-2010
OI Kramer, Holly/0000-0002-6374-837X; Myers, Richard/0000-0002-8365-2674;
Gu, Charles/0000-0002-8527-8145
FU NHLBI NIH HHS [N01-HC-55019, N01-HC-55015, N01-HC-55016, N01-HC-55018,
N01-HC-55020, N01-HC-55021, N01-HC-55022, N01HC55015, N01HC55016,
N01HC55018, N01HC55019, N01HC55020, N01HC55021, N01HC55022, U01
HL054509, U01 HL054509-10]
NR 57
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD MAY
PY 2009
VL 22
IS 5
BP 552
EP 558
DI 10.1038/ajh.2009.41
PG 7
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 435HP
UT WOS:000265335100019
PM 19265784
ER
PT J
AU Bagrov, A
Agalakova, NI
Kashkin, VA
Fedorova, OV
AF Bagrov, AlexeiY
Agalakova, Natalia I.
Kashkin, Vladimir A.
Fedorova, Olga V.
TI Endogenous Cardiotonic Steroids and Differential Patterns of Sodium Pump
Inhibition in NaCl-Loaded Salt-Sensitive and Normotensive Rats
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
ID DEPENDENT PROTEIN-KINASE; BLOOD-PRESSURE; HYPERTENSIVE-RATS;
NA/K-ATPASE; MARINOBUFAGENIN; ANP; PHOSPHORYLATION; STIMULATION;
DIGITALIS; ANTIBODY
AB BACKGROUND
Endogenous sodium pump inhibitors promote sodium excretion in normotensives and contribute to vasoconstriction in NaCl-sensitive hypertension. Marinobufagenin (MBG), an endogenous bufadienolide inhibitor of alpha-1 sodium pump, contributes to hypertension in Dahl salt-sensitive rats (DS). We hypothesized that in NaCl-loaded DS and normotensive Sprague-Dawley rats (S-D), MBG would elicit different patterns of sodium pump inhibition.
METHODS
We compared systolic blood pressure (SBP), renal sodium excretion, activity of the sodium pump in aorta and renal medulla, and levels of MBG, atrial natriuretic peptide (ANP), and cyclic guanosine monophosphate (cGMP) in salt-loaded DS and S-D (20% NaCl, 2.5 ml/kg, intraperitoneally).
RESULTS
NaCl loading produced sustained elevations in renal MBG excretion in both DS (2.41 +/- 0.24 vs. 0.79 +/- 0.08 pmol/h/kg, P < 0.01) and S-D (1.97 +/- 0.37 vs. 0.60 +/- 0.07 pmol/h/kg, P < 0.01) vs. that at baseline (n = 10 for each group). In NaCl-loaded DS, SBP rose by 18 mm Hg (P < 0.01) and aortic sodium pump was inhibited by 22% (P < 0.05 vs. control), while in S-D, SBP and activity of aortic sodium pump did not change. NaCl-loaded S-D excreted twice as much sodium as DS; in S-D, renal sodium pump was inhibited by 24% vs. 14% inhibition in DS (P < 0.05). NaCl loading elicited increases in plasma ANP and in renal cGMP excretion in S-D but not in DS.
CONCLUSIONS
Our present observations demonstrate that in NaCl-loaded S-D and DS, a comparable MBG response is associated with preferential inhibition of the sodium pump in the kidney and in vascular smooth muscle, respectively, resulting in an adaptive natriuresis in S-D but sodium retention and pressor response in DS.
C1 [Bagrov, AlexeiY; Agalakova, Natalia I.; Kashkin, Vladimir A.; Fedorova, Olga V.] NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
RP Fedorova, OV (reprint author), NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
EM FedorovO@mail.nih.gov
OI Kashkin, Vladimir/0000-0002-7202-0233
FU National Institute on Aging, NIH
FX This study has been supported by Intramural Research Program, National
Institute on Aging, NIH. The authors gratefully acknowledge critical
comments of Edward G. Lakatta, and David E. Anderson, and are grateful
for excellent technical assistance by Danielle Joseph, Chad Boily, and
Alexandra Newman (Namikas).
NR 30
TC 12
Z9 12
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD MAY
PY 2009
VL 22
IS 5
BP 559
EP 563
DI 10.1038/ajh.2009.22
PG 5
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 435HP
UT WOS:000265335100020
PM 19229192
ER
PT J
AU Madero, M
Sarnak, MJ
Wang, XL
Greene, T
Beck, GJ
Kusek, JW
Collins, AJ
Levey, AS
Menon, V
AF Madero, Magdalena
Sarnak, Mark J.
Wang, Xuelei
Greene, Tom
Beck, Gerald J.
Kusek, John W.
Collins, Allan J.
Levey, Andrew S.
Menon, Vandana
TI Uric Acid and Long-term Outcomes in CKD
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Kidney disease; uric acid; outcomes; cardiovascular; mortality; kidney
failure
ID CORONARY-HEART-DISEASE; CARDIOVASCULAR-DISEASE; KIDNEY-DISEASE;
RENAL-DISEASE; FOLLOW-UP; ESSENTIAL-HYPERTENSION; IGA NEPHROPATHY;
SCREENED COHORT; BLOOD-PRESSURE; RISK-FACTORS
AB Background: Hyperuricemia is prevalent in patients with chronic kidney disease (CKD); however, data are limited about the relationship of uric acid levels with long-term outcomes in this patient population.
Study Design: Cohort study.
Setting & Participants: The Modification of Diet in Renal Disease (MDRD) Study was a randomized controlled trial (N = 840) conducted from 1989 to 1993 to examine the effects of strict blood pressure control and dietary protein restriction on progression of stages 3 to 4 CKD. This analysis included 838 patients.
Predictor: Uric acid level.
Outcomes & Measurements: The study evaluated the association of baseline uric acid levels with all-cause mortality, cardiovascular disease (CVD) mortality, and kidney failure.
Results: Mean age was 52 12 (SD) years, glomerular filtration rate was 33 +/- 12 mL/min/1.73 m(2), and uric acid level was 7.63 +/- 1.66 mg/dL. During a median follow-up of 10 years, 208 (25%) participants died of any cause, 127 (15%) died of CVD, and 553 (66%) reached kidney failure. In multivariate models, the highest tertile of uric acid was associated with increased risk of all-cause mortality (hazard ratio [HR], 1.57; 95% confidence interval [CI], 1.07 to 2.32), a trend toward CVD mortality (HR, 1.47; 95% CI, 0.90 to 2.39), and no association with kidney failure (HR, 1.20; 95% CI, 0.95 to 1.51) compared with the lowest tertile. In continuous analyses, a 1-mg/dL greater uric acid level was associated with 17% increased risk of all-cause mortality (HR, 1.17; 95% CI, 1.05 to 1.30) and 16% increased risk of CVD mortality (HR, 1.16; 95% CI, 1.01 to 1.33), but was not associated with kidney failure (HR, 1.02; 95% CI, 0.97 to 1.07).
Limitations: Primary analyses were based on a single measurement of uric acid. Results are generalizable primarily to relatively young white patients with predominantly nondiabetic CKD.
Conclusions: In patients with stages 3 to 4 CKD, hyperuricemia appears to be an independent risk factor for all-cause and CVD mortality, but not kidney failure. Am J Kidney Dis 53:796-803. (C) 2009 by the National Kidney Foundation, Inc. All rights reserved.
C1 [Sarnak, Mark J.; Levey, Andrew S.; Menon, Vandana] Tufts Med Ctr, Div Nephrol, Dept Med, Boston, MA 02111 USA.
[Madero, Magdalena] Inst Nacl Cardiol Ignacio Chavez, Dept Med, Div Nephrol, Mexico City, DF, Mexico.
[Wang, Xuelei; Beck, Gerald J.] Cleveland Clin Fdn, Dept Biostat & Epidemiol, Cleveland, OH 44195 USA.
[Greene, Tom] Univ Utah, Div Clin Epidemiol, Salt Lake City, UT USA.
[Kusek, John W.] NIH, Bethesda, MD 20892 USA.
[Collins, Allan J.] Hennepin Cty Med Ctr, Div Nephrol, Minneapolis, MN 55415 USA.
RP Menon, V (reprint author), Tufts Med Ctr, Div Nephrol, Dept Med, Box 391,800 Washington St, Boston, MA 02111 USA.
EM vmenon@tuftsmedicalcenter.org
FU National Institute of Diabetes and Digestive and Kidney Diseases
(National Institutes of Health) [K23 DK067303, K23 DK02904, K24
DK078204, UO 1 DK35073]; TAP Pharmaceutical Products Inc
FX This study was supported by National Institute of Diabetes and Digestive
and Kidney Diseases (National Institutes of Health) Grants K23 DK067303,
K23 DK02904, K24 DK078204, and UO 1 DK35073, and TAP Pharmaceutical
Products Inc.
NR 32
TC 148
Z9 164
U1 3
U2 11
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD MAY
PY 2009
VL 53
IS 5
BP 796
EP 803
DI 10.1053/j.ajkd.2008.12.021
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 443PY
UT WOS:000265923500012
PM 19303683
ER
PT J
AU Greene, T
Daugirdas, JT
Depner, TA
Gotch, F
Kuhlman, M
AF Greene, Tom
Daugirdas, John T.
Depner, Thomas A.
Gotch, Frank
Kuhlman, Martin
CA Natl Inst Diabet & Digest & Kidney
TI Solute Clearances and Fluid Removal in the Frequent Hemodialysis Network
Trials
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Daily dialysis; nocturnal dialysis; kinetic modeling; clinical trials
ID BLOOD-FLOW; UREA; DIALYSIS; HEMO; KT/V; BETA(2)-MICROGLOBULIN; MODEL
AB Background: The Frequent Hemodialysis Network (FHN) is conducting 2 randomized clinical trials, a daytime in-center trial ("daily") comparing 6 versus 3 treatments/wk, and a home nocturnal trial comparing 6 nocturnal treatments versus 3 conventional treatments/wk. The goal of this study was to project separation between the treatment and control arms of these studies for measures of dialysis dose by using simulations based on 2-compartment variable-volume models.
Setting & Participants: Data from the most recent hemodialysis treatment in 100 patients dialyzed 3 times/wk at facilities of the Renal Research Institute in New York and from 2 data sets (n = 154 and 115 patients) from the Hemodialysis (HEMO) trial.
Design: Observational study.
Predictor: Dialysis prescriptions for the treatment and control arms in the FHN trials.
Dialysis Regimen Outcomes: Treatment time, ultrafiltration rate, standard Kt/V/wk for urea (stdKt/Vur.J, and continuous clearance estimates based on ratios of urea, creatinine, and normalized beta(2)-microglobulin generation rates (denoted by Gn) to time-averaged concentrations (TACs) of these solutes during 1 treatment week.
Results: The expected differences between median values in the experimental and control groups were weekly treatment time: daily trial, 29%; nocturnal trial, 234%; ultrafiltration rate: daily, -20%; nocturnal, -69%; stdKt/V(urea): daily, 52%; nocturnal, 133%; Gn(urea)/TAC(urea): daily, 34%; nocturnal, 130%; Gn(cr)/TAC(cr): daily, 31%; nocturnal, 135%; and Gn(beta 2)/TAC(beta 2): daily, 8%; nocturnal, 67%.
Limitations: Use of simulated data and assumption of equivalent volumes and ultrafiltration rates between treatment arms.
Conclusions: The nocturnal 6-times-weekly regimen produces substantially greater separation between the treatment and control arms than the daytime 6-times-weekly regimen for a wide range of treatment parameters. However, the 6-times-weekly interventions in both FHN trials will produce substantially greater separation than in the HEMO trial, where separations in median weekly treatment time and stdKt/V(urea). between the 3-times-weekly high- and standard-dose groups were 18% and 17%, respectively. The FHN trials will test whether substantial increases in solute clearance and other effects of frequent hemodialysis materially influence selected intermediate outcome measures. Am J Kidney Dis 53:835-844. (C) 2009 by the National Kidney Foundation, Inc.
C1 [Greene, Tom; Daugirdas, John T.; Depner, Thomas A.; Gotch, Frank; Kuhlman, Martin; Natl Inst Diabet & Digest & Kidney] NIDDK, NIH, Bethesda, MD USA.
RP Greene, T (reprint author), Univ Utah, Div Epidemiol, 85 N Med Dr,E Rm 201, Salt Lake City, UT 84112 USA.
EM tom.greene@hsc.utah.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health
FX The HEMO Study was funded by the National Institute of Diabetes and
Digestive and Kidney Diseases of the National Institutes of Health.
Baxter Healthcare and Fresenius Medical Care donated sonic of the
dialyzers used by study patients.
NR 26
TC 27
Z9 28
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD MAY
PY 2009
VL 53
IS 5
BP 835
EP 844
DI 10.1053/j.ajkd.2008.12.039
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA 443PY
UT WOS:000265923500016
PM 19339093
ER
PT J
AU Sperati, CJ
Parekh, RS
Berthier-Schaad, Y
Jaar, BG
Plantinga, L
Fink, N
Powe, NR
Smith, MW
Coresh, J
Kao, WHL
AF Sperati, C. John
Parekh, Rulan S.
Berthier-Schaad, Yvette
Jaar, Bernard G.
Plantinga, Laura
Fink, Nancy
Powe, Neil R.
Smith, Michael W.
Coresh, Josef
Kao, W. H. Linda
TI Association of Single-Nucleotide Polymorphisms in JAK3, STAT4, and STAT6
With New Cardiovascular Events in Incident Dialysis Patients
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Dialysis; cardiovascular diseases; inflammation; genes
ID IN-VIVO; PSEUDOKINASE DOMAIN; COMPETING RISKS; DEFICIENT MICE;
ATHEROSCLEROSIS; DISEASE; ACTIVATION; PATHWAY; INTERLEUKIN-10;
ATHEROGENESIS
AB Background: Increasing evidence supports a role for cell-mediated immunity in the pathogenesis of cardiovascular disease. Single-nucleotide polymorphisms (SNPs) in JAK3, STAT4, and STAT6 of the Janus kinase-signal transducer and activator of transcription (Jak-Stat) signal transduction pathway were examined for association with time to new cardiovascular events in incident dialysis patients from the Choices for Healthy Outcomes in Caring for End-Stage Renal Disease Study.
Study Design: Prospective cohort study.
Setting & Participants: 764 white (n = 518) and black (n = 246) participants from 79 dialysis centers.
Predictor: SNPs in JAK3, STAT4, and STAT6 selected using a pairwrise approach to identify a maximally informative set of tag SNPs for populations of European and African descent.
Outcomes & Measurements: Cox proportional hazards models were used to estimate unadjusted and multivariable-adjusted hazard ratios (HRs) for incident cardiovascular disease events after dialysis therapy initiation associated with each race-specific SNP.
Results: 2 European tag SNPs (rs3212780 and rs3213409) in JAK3 were associated with new cardiovascular disease events in white patients with unadjusted HRs of 1.92 (P < 0.001) and 1.82 (P = 0.07), respectively. One dual-tag SNP (rs3212752) in JAK3 was associated with new cardiovascular events in white patients with an unadjusted HR of 2.09 (P < 0.001) and in black patients with an HR of 2.07 (P = 0.007). SNP rs3213409 codes for a valine to isoleucine change at amino acid 722, a potentially functional mutation. SNPs in STAT4 and STAT6 were not associated with cardiovascular events after the initiation of dialysis therapy.
Limitations: This study does not provide direct evidence for the mechanism of increased risk. Replication in independent cohorts is necessary.
Conclusions: Genetic polymorphisms in the Jak-Stat signaling pathway are associated with an increased risk of new cardiovascular events in incident dialysis patients. Am J Kidney Dis 53:845-855. (C) 2009 by the National Kidney Foundation, Inc.
C1 [Sperati, C. John; Parekh, Rulan S.; Jaar, Bernard G.] Johns Hopkins Univ, Sch Med, Div Nephrol, Dept Med, Baltimore, MD 21205 USA.
[Parekh, Rulan S.; Berthier-Schaad, Yvette; Jaar, Bernard G.; Fink, Nancy; Powe, Neil R.; Coresh, Josef; Kao, W. H. Linda] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Parekh, Rulan S.; Jaar, Bernard G.; Plantinga, Laura; Powe, Neil R.; Coresh, Josef; Kao, W. H. Linda] Johns Hopkins Bloomberg Sch Publ Hlth, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
[Berthier-Schaad, Yvette; Smith, Michael W.] NCI, Lab Genom Div, Frederick, MD 21701 USA.
[Fink, Nancy; Powe, Neil R.; Coresh, Josef] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
RP Sperati, CJ (reprint author), Johns Hopkins Univ, Sch Med, Div Nephrol, Dept Med, 1830 Monument St,Rm 416, Baltimore, MD 21205 USA.
EM jsperati@jhmi.edu
RI Jaar, Bernard/B-5026-2011; Smith, Michael/B-5341-2012
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[T32-DK-007732]; NIDDK [K24-DK-00264, RO1-DK-59616]; National Heart,
Lung, and Blood Institute [RO1-HL62985]
FX Dr Sperati was supported by National Institute of Diabetes and Digestive
and Kidney Diseases (NIDDK) training grant T32-DK-007732, and Dr Powe
was supported by NIDDK grant K24-DK-00264. CHOICE was supported by
National Heart, Lung, and Blood Institute grant RO1-HL62985 and NIDDK
grant RO1-DK-59616.
NR 55
TC 12
Z9 12
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD MAY
PY 2009
VL 53
IS 5
BP 845
EP 855
DI 10.1053/j.ajkd.2008.12.025
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA 443PY
UT WOS:000265923500017
PM 19282076
ER
PT J
AU Solomon, BD
Lacbawan, F
Jain, M
Domene, S
Roessler, E
Moore, C
Dobyns, WB
Muenke, M
AF Solomon, Benjamin D.
Lacbawan, Felicitas
Jain, Mahim
Domene, Sabina
Roessler, Erich
Moore, Cynthia
Dobyns, William B.
Muenke, Maximilian
TI A Novel SIX3 Mutation Segregates With Holoprosencephaly in a Large
Family
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE holoprosencephaly; HPE; SIX3
ID FOREBRAIN DEVELOPMENT; VENTRAL FOREBRAIN; LINKAGE ANALYSIS; EYE
DEVELOPMENT; NEURAL PLATE; GENE; EXPRESSION; IDENTIFICATION;
SPECIFICATION; POPULATION
AB Holoprosencephaly is the most common structural malformation of the forebrain in humans and has a complex etiology including chromosomal aberrations, single gene mutations and environmental components. Here we present the pertinent clinical findings among members of an unusually large kindred ascertained over 1-5 years ago following the evaluation and subsequent genetic work-up of it female infant with congenital anomalies. A genome-wide scan and linkage analysis showed only suggestive evidence of linkage to markers on chromosome 2 among the most likely of several pedigree interpretations. We now, report that a novel missense mutation in the SIX3 holoprosencephaly gene is the likely cause in this family. Molecular genetic analysis and/or clinical characterization now show that at least 15 members of this family are presumed SIX3 mutation gene carriers, with clinical manifestations ranging from phenotypically nomial adults (non-penetrance) to alobar holoprosencephaly incompatible with postnatal life. This particular family represents it seminal example of the variable manifestations of gene mutations in holoprosencephaly and difficulties encountered in their elucidation. Published 2009 Wiley-Liss, Inc.
C1 [Solomon, Benjamin D.; Lacbawan, Felicitas; Jain, Mahim; Domene, Sabina; Roessler, Erich; Muenke, Maximilian] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Lacbawan, Felicitas] SUNY Hlth Sci Ctr, Dept Pathol, Brooklyn, NY 11203 USA.
[Moore, Cynthia] Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Dobyns, William B.] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA.
[Dobyns, William B.] Univ Chicago, Dept Neurol, Chicago, IL 60637 USA.
[Dobyns, William B.] Univ Chicago, Dept Pediat, Chicago, IL 60637 USA.
RP Muenke, M (reprint author), NHGRI, Med Genet Branch, NIH, Bldg 35,Room 1B-203, Bethesda, MD 20892 USA.
EM mamuenke@mail.nih.gov
OI Dobyns, William/0000-0002-7681-2844
FU Division of Intramural Research, National Human Genome Research
Institute, National Institutes of Health
FX The authors would like to thank Julia Fekecs for her help with
illustrations and would like to extend deep gratitude to the family
described here. This work was supported by the Division of Intramural
Research, National Human Genome Research Institute, National Institutes
of Health.
NR 41
TC 17
Z9 17
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD MAY
PY 2009
VL 149A
IS 5
BP 919
EP 925
DI 10.1002/ajmg.a.32813
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 441YG
UT WOS:000265805900015
PM 19353631
ER
PT J
AU Merideth, MA
Vincent, LM
Sparks, SE
Hess, RA
Manoli, I
O'Brien, KJ
Tsilou, E
White, JG
Huizing, M
Gahl, WA
AF Merideth, Melissa A.
Vincent, Lisa M.
Sparks, Susan E.
Hess, Richard A.
Manoli, Irini
O'Brien, Kevin J.
Tsilou, Ekaterina
White, James G.
Huizing, Marjan
Gahl, William A.
TI Hermansky-Pudlak Syndrome in Two African-American Brothers
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE albinism; Hermansky-Pudlak syndrome; platelet dense bodies; pulmonary
fibrosis; splice-site mutation; silent mutation
ID SUB-SAHARAN AFRICA; P-GENE-MUTATIONS; OCULOCUTANEOUS ALBINISM; LOCUS
HETEROGENEITY; DENSE BODIES; SEROTONIN; PLATELETS; DELETION; DISEASE;
PROTEIN
AB Hermansky-Pudlak syndrome (HPS) is an autosomal recessive disorder characterized by oculocutaneous albinism, a bleeding disorder, and, in some patients, granulomatous colitis and/or a fatal pulmonary fibrosis. There are eight different subtypes of HPS, each due to mutations in one of eight different genes,whose functions are thought to involve intracellular vesicle formation and trafficking. HPS has been identified in patients of nearly all ethnic groups, though it has primarily been associated with patients Of Puerto Rican, Northern European, Japanese and Israeli descent. We report oil the diagnosis of HPS type I in two African-American patients. Both brothers carried compound heterozygous Mutations in HPS1: previously reported p.M32.5WfsX6 (c.972deIC) and a novel silent mutation p.E169E (c.507G > A), which resulted in a splice defect. HPS may be under-diagnosed in African-American patients and other ethnic groups. A history of easy bruising or evidence of a bleeding disorder, combined with some degree of hypopigmentation, should prompt investigation into the diagnosis of HPS. Published 2009 Wiley-Liss, Inc.
C1 [Merideth, Melissa A.; Vincent, Lisa M.; Hess, Richard A.; Manoli, Irini; O'Brien, Kevin J.; Huizing, Marjan; Gahl, William A.] NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Merideth, Melissa A.; O'Brien, Kevin J.; Gahl, William A.] NIH, Intramural Off Rare Dis, Off Director, Bethesda, MD 20892 USA.
[Sparks, Susan E.] Childrens Natl Med Ctr, Div Genet & Metab, Washington, DC 20010 USA.
[Tsilou, Ekaterina] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
[White, James G.] Univ Minnesota, Dept Lab Med, Minneapolis, MN 55455 USA.
RP Merideth, MA (reprint author), NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, 10 Ctr Dr,MSC 1851,Bldg 10,Rm 10C-103, Bethesda, MD 20892 USA.
EM mmeridet@mail.nih.gov
OI Manoli, Irini/0000-0003-1543-2941
FU National Human Genome Research Institute, National Institutes of Health,
Bethesda, MD
FX We thank the patients and their family for participating in the NI H
protocol. We appreciate the nursing care provided by the NTH Clinical
Center nurses. This Study was supported by the Intramural Research
program of the National Human Genome Research Institute, National
Institutes of Health, Bethesda, MD.
NR 31
TC 3
Z9 3
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD MAY
PY 2009
VL 149A
IS 5
BP 987
EP 992
DI 10.1002/ajmg.a.32757
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 441YG
UT WOS:000265805900025
PM 19334085
ER
PT J
AU Taylor, HA
Akylbekova, EL
Garrison, RJ
Sarpong, D
Joe, J
Walker, E
Wyatt, SB
Steffes, MW
AF Taylor, Herman A., Jr.
Akylbekova, Ermeg L.
Garrison, Robert J.
Sarpong, Daniel
Joe, Jennifer
Walker, Evelyn
Wyatt, Sharon B.
Steffes, Michael W.
TI Dyslipidemia and the Treatment of Lipid Disorders in African Americans
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Article
DE African Americans; Cardiovascular disease; Cholesterol; Dyslipidemia;
Risk factors
ID CORONARY-HEART-DISEASE; RISK-FACTORS; ATHEROSCLEROSIS RISK; NHANES-I;
CARDIOVASCULAR HEALTH; MYOCARDIAL-INFARCTION; ETHNIC-DIFFERENCES; WHITE
MEN; CHOLESTEROL; ADULTS
AB BACKGROUND: Despite the high prevalence of cardiovascular disease documented among the African-American population, there has been little emphasis on the role of dyslipidemia as a prominent risk factor in this large subpopulation. Questions of medication efficacy also have been raised. Together, these factors may have affected awareness, diagnosis, and treatment rates.
METHODS AND RESULTS: Dyslipidemia was defined as the presence of either hypercholesterolemia or hypertriglyceridemia using National Cholesterol Education Program III criteria and the fasting lipid measurements, self-reported treatment history, and medication survey available from 5302 Jackson Heart Study participants. Dyslipidemia was more common in men ( compared with women) aged less than 50 years and increased with age in both genders. Hypercholesterolemia prevalence rates approached 50% in women aged more than 65 years. The lifestyle-related attributes found to be related to prevalence were being overweight and less physically active, and all disease status variables exhibited significant (P < .05) associations. Awareness of hypercholesterolemia is approximately 55% or more in both men and women aged more than 35 years. Treatment rates lag far behind awareness, particularly in younger adult men, and less than 50% of women and men aged less than 65 years were treated for hypercholesterolemia.
CONCLUSION: Higher rates of identification and effective treatment of dyslipidemia are clearly needed in this, and probably other African-American communities. Despite the less than optimal treatment, the identification and importance of the known cardiovascular disease states and risk factors in these analyses suggest the adoption of National Cholesterol Education Program III "high-risk strategy" algorithms in treatment recommendations and decisions by providers is occurring. (C) 2009 Elsevier Inc. All rights reserved. The American Journal of Medicine (2009) 122, 454-463
C1 [Taylor, Herman A., Jr.; Garrison, Robert J.; Wyatt, Sharon B.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Taylor, Herman A., Jr.; Akylbekova, Ermeg L.; Sarpong, Daniel] Jackson State Univ, Jackson Heart Study, Jackson, MS USA.
[Taylor, Herman A., Jr.] Tougaloo Coll, Jackson, MS USA.
[Joe, Jennifer] Georgetown Univ Hosp, Div Internal Med, Washington, DC 20007 USA.
[Walker, Evelyn] NHLBI, Jackson Heart Study, Jackson, MS USA.
[Steffes, Michael W.] Univ Minnesota, Minneapolis, MN 55455 USA.
RP Taylor, HA (reprint author), 350 W Woodrow Wilson,Suite 701, Jackson, MS 39213 USA.
FU National Institutes of Health [N01-HC-95170, N01-HC-95171, N01-HC-95172]
FX This research was supported by National Institutes of Health contracts
N01-HC-95170, N01-HC-95171, and N01-HC-95172, provided by the National
Heart, Lung, and Blood Institute and the National Center for Minority
Health and Health Disparities.
NR 44
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9343
J9 AM J MED
JI Am. J. Med.
PD MAY
PY 2009
VL 122
IS 5
BP 454
EP 463
DI 10.1016/j.amjmed.2008.09.049
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 433XB
UT WOS:000265238000013
PM 19375555
ER
PT J
AU Brubaker, L
Chiang, SN
Zyczynski, H
Norton, P
Kalinoski, L
Stoddard, A
Kusek, JW
Steers, W
AF Brubaker, Linda
Chiang, Seine
Zyczynski, Halina
Norton, Peggy
Kalinoski, Lynn
Stoddard, Anne
Kusek, John W.
Steers, William
CA Urinary Incontinence Treatment Net
TI The impact of stress incontinence surgery on female sexual function
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article; Proceedings Paper
CT 29th Annual Meeting of the American-Urogynecologic-Society
CY SEP 04-06, 2008
CL Chicago, IL
SP Amer Urogynecol Soc
DE Burch; Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire;
sexual function; sling; stress incontinence surgery
ID PELVIC ORGAN PROLAPSE; URINARY-INCONTINENCE; WOMEN; QUESTIONNAIRE; LIFE
AB OBJECTIVE: We sought to describe change in sexual function 2 years after surgery to treat stress urinary incontinence.
STUDY DESIGN: This analysis included 655 women randomized to Burch colposuspension or sling surgery. Sexual activity was assessed by the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ-12) among those sexually active at baseline and 2 years after surgery.
RESULTS: Mean PISQ-12 total score improved from baseline 32.23 +/- 6.85 to 36.85 +/- 5.89. After surgery, fewer subjects reported incontinence (9% vs 53%; P < .0001), restriction of sexual activity as a result of fear of incontinence (10% vs 52%; P < .0001), avoidance of intercourse because of vaginal bulging (3% vs 24%; P < .0001), or negative emotional reactions during sex (9% vs 35%; P < .0001). Women with successful surgery had greater improvement PISQ-12 scores (5.77 vs 3.79; P < .006). Sexually active women were younger, thinner, and had lower Medical, Epidemiological, and Social Aspects of Aging scores ( total and urge subscale) than sexually inactive women.
CONCLUSION: Sexual function improves after successful surgery and does not differ between Burch and sling.
C1 [Brubaker, Linda] Loyola Univ Chicago, Dept Obstet & Gynecol, Maywood, IL USA.
[Brubaker, Linda] Loyola Univ Chicago, Dept Urol, Maywood, IL USA.
[Chiang, Seine] Univ Washington, Dept Obstet & Gynecol, Seattle, WA 98195 USA.
[Zyczynski, Halina] Univ Pittsburgh, Div Urogynecol & Pelv Reconstruct Surg, Pittsburgh, PA USA.
[Norton, Peggy] Univ Utah, Dept Urol, Salt Lake City, UT USA.
[Kalinoski, Lynn] Univ Calif San Diego, Div Urol, San Diego, CA 92103 USA.
[Stoddard, Anne] New England Res Inst, Watertown, MA 02172 USA.
[Kusek, John W.] NIDDK, NIH, Bethesda, MD USA.
[Steers, William] Univ Virginia, Dept Urol, Charlottesville, VA USA.
RP Brubaker, L (reprint author), Loyola Univ Chicago, Dept Obstet & Gynecol, Maywood, IL USA.
FU NIDDK NIH HHS [U01 DK058231, U01 DK60401, U01 DK60395, U01 DK60380, U01
DK58229, U01 DK060397, U01 DK060379, U01 DK058234, U01 DK058225, U01
DK58234, U01 DK060379-01, U01 DK060393, U01 DK58225, U01 DK58231, U01
DK60379, U01 DK60397, U01 DK060401, U01 DK058229, U01 DK060380, U01
DK060395, U01 DK60393]
NR 21
TC 4
Z9 5
U1 1
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD MAY
PY 2009
VL 200
IS 5
AR 562.e1
DI 10.1016/j.ajog.2008.11.017
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 434CW
UT WOS:000265253800036
PM 19286143
ER
PT J
AU Levens, ED
Wesley, R
Premkumar, A
Blocker, W
Nieman, LK
AF Levens, Eric D.
Wesley, Robert
Premkumar, Ahalya
Blocker, Wendy
Nieman, Lynnette K.
TI Magnetic resonance imaging and transvaginal ultrasound for determining
fibroid burden: implications for research and clinical care
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE detection; imaging; magnetic resonance imaging; ultrasound; uterine
fibroids
ID HYSTEROSONOGRAPHIC EXAMINATION; UTERINE LEIOMYOMAS; REPRODUCIBILITY;
MYOMAS; HYSTEROSCOPY; SONOGRAPHY; DIAGNOSIS; MRI; US
AB OBJECTIVES: To compare magnetic resonance and ultrasound imaging for uterine fibroid measurement.
STUDY DESIGN: Eighteen women undergoing hysterectomy for symptomatic fibroids underwent preoperative pelvic ultrasound and magnetic resonance imaging. Resected fibroids were correlated with the images. Weighted kappa agreement statistics and Spearman correlations for patient characteristics were calculated.
RESULTS: Magnetic resonance imaging identified 121 of 151 pathologically confirmed fibroids, yielding 91% positive predictive value (95% confidence interval [CI], 85-95) and 80% sensitivity (95% CI, 73-86). Positive predictive value and sensitivity for ultrasound were 97% ( 95% CI, 89-100) and 40% (95% CI, 32-48), respectively. Mean diameter-equivalent discrepancies between imaging and pathologic measurements were 0.51 +/- 0.68 cm for magnetic resonance imaging and 0.76 +/- 0.88 cm for ultrasound. kappa statistics comparing imaging to pathology showed better agreement for magnetic resonance than ultrasound (kappa = 0.60 vs 0.36). The number of fibroids detected by magnetic resonance imaging predicted measurement errors (r = 0.76; P = .0002).
CONCLUSION: Superior sensitivity and minimal measurement discrepancies suggest magnetic resonance imaging may be preferentially used for fibroid assessment in clinical research.
C1 [Levens, Eric D.; Blocker, Wendy; Nieman, Lynnette K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Wesley, Robert] NIH, Dept Biostat Serv, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Premkumar, Ahalya] NIH, Dept Diagnost Radiol, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Nieman, LK (reprint author), NICHD, Program Reprod & Adult Endocrinol, NIH, Bldg 10,CRC,Room E1-3140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM niemanl@mail.nih.gov
FU National Institutes of Health, Bethesda, MD
FX This research was supported, in part, by the Program in Reproductive and
Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child
Health and Human Development, National Institutes of Health, Bethesda,
MD.
NR 13
TC 1
Z9 1
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD MAY
PY 2009
VL 200
IS 5
AR 537.e1
DI 10.1016/j.ajog.2008.12.037
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 434CW
UT WOS:000265253800027
PM 19268886
ER
PT J
AU Scifres, CM
Iams, JD
Klebanoff, M
Macones, GA
AF Scifres, Christina M.
Iams, Jay D.
Klebanoff, Mark
Macones, George A.
TI Metaanalysis vs large clinical trials: which should guide our
management?
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Editorial Material
DE metaanalysis; randomized clinical trial
ID LOW-DOSE ASPIRIN; INDIVIDUAL PATIENT DATA; RANDOMIZED-TRIAL;
PREGNANT-WOMEN; CALCIUM INTAKE; PREVENT PREECLAMPSIA; HYPERTENSION;
QUALITY; RISK; BIAS
AB Large, randomized clinical trials have long been considered the gold standard to guide clinical care. Metaanalysis is a type of analysis in which results of a number of randomized clinical trials are combined and a summary measure of effect for a given treatment is ascertained. The clinician in practice often is faced with a dilemma regarding the type of evidence that should be used to guide clinical practice; for many clinical problems, there are both randomized controlled trials and metaanalyses available. The cases of calcium and aspirin therapy for the prevention of preeclampsia afford an opportunity to explore the benefits and limitations of each type of study to guide clinical practice. We conclude that, when available, large randomized clinical trials should be used to guide clinical practice.
C1 [Scifres, Christina M.; Macones, George A.] Washington Univ, Sch Med, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
[Iams, Jay D.] Ohio State Univ, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
[Klebanoff, Mark] NICHHD, Div Epidemiol Stat & Prevent Res, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Scifres, CM (reprint author), Washington Univ, Sch Med, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
FU Intramural NIH HHS
NR 25
TC 2
Z9 2
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD MAY
PY 2009
VL 200
IS 5
AR 484.e1
DI 10.1016/j.ajog.2008.09.873
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 434CW
UT WOS:000265253800004
PM 19027095
ER
PT J
AU Vink, J
Incerti, M
Toso, L
Roberson, R
Abebe, D
Spong, CY
AF Vink, Joy
Incerti, Maddelena
Toso, Laura
Roberson, Robin
Abebe, Daniel
Spong, Catherine Y.
TI Prenatal NAP plus SAL prevents developmental delay in a mouse model of
Down syndrome through effects on N-methyl-D-aspartic acid and
gamma-aminobutyric acid receptors
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article; Proceedings Paper
CT 29th Annual Meeting of the Society-for-Maternal-Fetal-Medicine
CY JAN 26-31, 2009
CL San Diego, CA
SP Soc Mat Fetal Med
DE Down syndrome; gamma-aminobutyric acid; learning; N-methyl-D-aspartic
acid; NAPVSIPQ; SALLRSIPA; Ts65Dn
ID FETAL ALCOHOL SYNDROME; VASOACTIVE-INTESTINAL-PEPTIDE; TS65DN MICE;
LEARNING-DEFICITS; ABNORMALITIES; PROTEIN; GROWTH; MEMORY; NMDA
AB OBJECTIVE: Down syndrome (DS) affects 1/800 infants. Prenatal NAPVSIPQ (NAP) and SALLRSIPA (SAL) (NAP + SAL) prevent developmental delay in Ts65Dn mice, a mouse model of DS. We investigated whether this finding involves N-methyl-D-aspartic acid and gamma-aminobutyric acid (GABA) receptor subunits.
STUDY DESIGN: Pregnant Ts65Dn mice were treated with placebo or NAP + SAL on gestational days 8-12. After developmental delay prevention was shown, 4 trisomic (Ts), 4 control, and 3 Ts + NAP + SAL adult offspring brains (from 3 litters) were collected. Calibrator-normalized real-time polymerase chain reaction was performed using primers for N-methyl-D-aspartic acid subunits NR2A and NR2B, and for GABA subunits GABA(A)alpha 5 and GABA(A)beta 3 with glyceraldehyde-3-phosphate dehydrogenase stan-dardization. Statistics included analysis of variance and Fisher PLSD with P < .05 as significant.
RESULTS: NR2A, NR2B, and GABA(A)beta 3 levels were decreased in Ts vs control (all P < .05). Prenatal NAP + SAL increased NR2A, NR2B, and GABA(A)beta 3 to levels similar to control (all P < .05). A significant difference in GABA(A)alpha 5 levels was not found.
CONCLUSION: Prenatal NAP + SAL increases NR2A, NR2B, and GABA(A)beta 3 expression in adult DS mice to levels similar to controls. This may explain how NAP + SAL improve developmental milestone achievement.
C1 [Vink, Joy] Georgetown Univ Hosp, Dept Obstet & Gynecol, Washington, DC 20007 USA.
[Vink, Joy; Incerti, Maddelena; Roberson, Robin; Abebe, Daniel; Spong, Catherine Y.] NICHHD, Unit Perinatal & Dev Neurobiol, NIH, Bethesda, MD 20892 USA.
[Toso, Laura] George Washington Univ, Dept Obstet & Gynecol, Washington, DC USA.
RP Vink, J (reprint author), Georgetown Univ Hosp, Dept Obstet & Gynecol, 3800 Reservoir Rd,3 PHC, Washington, DC 20007 USA.
EM joyvink@gmail.com
FU Intramural NIH HHS
NR 26
TC 1
Z9 1
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD MAY
PY 2009
VL 200
IS 5
AR 524.e1
DI 10.1016/j.ajog.2009.01.052
PG 4
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 434CW
UT WOS:000265253800021
PM 19327737
ER
PT J
AU Chan, CC
Sauer, TC
AF Chan, Chi-Chao
Sauer, Theodor C.
TI Ocular Imaging in Primary Retinal Lymphoma
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Editorial Material
ID PRIMARY INTRAOCULAR LYMPHOMA; CENTRAL-NERVOUS-SYSTEM; DIAGNOSIS
C1 [Chan, Chi-Chao; Sauer, Theodor C.] NEI, NIH, Immunopathol Sect, Immunol Lab, Bethesda, MD 20892 USA.
RP Chan, CC (reprint author), NEI, NIH, Immunopathol Sect, Immunol Lab, 10 Ctr Dr,Bldg 10,Rm 10N103, Bethesda, MD 20892 USA.
EM chanc@nei.nih.gov
FU Intramural NIH HHS [Z01 EY000222-22]
NR 14
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD MAY
PY 2009
VL 147
IS 5
BP 764
EP 765
DI 10.1016/j.ajo.2008.12.029
PG 2
WC Ophthalmology
SC Ophthalmology
GA 441IQ
UT WOS:000265762900002
PM 19376328
ER
PT J
AU Liu, Y
Korn, EL
Oh, HS
Pearson, H
Xu, TM
Baumrind, S
AF Liu, Yan
Korn, Edward L.
Oh, Hee Soo
Pearson, Helmer
Xu, Tian-Min
Baumrind, Sheldon
TI Comparison of Chinese and US orthodontists' averaged evaluations of
"facial attractiveness'' from end-of-treatment facial photographs
SO AMERICAN JOURNAL OF ORTHODONTICS AND DENTOFACIAL ORTHOPEDICS
LA English
DT Article
ID DYNAMIC SMILE VISUALIZATION; SOFT-TISSUE PROFILE; PREFERENCES;
QUANTIFICATION; POPULATION; AMERICANS; FACES; AGE
AB Introduction: This study continues our assessment of agreement and disagreement among 25 Chinese and 20 US orthodontists in the ranking for facial attractiveness of end-of-treatment photographs of randomly sampled growing Chinese and white orthodontic patients. The main aims of this article were to (1) measure the overall pattern of agreement between the mean rankings of US and Chinese orthodontists, and (2) measure the strength of agreement between the rankings of the US and Chinese orthodontists for each patient. Methods: Each judge independently ranked standard clinical sets of profile, frontal, and frontal-smiling photographs of 43 US patients and 48 Chinese patients. For each patient, a separate mean rank was computed from the responses of each group of judges. Pearson correlations between the mean ranks of the 2 groups of judges were used to measure their overall agreement. Paired and unpaired t tests were used to measure the agreement between the judges of the 2 groups for each patient. Results: The overall agreement between the mean rankings of the US and Chinese judges was very high. For the US patients, the correlation between the Chinese and US judges means was r = 0.92, P <0.0001. For the Chinese patients, the analogous value was r = 0.86, P <0.0001. Agreement between the 2 groups of judges concerning each patient was also generally strong. For two thirds of the patients, the mean ranks of the US and Chinese judges differed by less than 1 unit in a scale of 12. However, for 6 patients considered individually (5 Chinese and 1 US), the assessment of the 2 groups of judges was statistically significantly different at P values ranging from 0.02 to less than 0.0001, even after the Bonferroni correction. Conclusions: These findings demonstrate that orthodontic clinicians can reliably identify and rank subtle differences between patients, and that differences between judges and between patients can be distinguished at a high level of statistical significance, given appropriate study designs. However, the reasons clinicians give for the differences in their judgments are more difficult to investigate and will require further study. (Am J Orthod Dentofacial Orthop 2009; 135: 621-34)
C1 [Baumrind, Sheldon] Univ Pacific, Sch Dent, Craniofacial Res Instrumentat Lab, San Francisco, CA 94115 USA.
[Oh, Hee Soo; Baumrind, Sheldon] Univ Pacific, Sch Dent, Dept Orthodont, San Francisco, CA 94115 USA.
[Liu, Yan; Xu, Tian-Min] Peking Univ, Dept Orthodont, Sch Stomatol, Beijing 100871, Peoples R China.
[Liu, Yan; Xu, Tian-Min] Peking Univ, Dept Orthodont, Hosp Stomatol, Beijing 100871, Peoples R China.
[Korn, Edward L.] NCI, Biometr Res Branch, NIH, Rockville, MD USA.
[Pearson, Helmer] Univ Med & Dent New Jersey, New Jersey Dent Sch, Dept Orthodont, Newark, NJ 07103 USA.
RP Baumrind, S (reprint author), Univ Pacific, Arthur A Dugoni Sch Dent, Craniofacial Res Instrumentat Lab, Room 617,2115 Webster St, San Francisco, CA 94115 USA.
EM sbaumrind@pacific.edu
FU NIH-NIDR [DE07332, DE08713]; American Association of Orthodontists
Foundation
FX Supported in part by NIH-NIDR grants DE07332 and DE08713, and the
American Association of Orthodontists Foundation.
NR 26
TC 6
Z9 8
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0889-5406
J9 AM J ORTHOD DENTOFAC
JI Am. J. Orthod. Dentofac. Orthop.
PD MAY
PY 2009
VL 135
IS 5
BP 621
EP 634
DI 10.1016/j.ajodo.2007.04.039
PG 14
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 439UH
UT WOS:000265652300024
PM 19409345
ER
PT J
AU Soulas, C
Donahue, RE
Dunbar, CE
Persons, DA
Alvarez, X
Williams, KC
AF Soulas, Caroline
Donahue, Robert E.
Dunbar, Cynthia E.
Persons, Derek A.
Alvarez, Xavier
Williams, Kenneth C.
TI Genetically Modified CD34(+) Hematopoietic Stem Cells Contribute to
Turnover of Brain Perivascular Macrophages in Long-Term Repopulated
Primates
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; SIMIAN IMMUNODEFICIENCY VIRUS; GREEN FLUORESCENT
PROTEIN; MARROW-DERIVED ELEMENTS; LENTIVIRAL VECTOR; MOUSE-BRAIN;
RAT-BRAIN; NONHUMAN-PRIMATES; BLOOD MONOCYTES; IN-SITU
AB Studies in rodents have shown that brain perivascular macrophages are derived from bone marrow precursors. Less is known about the origin and turnover of perivascular cells in the human central nervous system. we took advantage of non-human primates reconstituted with autologous CD34+ hematopoietic stem cells that had been transduced with a lentiviral vector expressing the enhanced green fluorescent protein (EGFP) to study the ontogeny of brain macrophages of rhesus macaques. Flow cytometry and immunohistochemistry/fluorescence microscopy showed long-term reconstitution of monocytes/macrophages in the blood, lymphoid, and brain tissues 4 years post-transplant. In the brain, EGFP+ cells were detected in the choroid plexus, cerebellum, and cerebrum, where the percent engraftment between animals reflected the percentage of EGFP+ monocytes in the blood. Morphology and location of brain EGFP+ cells exclusively in the vicinity of blood vessels were consistent with perivascular macrophages. Up to 85% of brain EGFP+ cells expressed CD163, a marker of perivascular macrophages, and greater than 70% were CD68+ macrophages. These findings clearly demonstrate that a subpopulation of CD163+/CD68+ brain perivascular macrophages in rhesus macaques are renewed by CD34+ hematopoietic stem cell-derived precursors and exhibit a continuous long-lasting turnover. Because perivascular macrophages are significant targets of productive HIV/simian immunodeficiency virus infection in the brain, these observations point to hematopoietic stem cells as targets of both HIV/simian immunodeficiency virus infection and potential gene therapy. (Am J Pathol 2009, 174:1808-1817; DOI: 10.2353/ajpath.2009.081010)
C1 [Soulas, Caroline; Williams, Kenneth C.] Boston Coll, Dept Biol, Chestnut Hill, MA 02467 USA.
[Donahue, Robert E.; Dunbar, Cynthia E.] NHLBI, Hematol Branch, Rockville, MD USA.
[Persons, Derek A.] St Jude Childrens Hosp, Dept Hematol, Memphis, TN 38105 USA.
[Alvarez, Xavier] Tulane Univ, Hlth Sci Ctr, Tulane Natl Primate Res Ctr, Div Comparat Pathol, Covington, LA USA.
RP Williams, KC (reprint author), Boston Coll, Dept Biol, Higgins Hall 445B,140 Commonwealth Ave, Chestnut Hill, MA 02467 USA.
EM williauy@bc.edu
FU NIH; National Heart Lung and Blood Institute Program Project
[P01HL05374921765]; Public Health Service [RR00164]; National Institute
of Neurologic Disease and Stroke [NS040237, NS037654]
FX Supported in part by the Intramural Research Program of the NIH (R.E.D.
and C.E.D.), by National Heart Lung and Blood Institute Program Project
P01HL05374921765 and American Lebanese Associated Charities (D.A.P.), by
Public Health Service Grants RR00164 (X.A.H.) and by grants from the
NIH, including the National Institute of Neurologic Disease and Stroke
NS040237 and NS037654 (to K.C.W.),
NR 41
TC 30
Z9 30
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD MAY
PY 2009
VL 174
IS 5
BP 1808
EP 1817
DI 10.2353/ajpath.2009.081010
PG 10
WC Pathology
SC Pathology
GA 438JK
UT WOS:000265551500025
PM 19349370
ER
PT J
AU Iliff, JJ
Wang, RK
Zeldin, DC
Alkayed, NJ
AF Iliff, Jeffrey J.
Wang, Ruikang
Zeldin, Darryl C.
Alkayed, Nabil J.
TI Epoxyeicosanoids as mediators of neurogenic vasodilation in cerebral
vessels
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE cerebral blood flow regulation; cytochrome P-450 epoxygenase;
epoxyeicosatrienoic acid; soluble epoxide hydrolase; perivascular nerves
ID SOLUBLE EPOXIDE HYDROLASE; ARACHIDONIC-ACID EPOXYGENASE; ASTROCYTIC
EPOXYEICOSATRIENOIC ACID; CORTICAL FUNCTIONAL HYPEREMIA; NITRIC-OXIDE;
BLOOD-FLOW; PERIVASCULAR NERVES; ENDOTHELIAL-CELLS; RAT; STIMULATION
AB Iliff JJ, Wang R, Zeldin DC, Alkayed NJ. Epoxyeicosanoids as mediators of neurogenic vasodilation in cerebral vessels. Am J Physiol Heart Circ Physiol 296: H1352-H1363, 2009. First published March 20, 2009; doi:10.1152/ajpheart.00950.2008.-Epoxyeicosatrienoic acids (EETs) are potent vasodilators produced from arachidonic acid by cytochrome P-450 (CYP) epoxygenases and metabolized to vicinal diols by soluble epoxide hydrolase (sEH). In the brain, EETs are produced by astrocytes and the vascular endothelium and are involved in the control of cerebral blood flow (CBF). Recent evidence, however, suggests that epoxygenases and sEH are present in perivascular vasodilator nerve fibers innervating the cerebral surface vasculature. In the present study, we tested the hypothesis that EETs are nerve-derived relaxing factors in the cerebral circulation. We first traced these fibers by retrograde labeling in the rat to trigeminal ganglia (TG) and sphenopalatine ganglia (SPG). We then examined the expression of CYP epoxygenases and sEH in these ganglia. RT-PCR and Western blot analysis identified CYP2J3 and CYP2J4 epoxygenase isoforms and sEH in both TG and SPG, and immunofluorescence double labeling identified CYP2J and sEH immunoreactivity in neuronal cell bodies of both ganglia. To evaluate the functional role of EETs in neurogenic vasodilation, we elicited cortical hyperemia by electrically stimulating efferent cerebral perivascular nerve fibers and by chemically stimulating oral trigeminal fibers with capsaicin. Cortical blood flow responses were monitored by laser-Doppler flowmetry. Local administration to the cortical surface of the putative EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (30 mu mol/l) attenuated CBF responses to electrical and chemical stimulation. These results suggest that EETs are produced by perivascular nerves and play a role in neurogenic vasodilation of the cerebral vasculature. The findings have important implications to such clinical conditions as migraine, vasospasm after subarachnoid hemorrhage, and stroke.
C1 [Iliff, Jeffrey J.; Alkayed, Nabil J.] Oregon Hlth & Sci Univ, Dept Anesthesiol & Peri Operat Med, Portland, OR 97239 USA.
[Iliff, Jeffrey J.; Alkayed, Nabil J.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97239 USA.
[Wang, Ruikang] Oregon Hlth & Sci Univ, Dept Biomed Engn, Portland, OR 97239 USA.
[Zeldin, Darryl C.] Natl Inst Environm Hlth Sci, Div Intramural Res, Natl Inst Hlth, Res Triangle Pk, NC USA.
RP Alkayed, NJ (reprint author), Oregon Hlth & Sci Univ, Dept Anesthesiol & Peri Operat Med, 3181 SW Sam Jackson Pk Rd,UHS 2, Portland, OR 97239 USA.
EM alkayedn@ohsu.edu
FU Vertex Pharmaceuticals; National Institutes of Health (NIH)
[F31-NS-060498, RO1-NS-044313, P01-NS-049210, 1-R01-HL-093140-01,
Z01-ES-025034]
FX This work was supported by an Oregon Health and Science University
Graduate Student Fellowship for the Neurobiology of Disease funded by
Vertex Pharmaceuticals; National Institutes of Health (NIH) Grants
F31-NS-060498 (to J. J. Iliff), RO1-NS-044313 and P01-NS-049210 (to N.
J. Alkayed), 1-R01-HL-093140-01 (to R. Wang), and Z01-ES-025034 (to D.
C. Zeldin); and the Intramural Research Program of the NIH (to D. C.
Zeldin).
NR 36
TC 34
Z9 35
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD MAY
PY 2009
VL 296
IS 5
BP H1352
EP H1363
DI 10.1152/ajpheart.00950.2008
PG 12
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 439WU
UT WOS:000265659100023
PM 19304946
ER
PT J
AU Mukhopadhyay, P
Rajesh, M
Batkai, S
Kashiwaya, Y
Hasko, G
Liaudet, L
Szabo, C
Pacher, P
AF Mukhopadhyay, Partha
Rajesh, Mohanraj
Batkai, Sandor
Kashiwaya, Yoshihiro
Hasko, Gyoergy
Liaudet, Lucas
Szabo, Csaba
Pacher, Pal
TI Role of superoxide, nitric oxide, and peroxynitrite in
doxorubicin-induced cell death in vivo and in vitro
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE heart failure; apoptosis; inducible nitric oxide synthase; hemodynamics
ID INDUCED HEART-FAILURE; HEPATIC ISCHEMIA/REPERFUSION INJURY;
LEFT-VENTRICULAR DYSFUNCTION; INDUCED CARDIAC DYSFUNCTION; INDUCED
CARDIOMYOPATHY; INDUCED CARDIOTOXICITY; MATRIX METALLOPROTEINASE-2;
ISCHEMIA-REPERFUSION; NITROSATIVE STRESS; HYDROGEN-PEROXIDE
AB Mukhopadhyay P, Rajesh M, Batkai S, Yoshihiro K, Hasko G, Liaudet L, Szabo C, Pacher P. Role of superoxide, nitric oxide, and peroxynitrite in doxorubicin-induced cell death in vivo and in vitro. Am J Physiol Heart Circ Physiol 296: H1466-H1483, 2009. First published March 13, 2009; doi:10.1152/ajpheart.00795.2008.-Doxorubicin (DOX) is a potent available antitumor agent; however, its clinical use is limited because of its cardiotoxicity. Cell death is a key component in DOX-induced cardiotoxicity, but its mechanisms are elusive. Here, we explore the role of superoxide, nitric oxide (NO), and peroxynitrite in DOX-induced cell death using both in vivo and in vitro models of cardiotoxicity. Western blot analysis, real-time PCR, immunohistochemistry, flow cytometry, fluorescent microscopy, and biochemical assays were used to determine the markers of apoptosis/necrosis and sources of NO and superoxide and their production. Left ventricular function was measured by a pressure-volume system. We demonstrated increases in myocardial apoptosis (caspase-3 cleavage/activity, cytochrome c release, and TUNEL), inducible NO synthase (iNOS) expression, mitochondrial superoxide generation, 3-nitrotyrosine (NT) formation, matrix metalloproteinase (MMP)-2/MMP-9 gene expression, poly(ADP-ribose) polymerase activation [without major changes in NAD(P) H oxidase isoform 1, NAD(P) H oxidase isoform 2, p22(phox), p40(phox), p47(phox), p67(phox), xanthine oxidase, endothelial NOS, and neuronal NOS expression] and decreases in myocardial contractility, catalase, and glutathione peroxidase activities 5 days after DOX treatment to mice. All these effects of DOX were markedly attenuated by peroxynitrite scavengers. Doxorubicin dose dependently increased mitochondrial superoxide and NT generation and apoptosis/necrosis in cardiac-derived H9c2 cells. DOX- or peroxynitrite-induced apoptosis/necrosis positively correlated with intracellular NT formation and could be abolished by peroxynitrite scavengers. DOX-induced cell death and NT formation were also attenuated by selective iNOS inhibitors or in iNOS knockout mice. Various NO donors when coadministered with DOX but not alone dramatically enhanced DOX-induced cell death with concomitant increased NT formation. DOX-induced cell death was also attenuated by cell-permeable SOD but not by cell-permeable catalase, the xanthine oxidase inhibitor allopurinol, or the NADPH oxidase inhibitors apocynine or diphenylene iodonium. Thus, peroxynitrite is a major trigger of DOX-induced cell death both in vivo and in vivo, and the modulation of the pathways leading to its generation or its effective neutralization can be of significant therapeutic benefit.
C1 [Mukhopadhyay, Partha; Rajesh, Mohanraj; Batkai, Sandor; Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Kashiwaya, Yoshihiro] NIAAA, Lab Metab Control, NIH, Bethesda, MD 20892 USA.
[Hasko, Gyoergy] Univ Med & Dent New Jersey, Sch Med, Dept Surg, Newark, NJ 07103 USA.
[Liaudet, Lucas] Univ Lausanne Hosp, Dept Intens Care Med, Lausanne, Switzerland.
[Szabo, Csaba] Univ Texas Med Branch, Dept Anesthesiol, Galveston, TX USA.
RP Pacher, P (reprint author), NIAAA, Sect Oxidat Stress & Tissue Injury, Lab Physiol Studies, NIH, 5625 Fishers Lane,MSC-9413, Bethesda, MD 20892 USA.
EM pacher@mail.nih.gov
RI MUKHOPADHYAY, PARTHA/G-3890-2010; Batkai, Sandor/G-3889-2010; Pacher,
Pal/B-6378-2008; Batkai, Sandor/H-7983-2014; Liaudet, Lucas/E-1322-2017
OI MUKHOPADHYAY, PARTHA/0000-0002-1178-1274; Pacher,
Pal/0000-0001-7036-8108; Liaudet, Lucas/0000-0003-2670-4930
FU National Institute on Alcohol Abuse and Alcoholism/National Institutes
of Health (NIH) [R01-GM-60915]; Swiss National Fund [PP00B-68882/1]
FX This work was supported by the Intramural Research Program of the
National Institute on Alcohol Abuse and Alcoholism/National Institutes
of Health (NIH) (to P. Pacher), NIH Grant R01-GM-60915 (to C. Szabo),
and Swiss National Fund PP00B-68882/1 (to L. Liaudet).
NR 65
TC 144
Z9 151
U1 3
U2 26
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD MAY
PY 2009
VL 296
IS 5
BP H1466
EP H1483
DI 10.1152/ajpheart.00795.2008
PG 18
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 439WU
UT WOS:000265659100036
PM 19286953
ER
PT J
AU Paolocci, N
Wink, DA
AF Paolocci, Nazareno
Wink, David A.
TI The shy Angeli and his elusive creature: the HNO route to vasodilation
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
ID CARDIAC SARCOPLASMIC-RETICULUM; NO-CENTER-DOT; NITRIC-OXIDE; IN-VIVO;
NITROXYL HNO; S-NITROSOTHIOLS; L-CYSTEINE; MUSCLE; CHEMISTRY; SALT
C1 [Paolocci, Nazareno] Johns Hopkins Med Inst, Dept Med, Div Cardiol, Baltimore, MD 21205 USA.
[Paolocci, Nazareno] Univ Perugia, Dept Clin Med, Sect Gen Pathol, I-06100 Perugia, Italy.
[Wink, David A.] NCI, Radiat Biol Branch, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Paolocci, N (reprint author), Johns Hopkins Sch Med, Div Cardiol, Ross 858,720 Rutland Ave, Baltimore, MD 21205 USA.
EM npaoloc1@jhmi.edu
OI Paolocci, Nazareno/0000-0001-7011-997X
FU NHLBI NIH HHS [R01 HL-075265]
NR 44
TC 14
Z9 14
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD MAY
PY 2009
VL 296
IS 5
BP H1217
EP H1220
DI 10.1152/ajpheart.00243.2009
PG 4
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 439WU
UT WOS:000265659100005
PM 19286958
ER
PT J
AU Sanchez-Lemus, E
Benicky, J
Pavel, J
Larrayoz, IM
Zhou, J
Baliova, M
Nishioku, T
Saavedra, JM
AF Sanchez-Lemus, Enrique
Benicky, Julius
Pavel, Jaroslav
Larrayoz, Ignacio M.
Zhou, Jin
Baliova, Martina
Nishioku, Tsuyoshi
Saavedra, Juan M.
TI Angiotensin II AT(1) blockade reduces the lipopolysaccharide-induced
innate immune response in rat spleen
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
PHYSIOLOGY
LA English
DT Article
DE CD14; cyclooxygenase-2; NAPDH oxidase; inducible nitric oxide synthase;
proinflammatory cytokines
ID NF-KAPPA-B; NITRIC-OXIDE SYNTHASE; SPONTANEOUSLY HYPERTENSIVE-RATS;
TYPE-1 RECEPTOR ANTAGONIST; CYCLOOXYGENASE-2 EXPRESSION; ENDOTHELIAL
DYSFUNCTION; VASCULAR INFLAMMATION; BRAIN MICROVESSELS; PASTE STANDARDS;
INOS EXPRESSION
AB Sanchez-Lemus E, Benicky J, Pavel J, Larrayoz IM, Zhou J, Baliova M, Nishioku T, Saavedra JM. Angiotensin II AT1 blockade reduces the lipopolysaccharide- induced innate immune response in rat spleen. Am J Physiol Regul Integr Comp Physiol 296: R1376-R1384, 2009. First published February 18, 2009; doi: 10.1152/ajpregu.90962.2008.- ANG II AT1 receptor blockade reduces inflammation in hypertension. To determine whether ANG II AT1 receptor blockers (ARBs) influence the innate immune inflammatory response in normotensive rats, we studied rat plasma and spleen after a 3-day subcutaneous pretreatment with the ARB candesartan followed by a single dose of the bacterial endotoxin LPS ( 50 mu g/kg ip). Peripheral administration of LPS to rodents produced a generalized inflammatory response with increased release of TNF-alpha, IL-1 beta, and IL-6 into the circulation. Candesartan pretreatment reduced the LPS-induced release of TNF-alpha, IL-1 beta, and IL-6 into the circulation. The red pulp of rat spleen expressed large numbers of AT1 receptors and the LPS receptors Toll-like receptor 4 and CD14. Candesartan administration significantly blocked AT1 receptors. The ARB reduced the LPS-induced upregulation of CD14 gene expression; expression of TNF-alpha and IL-6 mRNA and protein; expression of IL-1 beta and I kappa B-alpha mRNA; COX-2 mRNA and protein expression and PGE2 concentration; inducible nitric oxide synthase (iNOS) gene and protein expression and iNOS activity; and Nox2 gene expression and 8-isoprostane levels. In addition, candesartan reduced the CD14 protein expression in saline- and LPS-treated rats. Our results suggest that AT1 receptors are essential for the development of the full innate immune response to bacterial endotoxin. The ARB decreased the general peripheral inflammatory reaction to LPS and partially decreased the inflammatory response in the spleen. An unrestricted innate immune response to the bacterial endotoxin may have deleterious effects for the organism and may lead to development of chronic inflammatory disease. We postulate that ARBs may have therapeutic effects on inflammatory conditions.
C1 [Sanchez-Lemus, Enrique; Benicky, Julius; Pavel, Jaroslav; Larrayoz, Ignacio M.; Zhou, Jin; Baliova, Martina; Nishioku, Tsuyoshi; Saavedra, Juan M.] NIMH, Pharmacol Sect, NIH, DHHS, Bethesda, MD 20892 USA.
RP Sanchez-Lemus, E (reprint author), NIMH, Pharmacol Sect, NIH, DHHS, 10 Ctr Dr,Bldg 10,Rm 2D-57, Bethesda, MD 20892 USA.
EM sancheze@mail.nih.gov
RI Larrayoz, Ignacio/I-5613-2012
OI Larrayoz, Ignacio/0000-0003-1629-152X
FU Division of Intramural Research Programs; National Institute of Mental
Health
FX This study was supported by the Division of Intramural Research
Programs, National Institute of Mental Health.
NR 63
TC 26
Z9 26
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6119
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD MAY
PY 2009
VL 296
IS 5
BP R1376
EP R1384
DI 10.1152/ajpregu.90962.2008
PG 9
WC Physiology
SC Physiology
GA 448EW
UT WOS:000266246900011
PM 19225144
ER
PT J
AU Elkareh, J
Periyasamy, SM
Shidyak, A
Vetteth, S
Schroeder, J
Raju, V
Hariri, IM
El-Okdi, N
Gupta, S
Fedorova, L
Liu, J
Fedorova, OV
Kahaleh, MB
Xie, ZJ
Malhotra, D
Watson, DK
Bagrov, AY
Shapiro, JI
AF Elkareh, Jihad
Periyasamy, Sankaridrug M.
Shidyak, Amjad
Vetteth, Sandeep
Schroeder, Jeremy
Raju, Vanamala
Hariri, Imad M.
El-Okdi, Nasser
Gupta, Shalini
Fedorova, Larisa
Liu, Jiang
Fedorova, Olga V.
Kahaleh, M. Bashar
Xie, Zijian
Malhotra, Deepak
Watson, Dennis K.
Bagrov, Alexei Y.
Shapiro, Joseph I.
TI Marinobufagenin induces increases in procollagen expression in a process
involving protein kinase C and Fli-1: implications for uremic
cardiomyopathy
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article; Proceedings Paper
CT 40th Annual Meeting of the American-Society-of-Nephrology/Annual Renal
Week
CY OCT 31-NOV 05, 2007
CL San Francisco, CA
SP Amer Soc Nephrol
DE renal failure; cardiotonic steroids; fibrosis
ID ETS ONCOGENE FAMILY; TRANSCRIPTION FACTOR; DERMAL FIBROBLASTS;
GENE-EXPRESSION; COLLAGEN; RAT; ASSOCIATION; ACTIVATION; DISEASE
AB Elkareh J, Periyasamy SM, Shidyak A, Vetteth S, Schroeder J, Raju V, Hariri IM, El-Okdi N, Gupta S, Fedorova L, Liu J, Fedorova OV, Kahaleh MB, Xie Z, Malhotra D, Watson DK, Bagrov AY, Shapiro JI. Marinobufagenin induces increases in procollagen expression in a process involving protein kinase C and Fli-1: implications for uremic cardiomyopathy. Am J Physiol Renal Physiol 296: F1219-F1226, 2009. First published March 4, 2009; doi:10.1152/ajprenal.90710.2008.-The cardiotonic steroid marinobufagenin (MBG) has been implicated in the pathogenesis of experimental uremic cardiomyopathy, which is characterized by progressive cardiac fibrosis. We examined whether the transcription factor Friend leukemia integration-1 (Fli-1) might be involved in this process. Fli-1-knockdown mice demonstrated greater cardiac collagen-1 expression and fibrosis compared with wild-type mice; both developed increased cardiac collagen expression and fibrosis after 5/6 nephrectomy. There was a strong inverse relationship between the expressions of Fli-1 and procollagen in primary culture of rat cardiac and human dermal fibroblasts as well as a cell line derived from renal fibroblasts and MBG-induced decreases in nuclear Fli-1 as well as increases in procollagen-1 expression in these cells. Transfection of a Fli-1 expression vector prevented increased procollagen-1 expression from MBG. MBG exposure induced a rapid translocation of the delta-isoform of protein kinase C (PKC delta) to the nucleus. This translocation was prevented by pharmacological inhibition of phospholipase C, and MBG-induced increases in procollagen-1 expression were prevented with a PKC delta-but not a PKC delta-specific inhibitor. Finally, immunoprecipitation studies strongly suggest that MBG induced phosphorylation of Fli-1. We feel these data support a causal relationship with MBG-induced translocation of PKC delta, which results in phosphorylation of as well as decreases in nuclear Fli-1 expression, which, in turn, leads to increases in collagen production. Should these findings be confirmed, we speculate that this pathway may represent a therapeutic target for uremic cardiomyopathy as well as other conditions associated with excessive fibrosis.
C1 [Elkareh, Jihad; Periyasamy, Sankaridrug M.; Shidyak, Amjad; Vetteth, Sandeep; Schroeder, Jeremy; Raju, Vanamala; Hariri, Imad M.; El-Okdi, Nasser; Gupta, Shalini; Fedorova, Larisa; Liu, Jiang; Kahaleh, M. Bashar; Xie, Zijian; Malhotra, Deepak; Shapiro, Joseph I.] Univ Toledo, Coll Med, Dept Med, Toledo, OH 43614 USA.
[Elkareh, Jihad; Periyasamy, Sankaridrug M.; Shidyak, Amjad; Vetteth, Sandeep; Schroeder, Jeremy; Raju, Vanamala; Hariri, Imad M.; El-Okdi, Nasser; Gupta, Shalini; Fedorova, Larisa; Liu, Jiang; Kahaleh, M. Bashar; Xie, Zijian; Malhotra, Deepak; Shapiro, Joseph I.] Univ Toledo, Coll Med, Dept Pharmacol, Toledo, OH 43614 USA.
[Watson, Dennis K.] Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA.
[Watson, Dennis K.] Med Univ S Carolina, Hollings Canc Ctr, Charleston, SC 29425 USA.
[Fedorova, Olga V.; Bagrov, Alexei Y.] NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA.
RP Shapiro, JI (reprint author), Univ Toledo, Coll Med, Dept Med, Mail Stop 1186 Hlth Sci Campus,3000 Arlington Ave, Toledo, OH 43614 USA.
EM joseph.shapiro@utoledo.edu
FU Intramural NIH HHS [Z01 AG000609-17]; NCI NIH HHS [P01-CA-78582]; NHLBI
NIH HHS [R01-HL-67963]
NR 22
TC 34
Z9 34
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD MAY
PY 2009
VL 296
IS 5
BP F1219
EP F1226
DI 10.1152/ajprenal.90710.2008
PG 8
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 438AZ
UT WOS:000265529600032
PM 19261738
ER
PT J
AU Neubauer, B
Machura, K
Chen, M
Weinstein, LS
Oppermann, M
Sequeira-Lopez, ML
Gomez, RA
Schnermann, J
Castrop, H
Kurtz, A
Wagner, C
AF Neubauer, Bjoern
Machura, Katharina
Chen, Min
Weinstein, Lee S.
Oppermann, Mona
Sequeira-Lopez, Maria Luisa
Gomez, R. Ariel
Schnermann, Juergen
Castrop, Hayo
Kurtz, Armin
Wagner, Charlotte
TI Development of vascular renin expression in the kidney critically
depends on the cyclic AMP pathway
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE fetal kidney; transgenic mice
ID CONTAINING CELLS; GENE-EXPRESSION; JUXTAGLOMERULAR APPARATUS; RESPONSIVE
ELEMENT; FETAL DEVELOPMENT; STIMULATED RENIN; MESSENGER-RNA; RAT
KIDNEYS; INHIBITION; MOUSE
AB Neubauer B, Machura K, Chen M, Weinstein LS, Oppermann M, Sequeira-Lopez ML, Gomez RA, Schnermann J, Castrop H, Kurtz A, Wagner C. Development of vascular renin expression in the kidney critically depends on the cyclic AMP pathway. Am J Physiol Renal Physiol 296: F1006-F1012, 2009. First published March 4, 2009; doi:10.1152/ajprenal.90448.2008.-During metanephric kidney development, renin expression in the renal vasculature begins in larger vessels, shifting to smaller vessels and finally remaining restricted to the terminal portions of afferent arterioles at the entrance into the glomerular capillary network. The mechanisms determining the successive expression of renin along the vascular axis of the kidney are not well understood. Since the cAMP signaling cascade plays a central role in the regulation of both renin secretion and synthesis in the adult kidney, it seemed feasible that this pathway might also be critical for renin expression during kidney development. In the present study we determined the spatiotemporal development of renin expression and the development of the preglomerular arterial tree in mouse kidneys with renin cell-specific deletion of G(s alpha), a core element for receptor activation of adenylyl cyclases. We found that in the absence of the G(s alpha) protein, renin expression was largely absent in the kidneys at any developmental stage, accompanied by alterations in the development of the preglomerular arterial tree. These data indicate that the maintenance of renin expression following a specific spatiotemporal pattern along the preglomerular vasculature critically depends on the availability of G(s alpha). We infer from our data that the cAMP signaling pathway is not only critical for the regulation of renin synthesis and secretion in the mature kidney but that it also is critical for establishing the juxtaglomerular expression site of renin during development.
C1 [Wagner, Charlotte] Univ Regensburg, Inst Physiol, Dept Physiol, D-93040 Regensburg, Germany.
[Chen, Min; Weinstein, Lee S.; Schnermann, Juergen] NIH, Bethesda, MD 20892 USA.
[Oppermann, Mona] Univ Regensburg, Fac Med, Dept Pediat, D-93040 Regensburg, Germany.
[Sequeira-Lopez, Maria Luisa; Gomez, R. Ariel] Univ Virginia, Charlottesville, VA USA.
RP Wagner, C (reprint author), Univ Regensburg, Inst Physiol, Dept Physiol, D-93040 Regensburg, Germany.
EM charlotte.schmid@vkl.uni-regensburg.de
OI Weinstein, Lee/0000-0002-1899-5152
FU Deutsche Forschungsgemeinschaft [SFB 699]
FX The study was financially supported by Deutsche Forschungsgemeinschaft
Grant SFB 699.
NR 45
TC 26
Z9 26
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD MAY
PY 2009
VL 296
IS 5
BP F1006
EP F1012
DI 10.1152/ajprenal.90448.2008
PG 7
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 438AZ
UT WOS:000265529600008
PM 19261741
ER
PT J
AU Bowen, DJ
Kreuter, M
Spring, B
Cofta-Woerpel, L
Linnan, L
Weiner, D
Bakken, S
Kaplan, CP
Squiers, L
Fabrizio, C
Fernandez, M
AF Bowen, Deborah J.
Kreuter, Matthew
Spring, Bonnie
Cofta-Woerpel, Ludmila
Linnan, Laura
Weiner, Diane
Bakken, Suzanne
Kaplan, Cecilia Patrick
Squiers, Linda
Fabrizio, Cecilia
Fernandez, Maria
TI How We Design Feasibility Studies
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID CANCER; ISSUES
AB Public health is moving toward the goal of implementing evidence-based interventions. To accomplish this, there is a need to select, adapt, and evaluate intervention studies. Such selection relies, in part, on making judgments about the feasibility of possible interventions and determining whether comprehensive and multilevel evaluations are justified. There exist few published standards and guides to aid these judgments. This article describes the diverse types of feasibility studies conducted in the field of cancer prevention, using a group of recently funded grants from the National Cancer Institute. The grants were submitted in response to a request for applications proposing research to identify feasible interventions for increasing the utilization of the Cancer Information Service among underserved populations. (Am J Prev Med 2009;36(5):452-457) (c) 2009 Published by Elsevier Inc. oil behalf of American Journal of Preventive Medicine.
C1 [Bowen, Deborah J.] Boston Univ, Dept Social & Behav Sci, Sch Publ Hlth, Boston, MA 02118 USA.
[Kreuter, Matthew] St Louis Univ, Hlth Commun Res Lab, Sch Publ Hlth, St Louis, MO 63103 USA.
[Spring, Bonnie] Northwestern Univ, Dept Behav Med, Chicago, IL 60611 USA.
[Fernandez, Maria] Univ Texas Houston, Hlth Sci Ctr, Ctr Hlth Promot & Prevent Res, Houston, TX 77030 USA.
[Cofta-Woerpel, Ludmila] Univ Texas Houston, MD Anderson Canc Ctr, NCI, Canc Informat Serv, Houston, TX 77030 USA.
[Cofta-Woerpel, Ludmila] Univ Texas Houston, MD Anderson Canc Ctr, Dept Behav Sci, Houston, TX 77030 USA.
[Linnan, Laura] Univ N Carolina, Sch Publ Hlth, Dept Hlth Behav & Hlth Educ, Chapel Hill, NC USA.
[Weiner, Diane] Mashantucket Pcquot Tribal Nation, Mashantucket, CT USA.
[Fabrizio, Cecilia] Yale Canc Ctr, NCI, Canc Informat Serv, New Haven, CT USA.
[Bakken, Suzanne] Columbia Univ, Sch Nursing, New York, NY USA.
[Kaplan, Cecilia Patrick] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Squiers, Linda] NCI, Canc Informat Serv, Bethesda, MD 20892 USA.
RP Bowen, DJ (reprint author), Boston Univ, Dept Social & Behav Sci, Sch Publ Hlth, 801 Massachusetts Ave,3rd Floor, Boston, MA 02118 USA.
EM dbowen@bu.edu
FU National Cancer Institute [1R21CA126325-01, 1R21CA126990-01,
1R21CA126326-01, 1R21CA126373-01, 1R21CA126450-01, 1R21CA126321-01]
FX The projects described were supported by the following six grants from
the National Cancer Institute: 1R21CA126325-01, 1R21CA126990-01,
1R21CA126326-01, 1R21CA126373-01, 1R21CA126450-01, and 1R21CA126321-01.
The contents of this manuscript are solely the responsibility of the
authors and do not necessarily represent the official views of the
National Cancer Institute.
NR 13
TC 200
Z9 202
U1 7
U2 27
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD MAY
PY 2009
VL 36
IS 5
BP 452
EP 457
DI 10.1016/j.amepre.2009.02.002
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 435AI
UT WOS:000265315200013
PM 19362699
ER
PT J
AU Zheng, L
Mack, WJ
Dagerman, KS
Hsiao, JK
Lebowitz, BD
Lyketsos, CG
Stroup, TS
Sultzer, DL
Tariot, PN
Vigen, C
Schneider, LS
AF Zheng, Ling
Mack, Wendy J.
Dagerman, Karen S.
Hsiao, John K.
Lebowitz, Barry D.
Lyketsos, Constantine G.
Stroup, T. Scott
Sultzer, David L.
Tariot, Pierre N.
Vigen, Cheryl
Schneider, Lon S.
TI Metabolic Changes Associated With Second-Generation Antipsychotic Use in
Alzheimer's Disease Patients: The CATIE-AD Study
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article; Proceedings Paper
CT International Conference on Alzheimers Disease
CY JUL 26-31, 2008
CL Chicago, IL
ID PLACEBO-CONTROLLED TRIALS; DOUBLE-BLIND; BEHAVIORAL DISTURBANCES;
CARDIOVASCULAR-DISEASE; CLINICAL-TRIAL; DEMENTIA; PSYCHOSIS;
RISPERIDONE; OLANZAPINE; SCHIZOPHRENIA
AB Objective: The second-generation antipsychotics are associated with metabolic abnormalities in patients with schizophrenia. Elderly patients with Alzheimer's disease are frequently treated with these antipsychotics, but limited data are available on their metabolic effects.
Method: The authors assessed 186 male and 235 female Alzheimer's disease outpatients from the Clinical Antipsychotic Trials of Intervention Effectiveness-Alzheimer's Disease (CATIE-AD) for changes in weight, waist circumference, blood pressure, fasting glucose, and lipids in relation to duration of second-generation antipsychotic use (i.e., olanzapine, quetiapine, and risperidone) throughout the 36-week trial, using logistic regression and mixed-effects models.
Results: Women showed significant weight gain (0.14 lb/week of use) while change was nonsignificant in men. Clinically significant weight gain (i.e., >= 7% of body weight) was seen among patients with antipsychotic use <= 12 weeks (odds ratio [OR]=1.56, 95% CI=0.53 to 4.58), between 12 and 24 weeks (OR=2.89, 95% CI=0.97 to 8.64), and >24 weeks (OR= 3.38, 95% CI=1.24 to 9.23) relative to patients who did not use antipsychotics during the trial. Olanzapine and quetiapine treatments were significantly associated with weight gain (0.12 and 0.14 lb/week, respectively). In addition, olanzapine was significantly associated with decreases in HDL cholesterol (-0.19 mg/dl/week) and increased girth (0.07 inches/week) relative to the placebo group. No treatment effects were noted for changes in blood pressure, glucose, and triglycerides.
Conclusion: Second-generation antipsychotic use was associated with weight gain in women, with olanzapine and quetiapine in particular, and with unfavorable change in HDL cholesterol and girth with olanzapine. The potential consequences of these effects suggest that patients with Alzheimer's disease treated with second-generation antipsychotics should be monitored closely.
C1 Univ So Calif, Keck Sch Med, Dept Psychiat & Behav Sci, Los Angeles, CA 90033 USA.
Univ So Calif, Keck Sch Med, Dept Neurol, Los Angeles, CA 90033 USA.
Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
Univ Calif San Diego, Sch Med, Div Geriatr Psychiat, La Jolla, CA 92093 USA.
NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
Johns Hopkins Bayview Med Ctr, Dept Psychiat, Baltimore, MD USA.
Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
VA Greater Angeles Healthcare Syst, Gero Neuropsychiat Div, Los Angeles, CA USA.
Banner Alzheimers Inst, Phoenix, AZ USA.
RP Schneider, LS (reprint author), 1510 San Pablo St, Los Angeles, CA 90033 USA.
EM lschneid@usc.edu
RI Stroup, Thomas/F-9188-2014
OI Stroup, Thomas/0000-0002-3123-0672
FU NIMH NIH HHS [N01 MH-9001, N01 MH90001]
NR 29
TC 36
Z9 38
U1 1
U2 7
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD MAY
PY 2009
VL 166
IS 5
BP 583
EP 590
DI 10.1176/appi.ajp.2008.08081218
PG 8
WC Psychiatry
SC Psychiatry
GA 439YA
UT WOS:000265662500013
PM 19369318
ER
PT J
AU Nowicki, S
Izban, MG
Pawelczyk, E
Agboto, VK
Pratap, S
Olson, G
Nowicki, B
AF Nowicki, Stella
Izban, Michael G.
Pawelczyk, Edyta
Agboto, Vincent K.
Pratap, Siddarth
Olson, Gayle
Nowicki, Bogdan
TI Preterm Labor: CD55 in Maternal Blood Leukocytes
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE Infection; maternal circulatory immune response; preterm birth; preterm
labor
ID DECAY-ACCELERATING FACTOR; COMPLEMENT REGULATORY PROTEIN; FETAL MEMBRANE
DISTENSION; ESCHERICHIA-COLI; FETOMATERNAL INTERFACE; HUMAN TROPHOBLAST;
NITRIC-OXIDE; IN-VITRO; EXPRESSION; INFECTION
AB Intrauterine inflammation is a frequent and significant factor associated with the pathogenesis of preterm labor/birth (PTL/PTB). However, it remains unclear whether the intrauterine inflammatory responses activate the maternal peripheral circulation. We explored the association between PTL/PTB and the 'activation' of the peripheral circulatory system by determining whether CD55 mRNA expression within peripheral WBCs differed between PTL and control patients not in labor.
RNA was purified from white blood cells collected from pregnant women with preterm labor (n = 45), and from pregnant (n = 30) control women. CD55 gene expression was evaluated by quantitative PCR.
The mean CD55 mRNA level within the PTL group (0.77 +/- 0.03) was 1.48-fold higher than that observed (0.52 +/- 0.02) within the control group (P < 0.0001); 71% of PTL patients and only 6.7% of control subjects expressed elevated CD55 mRNA. The receiver operating characteristics (with 95% CI) of CD55 as a marker for PTL were as follows: Sensitivity, 69% (53-82%); Specificity, 93% (78-99%); Positive Predictive Value, 94% (80-99%); and Negative Predictive Value, 67% (51-80%). In the patient population that delivered prematurely (before 37 weeks), 81% expressed elevated CD55 mRNA levels with a mean of 0.78 +/- 0.03 and 95% CI of 0.71-0.84. The receiver operating characteristics were as follows: Sensitivity, 73% (54-88%); Specificity, 86% (71-95%); Positive Predictive Value, 81.5% (62-94%); and Negative Predictive Value, 80% (64-91%).
Here we report for the first time that CD55 mRNA expression was elevated in the peripheral WBCs of subjects with preterm labor compared with control gestationally-matched pregnant woman and that elevated leukocyte CD55 may be a useful predictor of subsequent PTB.
C1 [Nowicki, Stella; Izban, Michael G.; Nowicki, Bogdan] Meharry Med Coll, Dept Microbial Pathogenesis, Nashville, TN 37208 USA.
[Nowicki, Stella; Izban, Michael G.; Nowicki, Bogdan] Meharry Med Coll, Dept Immune Response, Nashville, TN 37208 USA.
[Nowicki, Stella; Izban, Michael G.; Nowicki, Bogdan] Meharry Med Coll, Dept Obstr & Gynocol, Nashville, TN 37208 USA.
[Agboto, Vincent K.] Meharry Med Coll, Clin Res Ctr, Nashville, TN 37208 USA.
[Pawelczyk, Edyta] NIH, Ctr Clin, Expt Neuroimaging Sect, Bethesda, MD 20892 USA.
[Pratap, Siddarth] Meharry Med Coll, Dept Microbial Pathogenesis & Immune Response, Nashville, TN 37208 USA.
[Olson, Gayle] Univ Texas Med Branch, Dept Obster & Gynecol, Galveston, TX USA.
RP Nowicki, S (reprint author), Meharry Med Coll, Dept Obstet & Gynecol, 1005 Dr DB Todd Jr Blvd, Nashville, TN 37208 USA.
EM snowicki@mmc.edu
OI Pratap, Siddharth/0000-0003-2200-0848
FU National Institute of Child Health and Human Development [HD41687];
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[DK42029]; National Institutes of Health [P20RR011792]; RCMI
[U54HD044315]
FX This work was supported by Public Health Service grant HD41687 from the
National Institute of Child Health and Human Development to S. Nowicki
and B.J. Nowicki, and in part by grant DK42029 from the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) to B.J.
Nowicki. This research was supported in part by the Clinical Research
Center of Meharry Medical College, grant #P20RR011792 from the National
Institutes of Health and RCMI Clinical Research Infrastructure
Initiative and U54HD044315 to B.J. Nowicki. We express our gratitude to
Dr G. Anderson and Dr G. Hankins for assisting us with sample
acquisition.
NR 42
TC 8
Z9 9
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1046-7408
EI 1600-0897
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD MAY
PY 2009
VL 61
IS 5
BP 360
EP 367
DI 10.1111/j.1600-0897.2009.00702.x
PG 8
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 428BP
UT WOS:000264823300006
PM 19341386
ER
PT J
AU Tomita, T
Yamada, A
Miyakoshi, M
Kido, T
Sheikh, F
Srisodsai, A
Miyajima, A
Donnelly, RP
Kimura, S
AF Tomita, Takeshi
Yamada, Atsushi
Miyakoshi, Masaaki
Kido, Taketomo
Sheikh, Faruk
Srisodsai, Achara
Miyajima, Atsushi
Donnelly, Raymond P.
Kimura, Shioko
TI Oncostatin M Regulates Secretoglobin 3A1 and 3A2 Expression in a
Bidirectional Manner
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE oncostatin M; gene regulation; secretoglobin 3A1; secretoglobin 3A2;
lung
ID UTEROGLOBIN-RELATED PROTEIN-1; ALLERGIC AIRWAY INFLAMMATION; MUCIN
GENE-EXPRESSION; IN-VITRO; EPITHELIAL-CELLS; MOUSE; HIN-1; MICE;
FIBROBLASTS; LUNG
AB Secretoglobin (SCGB) 3A1 and 3A2 are members of the small molecular weight secretoglobin gene superfamily. SCGB3A1 is a tumor suppressor gene, whereas SCGB3A2 has anti-inflammatory properties. Both genes are mainly expressed in the lung and trachea in mice. Whether the expression and/or function of these two genes are related is not known. Here we show that the expression of SCGB3A1 and SCGB3A2 are bidirectionally regulated by oncostatin M (OSM) when examined in a mouse transformed Clara cell line (mtCC); SCGB3A1 is up-regulated by OSM, while SCGB3A2 is downregulated in a time- and dose-dependent manner. OSM-activated STAT3/5, through binding to the STAT-binding element located at -201 to -209 by in the mouse Scgb3a1 gene promoter, and the extracellular signal-regulated kinase (ERK)- and p38-mitogen-activated protein kinase (MAPK) pathways are responsible for the OSM-induced up-regulation of SCGB3A1 expression. On the other hand, the -113 to -273 by region in the Scgb3a2 promoter appears to be responsible for the OSM induced down-regulation of the gene. No significant differences in the levels or patterns of specific DNA-binding proteins were found in the -113 to -273 by region as determined by electrophoretic mobility shift assays. Neither the ERK- nor p38-MAPK pathways were involved in the OSM-induced reduction of Scgb3a2 promoter activity. These results suggest that OSM-induced suppression of SCGB3A2 expression is an indirect effect of OSM. Expression of the Clara cell marker, CYP2F2, was markedly decreased upon OSM treatment in parallel with the decrease of SCGB3A2 expression in mtCC cells. The differential regulation of Scgb3a1 and Scgb3a2 gene expression by OSM may explain the unique functions of these genes in the lung.
C1 [Tomita, Takeshi; Yamada, Atsushi; Miyakoshi, Masaaki; Kido, Taketomo; Srisodsai, Achara; Kimura, Shioko] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
[Sheikh, Faruk; Donnelly, Raymond P.] US FDA, Div Therapeut Prot, Ctr Drug Evaluat & Res, Bethesda, MD USA.
[Srisodsai, Achara] Khon Kaen Univ, Fac Pharmaceut Sci, Khon Kaen, Thailand.
[Miyajima, Atsushi] Univ Tokyo, Inst Mol & Cellular Biosci, Tokyo, Japan.
RP Kimura, S (reprint author), NCI, Lab Metab, NIH, Bldg 37,Rm 3118, Bethesda, MD 20892 USA.
EM kimuras@mail.nih.gov
FU National Cancer Institute
FX This research was supported by the Intramural Research Program of the
National Cancer Institute, Center for Cancer Research.
NR 47
TC 2
Z9 2
U1 0
U2 2
PU AMER THORACIC SOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA
SN 1044-1549
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD MAY
PY 2009
VL 40
IS 5
BP 620
EP 630
DI 10.1165/rcmb.2008-0062OC
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA 439IH
UT WOS:000265620300012
PM 18978304
ER
PT J
AU El-Khouli, R
Macura, K
Barker, P
Jacobs, M
Kamel, I
Bluemke, D
AF El-Khouli, R.
Macura, K.
Barker, P.
Jacobs, M.
Kamel, I
Bluemke, D.
TI Dynamic MRI of the Breast: Quantitative Method for Kinetic Curve Shape
Assessment
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Meeting Abstract
CT 109th Annual Meeting of the American-Roentgen-Ray-Society
CY APR 27-MAY 01, 2009
CL Boston, MA
SP Amer Roentgen Ray Soc
C1 [El-Khouli, R.; Bluemke, D.] NIH, Silver Spring, MD USA.
[Macura, K.; Barker, P.; Jacobs, M.; Kamel, I] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
EM elkhoulir@cc.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD MAY
PY 2009
VL 192
IS 5
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 436BI
UT WOS:000265387200132
ER
PT J
AU El-Khouli, R
Jacobs, M
Macura, K
Barker, P
Bluemke, D
AF El-Khouli, R.
Jacobs, M.
Macura, K.
Barker, P.
Bluemke, D.
TI Diffusion-Weighted Imaging and Apparent Diffusion Coefficients Mapping
for Characterization of Focal Breast Lesions at 3T
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Meeting Abstract
CT 109th Annual Meeting of the American-Roentgen-Ray-Society
CY APR 27-MAY 01, 2009
CL Boston, MA
SP Amer Roentgen Ray Soc
C1 [El-Khouli, R.; Bluemke, D.] NIH, Bethesda, MD 20892 USA.
[Jacobs, M.; Macura, K.; Barker, P.; Bluemke, D.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
EM elkhoulir@cc.nih.gov
RI Jacobs, Michael/G-2901-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD MAY
PY 2009
VL 192
IS 5
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 436BI
UT WOS:000265387200129
ER
PT J
AU Fayad, L
Salibi, N
Jacobs, M
Ouwerker, R
Okollie, B
Eng, J
Weber, K
Barker, P
Bluemke, D
AF Fayad, L.
Salibi, N.
Jacobs, M.
Ouwerker, R.
Okollie, B.
Eng, J.
Weber, K.
Barker, P.
Bluemke, D.
TI Quantitative Molecular Characterization of Musculoskeletal Lesions by
Proton MR Spectroscopy
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Meeting Abstract
CT 109th Annual Meeting of the American-Roentgen-Ray-Society
CY APR 27-MAY 01, 2009
CL Boston, MA
SP Amer Roentgen Ray Soc
C1 [Fayad, L.; Jacobs, M.; Ouwerker, R.; Okollie, B.; Eng, J.; Weber, K.; Barker, P.; Bluemke, D.] Johns Hopkins Univ, Baltimore, MD USA.
[Bluemke, D.] NIH, Bethesda, MD 20892 USA.
EM lfayad1@jhmi.edu
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD MAY
PY 2009
VL 192
IS 5
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 436BI
UT WOS:000265387200199
ER
PT J
AU Rasiej, M
Uldrick, T
Joffe, R
Austin, J
Taub, R
Ichise, M
AF Rasiej, M.
Uldrick, T.
Joffe, R.
Austin, J.
Taub, R.
Ichise, M.
TI Malignant Peritoneal Mesothelioma: Characterization by CT, PET and
PET-CT
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Meeting Abstract
CT 109th Annual Meeting of the American-Roentgen-Ray-Society
CY APR 27-MAY 01, 2009
CL Boston, MA
SP Amer Roentgen Ray Soc
C1 [Rasiej, M.; Joffe, R.; Austin, J.; Taub, R.; Ichise, M.] Columbia Univ, NewYork Presbyterian Hosp, New York, NY USA.
[Uldrick, T.] NCI, Bethesda, MD 20892 USA.
EM rasiej@gmail.com
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD MAY
PY 2009
VL 192
IS 5
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 436BI
UT WOS:000265387200726
ER
PT J
AU Yao, L
Gai, N
AF Yao, L.
Gai, N.
TI Phase Sensitive Fat-Water Separation for Musculoskeletal Imaging: Core
Concepts and Methodologies
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Meeting Abstract
CT 109th Annual Meeting of the American-Roentgen-Ray-Society
CY APR 27-MAY 01, 2009
CL Boston, MA
SP Amer Roentgen Ray Soc
C1 [Yao, L.; Gai, N.] NIH, Bethesda, MD 20892 USA.
EM lyao@cc.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD MAY
PY 2009
VL 192
IS 5
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 436BI
UT WOS:000265387200633
ER
PT J
AU Moore, CC
Jacob, ST
Pinkerton, R
Banura, P
Meya, DB
Reynolds, SJ
Kenya-Mugisha, N
Mayanja-Kizza, H
Scheld, WM
AF Moore, Christopher C.
Jacob, Shevin T.
Pinkerton, Relana
Banura, Patrick
Meya, David B.
Reynolds, Steven J.
Kenya-Mugisha, Nathan
Mayanja-Kizza, Harriet
Scheld, W. Michael
CA PRISM U Study Grp
TI Treatment of Severe Sepsis with Artemether-Lumefantrine Is Associated
with Decreased Mortality in Ugandan Patients without Malaria
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID PLASMODIUM-FALCIPARUM MALARIA; SULFADOXINE-PYRIMETHAMINE;
RANDOMIZED-TRIAL; SEPTIC SHOCK; CHILDREN; BACTEREMIA; MICROSCOPY;
THERAPIES; AFRICA; ADULTS
AB We enrolled 382 patients at two hospitals in Uganda ill a prospective observational Study of severe sepsis. Because artemisinins improve Survival in murine sepsis models, we performed a post hoc analysis of the association between the use of artemether-lumefantrine (A-L) and mortality in patients with or without malaria. In patients with negative malaria smears (N = 328 of 379), Kaplan-Meier Curves revealed decreased combined inpatient and 30-day mortality among patients receiving A-L versus those who did not (20.6%, SE = 10.6 versus 48.8%, SE = 3.2; Log rank chi(2) = 3.93, P = 0.048). The decrease in mortality associated with A-L was maintained in the most clinically ill patients determined by Karnofsky Performance Scores <= 50 (16.7%, SE = 15.2 versus 58.3%, SE = 3.7; Log rank chi(2) 3.94, P = 0.041). Research into the properties of A-L is needed to improve treatment of sepsis without compromising malarial susceptibility.
C1 [Moore, Christopher C.; Pinkerton, Relana; Scheld, W. Michael] Univ Virginia, Dept Med, Div Infect Dis & Int Hlth, Charlottesville, VA 22908 USA.
[Jacob, Shevin T.] Univ Washington, Div Allergy & Infect Dis, Seattle, WA 98195 USA.
[Banura, Patrick] Masaka Reg Referral Hosp, Dept Internal Med, Masaka, Uganda.
[Meya, David B.; Mayanja-Kizza, Harriet] Makerere Univ, Fac Med, Infect Dis Inst, Kampala, Uganda.
[Reynolds, Steven J.] NIAID, NIH, Washington, DC 20521 USA.
[Kenya-Mugisha, Nathan] Minist Hlth, Kampala, Uganda.
NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RP Moore, CC (reprint author), Univ Virginia, Dept Med, Div Infect Dis & Int Hlth, 409 Land Rd,MR-4 Bldg,Room 2112, Charlottesville, VA 22908 USA.
EM ccm5u@virginia.edu; sjacob@post.harvard.edu; rcp3w@virginia.edu;
banura2003@yahoo.com; david.meya@gmail.com; sjr@jhmi.edu;
nkmugisha@yahoo.com; hmk@mucwru.or.ug; wms@virginia.edu
FU Pfizer Initiative in International Health at the University of Virginia;
University Of Virginia; Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health
FX Christopher C. Moore and Shevin T.Jacob received fellowships from the
Pfizer Initiative in International Health at the University of Virginia
to support this work. This Initiative was conceived 10 fund exchange
programs of post-doctoral fellows and students between the University Of
Virginia and several international partners to conduct research oil
global health issues. The major purpose of this program is to foster and
enhance bidirectional research training. An independent board at the
University of Virginia determines which research proposals are funded.
Pfizer provided funds to promote the Initiative, but has no role in the
planning or execution of research protocols including the study
described in our Manuscript. This work was also supported in part by the
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health.
NR 27
TC 9
Z9 9
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD MAY
PY 2009
VL 80
IS 5
BP 723
EP 728
PG 6
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 443GS
UT WOS:000265898800008
PM 19407113
ER
PT J
AU Juliano, JJ
Bacon, DJ
Mu, JB
Wang, XH
Meshnick, SR
AF Juliano, Jonathan J.
Bacon, David J.
Mu, Jianbing
Wang, Xinhua
Meshnick, Steven R.
TI Novel dhps and pfcrt Polymorphisms in Plasmodium falciparum Detected by
Heteroduplex Tracking Assay
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID INFECTIONS; RESISTANCE; MALARIA
AB Several single nucleotide polymorphisms (SNPs) have been linked to antimalarial drug resistance in Plasmodium falciparum. However, standard polymerase chain reaction (PCR) methods to detect these polymorphisms are unable to detect SNPs in variants representing <20% of the parasites in a mixed infection, nor can they detect polymorphisms at nearby loci. Here we use heteroduplex tracking assays (HTAs) to analyze dhps540 mutations in 96 samples from Peru and pfcrt76 mutations in 70 samples from China. All samples had been previously analyzed by standard PCR. We detected drug-resistant minority variants and two novel non-synonymous pfcrt mutations in China. In Peru, we found no drug-resistant minority variants and a synonymous mutation in dhps. Thus, even in regions of low malaria transmission, HTA assays are more informative than PCR with agarose gel electrophoresis.
C1 [Juliano, Jonathan J.] Univ N Carolina, Sch Med, Div Infect Dis, Chapel Hill, NC 27599 USA.
[Bacon, David J.] UN Environm & Preventat Med Unit 2, Norfolk, VA 23511 USA.
[Mu, Jianbing] NIH, Lab Malaria & Vector Res, Bethesda, MD 20892 USA.
[Wang, Xinhua] Guangzhou Univ Tradit Chinese Med, Guangzhou 510006, Guangdong, Peoples R China.
[Meshnick, Steven R.] Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
US Naval Med Res Ctr Detachment, Lima, Peru.
NIH, Lab Malaria & Vector Res, Rockville, MD USA.
Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA.
RP Juliano, JJ (reprint author), Univ N Carolina, Sch Med, Div Infect Dis, CB 7300, Chapel Hill, NC 27599 USA.
EM jjuliano@med.unc.edu; david.bacon@med.navy.mil; jmu@niaid.nih.gov;
xinhuaw@gzhtcm.edu.cn; meshnick@email.unc.edu
FU NIH [1R21AI07-6785]; National Center for Research Resources
[KL2RR025746]; Department of Defense-Global Emerging Infectious System
(DoD-GEIS) [847705.82000.25GB.B0016]
FX This project was funded in part by NIH 1R21AI07-6785 and the 2007 IDSA
ERF/NFID Merle A. Sande/Pfizer Fellowship in International Infectious
Diseases, KL2RR025746 from the National Center for Research Resources,
and funds provided by the Department of Defense-Global Emerging
Infectious System (DoD-GEIS) under Unit 847705.82000.25GB.B0016. These
agencies had no involvement in the design, collection, analysis, or
interpretation of data in this study or in writing this paper or
submitting it for publication.
NR 8
TC 2
Z9 3
U1 0
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD MAY
PY 2009
VL 80
IS 5
BP 734
EP 736
PG 3
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 443GS
UT WOS:000265898800010
PM 19407115
ER
PT J
AU Sapsford, KE
Francis, J
Sun, S
Kostov, Y
Rasooly, A
AF Sapsford, Kim E.
Francis, Jesse
Sun, Steven
Kostov, Yordan
Rasooly, Avraham
TI Miniaturized 96-well ELISA chips for staphylococcal enterotoxin B
detection using portable colorimetric detector
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Electroluminescent (EL) illumination; CCD; Miniature ELISA;
Staphylococcal enterotoxin B (SEB); Food; Colorimetric measurement;
Biosensor
ID ATOPIC-DERMATITIS; RHEUMATOID-ARTHRITIS; FOOD; IMMUNOASSAY; SEB;
SUPERANTIGENS; CHROMATOGRAPHY; CONFIRMATION; PREVALENCE; ANTIBODIES
AB A previously developed fluorescence sensing platform, combining spatial illumination using electroluminescence (EL) semiconductor strips with charge coupled device (CCD)-based detection (EL-CCD), was adapted to a new 96-well chip for colorimetric immunological assays, enhancing the capabilities of the EL-CCD platform. The modified system was demonstrated using a colorimetric-based enzyme linked immunosorbent assay (ELISA) for detection of staphylococcal enterotoxin B (SEB). Limits of detection (LODs) of 3.9 ng/mL (+/- 2.4 ng/mL) SEB were determined with the ELISA chip measured using the EL-CCD platform, following a standard 4-h ELISA protocol. The LODs were comparable to those obtained using standard 96-well ELISA plates measured using a standard laboratory 96-well plate reader. The miniature 96-well ELISA chip however required as little as 5-mu L samples, representing a tenfold reduction in sample volume compared to a standard 96-well ELISA plates. The ELISA chip also demonstrated detection of SEB spiked into various food matrices (milk, mushrooms, and mayonnaise) using limited-to-no sample preparation, with LODs ranging from 3.9 to 18.5 ng/mL depending on the matrix. The EL-CCD platform is versatile, capable of multi-mode detection (e. g., fluorescent and colorimetric along with solution and solid phase assays), and could readily be applied to other field portable or point-of-care applications.
C1 [Rasooly, Avraham] NCI, NIH, Bethesda, MD 20892 USA.
[Sapsford, Kim E.; Francis, Jesse; Sun, Steven; Rasooly, Avraham] US FDA, Div Biol, CDRH, Off Sci & Engn Labs, Silver Spring, MD 20903 USA.
[Francis, Jesse; Sun, Steven; Kostov, Yordan] Univ Maryland Baltimore Cty, Ctr Adv Sensor Technol, Baltimore, MD 21227 USA.
RP Rasooly, A (reprint author), NCI, NIH, 6130 Executive Blvd EPN,Room 6035A, Bethesda, MD 20892 USA.
EM rasoolya@mail.nih.gov
FU Office of Public Health emergency Preparedness (OPHEP) [IAG224-05-655,
HHSF223200610765P]; CDRH/OSEL/Division of Biology funds
FX This work was supported in part by the Office of Public Health emergency
Preparedness (OPHEP) IAG224-05-655 (to A. Rasooly and by FDA contract)
and HHSF223200610765P (to Dr. Yordan Kostov) and CDRH/OSEL/Division of
Biology funds. The mention of commercial products, their sources, or
their use in connection with material reported herein is not to be
construed as either an actual or implied endorsement of such products by
the Department of Health and Human Services
NR 35
TC 26
Z9 27
U1 0
U2 17
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD MAY
PY 2009
VL 394
IS 2
BP 499
EP 505
DI 10.1007/s00216-009-2730-z
PG 7
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 436BU
UT WOS:000265388400013
PM 19290511
ER
PT J
AU Concheiro-Guisan, M
Shakleya, DM
Huestis, MA
AF Concheiro-Guisan, Marta
Shakleya, Diaa M.
Huestis, Marilyn A.
TI Simultaneous quantification of buprenorphine, norbuprenorphine,
buprenorphine glucuronide, and norbuprenorphine glucuronide in human
placenta by liquid chromatography mass spectrometry
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Placenta; Buprenorphine; LCMS; Ion trap
ID N-DEALKYLATED METABOLITE; HUMAN-PLASMA; GAS-CHROMATOGRAPHY; HUMAN-URINE;
ENZYME-IMMUNOASSAY; PREGNANT-WOMEN; HAIR SAMPLES; VALIDATION; ASSAY;
METHADONE
AB A LCMS method was developed and validated for the determination of buprenorphine (BUP), norbuprenorphine (NBUP), buprenorphine glucuronide (BUP-Gluc), and norbuprenorphine glucuronide (NBUP-Gluc) in placenta. Quantification was achieved by selected ion monitoring of m/z 468.4 (BUP), 414.3 (NBUP), 644.4 (BUP-Gluc), and 590 (NBUP-Gluc). BUP and NBUP were identified monitoring MS(2) fragments m/z 396, 414 and 426 for BUP, and 340, 364 and 382 for NBUP, and glucuronide conjugates monitoring MS(3) fragments m/z 396 and 414 for BUP-Gluc, and 340 and 382 for NBUP-Gluc. Linearity was 1-50 ng/g. Intra-day, inter-day and total assay imprecision (% RSD) were <13.4%, and analytical recoveries were 96.2-113.1%. Extraction efficiencies ranged from 40.7-68%, process efficiencies 38.8-70.5%, and matrix effect 1.3-15.4%. Limits of detection were 0.8 ng/g for all compounds. An authentic placenta from an opioid-dependent pregnant woman receiving BUP pharmacotherapy was analyzed. BUP was not detected but metabolite concentrations were NBUP-Gluc 46.6, NBUP 15.7 and BUP-Gluc 3.2 ng/g.
C1 [Concheiro-Guisan, Marta; Shakleya, Diaa M.; Huestis, Marilyn A.] Natl Inst Drug Abuse, Intramural Res Program, Natl Inst Hlth, BRC, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), Natl Inst Drug Abuse, Intramural Res Program, Natl Inst Hlth, BRC, 251 Bayview Blvd,Suite 200,Room 05A721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU National Institutes of Health; Intramural Research Program; National
Institute on Drug Abuse; Ministerio de Educacion y Ciencia of Spain
[EX-2007-1194]
FX This research was supported by the National Institutes of Health,
Intramural Research Program, National Institute on Drug Abuse, and
funding for Marta Concheiro, Ph. D. from the Ministerio de Educacion y
Ciencia of Spain (Grant number EX-2007-1194). The authors would like to
thank Drs. Fred Askin, Gerrun March, and Leigh Ruane from Johns Hopkins
Bayview Medical Center (Baltimore, MD) for their help in providing
placenta samples.
NR 47
TC 13
Z9 13
U1 2
U2 7
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD MAY
PY 2009
VL 394
IS 2
BP 513
EP 522
DI 10.1007/s00216-009-2706-z
PG 10
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 436BU
UT WOS:000265388400015
PM 19247639
ER
PT J
AU Zhu, AP
Romero, R
Petty, HR
AF Zhu, Aiping
Romero, Roberto
Petty, Howard R.
TI An enzymatic fluorimetric assay for glucose-6-phosphate: Application in
an in vitro Warburg-like effect
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE Leukocyte; Metabolism; Glucose-6-phosphate; Sugar phosphate;
L-Phenylalanine
ID 2-DEOXYGLUCOSE 6-PHOSPHATE; ELECTROSPRAY-IONIZATION; ESCHERICHIA-COLI;
CHROMATOGRAPHY; AMPLIFICATION; METABOLITES; VALIDATION; CELLS
AB Recently, there has been a resurgence of interest in the regulatory role of cell metabolism in tumor biology and immunology. To assess changes in metabolite levels in cell Populations and tissues, especially from small clinical samples, highly sensitive assays are required. Based on the reaction of glucose-6-phosphate (G6P) and the diaphorase-resazurin amplifying system, we have developed a fluorescence methodology to measure G6P concentrations in cell extracts. In this approach, G6P is oxidized by G6P dehydrogenase in the presence of NADP(+), and the stoichiometrically generated NADPH is then amplified by the diaphorase cycling system to produce a highly fluorescent molecule-resorufin. The limit of detection (LOD) of the assay is 10 pmol. The assay has a Z' factor of 0.81. Its usefulness is demonstrated by experiments in which the pyruvate kinase inhibitor, phenylalanine, is added to cells. After 2 h of incubation at 37 degrees C, G6P levels rose by 20%, thereby illustrating an in vitro Warburg-like effect on cell metabolism. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Zhu, Aiping; Petty, Howard R.] Univ Michigan, Sch Med, Dept Ophthalmol & Visual Sci, Ann Arbor, MI 48105 USA.
[Romero, Roberto] NICHHD, Perinatol Res Branch, Bethesda, MD 20892 USA.
[Romero, Roberto] Hutzel Hosp, Detroit, MI 48201 USA.
[Petty, Howard R.] Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48105 USA.
RP Petty, HR (reprint author), Univ Michigan, Sch Med, Dept Ophthalmol & Visual Sci, 1000 Wall St, Ann Arbor, MI 48105 USA.
EM hpetty@umich.edu
FU National Institute of Child Health and Human Development; National
Institutes of Health, U.S. Department of Health and Human Services
FX This work was supported, in part, by the Intramural Program of the
National Institute of Child Health and Human Development, National
Institutes of Health, U.S. Department of Health and Human Services.
NR 20
TC 28
Z9 28
U1 2
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD MAY 1
PY 2009
VL 388
IS 1
BP 97
EP 101
DI 10.1016/j.ab.2009.02.009
PG 5
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 433TR
UT WOS:000265229200013
PM 19454216
ER
PT J
AU Tan, HY
AF Tan, Hao Yang
TI Cognitive Dysfunction in Schizophrenia: A Perspective from the Clinic to
Genetic Brain Mechanisms
SO ANNALS ACADEMY OF MEDICINE SINGAPORE
LA English
DT Review
DE Cognitive neuroscience; COMT; GRM3; Magnetic resonance imaging
ID CATECHOL-O-METHYLTRANSFERASE; CORTICAL PYRAMIDAL NEURONS;
WORKING-MEMORY; METABOTROPIC GLUTAMATE-RECEPTOR-3; PREFRONTAL CORTEX;
FUNCTIONAL POLYMORPHISM; NEUROPSYCHOLOGICAL DYSFUNCTION; INTERMEDIATE
PHENOTYPES; ANTIPSYCHOTIC-DRUGS; DOPAMINE MODULATION
AB Schizophrenia is a brain disease with differing symptomatic presentations, outcomes, and complex genetic mechanisms. A selection of recent work integrating clinical observations, human brain imaging and genetics will be reviewed. While the mechanics of brain dysfunction in schizophrenia remains to be well understood, the emerging evidence suggests that a number of interacting genetic mechanisms in dopaminergic and glutamatergic systems affect fundamental disease-related cognitive brain processes and may do so early in disease neurodevelopment. The availability of new imaging and genetic technologies, and institutional support for research in the translational neurosciences, extends the hope that increased understanding of these brain processes could yield meaningful clinical applications.
C1 NIMH, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
RP Tan, HY (reprint author), NIMH, Genes Cognit & Psychosis Program, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM tanh@mail.nih.gov
NR 72
TC 3
Z9 3
U1 2
U2 4
PU ACAD MEDICINE SINGAPORE
PI REPUBLIC SINGAPORE
PA 142 NEIL RD, REPUBLIC SINGAPORE 088871, SINGAPORE
SN 0304-4602
J9 ANN ACAD MED SINGAP
JI Ann. Acad. Med. Singap.
PD MAY
PY 2009
VL 38
IS 5
BP 420
EP 424
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 460PH
UT WOS:000267199100008
PM 19521642
ER
PT J
AU Taber, DR
Stevens, J
Murray, DM
Elder, JP
Webber, LS
Jobe, JB
Lytle, LA
AF Taber, Daniel R.
Stevens, June
Murray, David M.
Elder, John P.
Webber, Larry S.
Jobe, Jared B.
Lytle, Lelie A.
TI The Effect of a Physical Activity Intervention on Bias in Self-Reported
Activity
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Bias (epidemiology); Intervention Studies; Adolescent; Exercise;
Questionnaires; Social Desirability
ID ADOLESCENT GIRLS TAAG; SOCIAL DESIRABILITY; OBESITY PREVENTION;
CHILDREN; ACCELEROMETER; VALIDATION; TRIAL; QUESTIONNAIRES; CALIBRATION;
INTENSITIES
AB PURPOSE: A positive outcome in self-reported behavior could be detected erroneously if an intervention caused over-reporting of the targeted behavior. Data collected from a multi-site randomized trial were examined to determine if adolescent girls who received a physical activity intervention over-reported their activity more than girls who received no intervention.
METHODS: Activity was measured using accelerometers and self-reports (3-Day Physical Activity Recall, 3DPAR) in cross-sectional samples preintervention (6th grade, n = 1,464) and post-intervention (8th grade, n = 3,114). Log-transformed accelerometer minutes were regressed on 3DPAR blocks, treatment group, and their interaction, while adjusting for race, body mass index, and timing of data collection.
RESULTS: Preintervention, the association between measures did not differ between groups, but postintervention 3DPAR blocks were associated with fewer log-accelerometer minutes of moderate-vigorous physical activity (MVPA) in intervention girls than in control girls (p = 0.002). The group difference was primarily in the upper 15% of the 3DPAR distribution, where control girls had > 1.7 more accelerometer minutes of MVPA than intervention girls who reported identical activity levels. Group differences in this subsample were 8.5%-16.2% of the mean activity levels; the intervention was powered to detect a difference of 10%.
CONCLUSION: Self-report measures should be interpreted with caution when used to evaluate a physical activity intervention. Ann Epidemiol 2009;19:316-322. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Taber, Daniel R.; Stevens, June] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Stevens, June] Univ N Carolina, Dept Nutr, Chapel Hill, NC 27599 USA.
[Murray, David M.] Ohio State Univ, Coll Publ Hlth, Div Epidemiol, Columbus, OH 43210 USA.
[Elder, John P.] San Diego State Univ, Div Hlth Promot & Behav Sci, San Diego, CA 92182 USA.
[Webber, Larry S.] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Biostat, New Orleans, LA USA.
[Jobe, Jared B.] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Lytle, Lelie A.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
RP Taber, DR (reprint author), Univ N Carolina, Dept Epidemiol, CB 7435, Chapel Hill, NC 27599 USA.
EM dtaber@email.unc.edu
RI Schmoelz, Camilie/D-1707-2012
OI Schmoelz, Camilie/0000-0003-2221-9954
FU NHLBI [HL66845, HL66852, HL66853, HL66855, HL66856, HL66857, HL66858]
FX This study was supported by funds from the NHLBI grant numbers HL66845,
HL66852, HL66853, HL66855, HL66856, HL66857, and HL66858.
NR 25
TC 20
Z9 22
U1 0
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1047-2797
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD MAY
PY 2009
VL 19
IS 5
BP 316
EP 322
DI 10.1016/j.annepidem.2009.01.001
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 435IL
UT WOS:000265337500005
PM 19230711
ER
PT J
AU Hou, LF
Shu, XO
Gao, YT
Ji, BT
Weiss, JM
Yang, G
Li, HL
Blair, A
Zheng, W
Chow, WH
AF Hou, Lifang
Shu, Xiao-Ou
Gao, Yu-Tang
Ji, Bu-Tian
Weiss, Jocelyn M.
Yang, Gong
Li, Hong-Lan
Blair, Aaron
Zheng, Wei
Chow, Wong-Ho
TI Anthropometric Measurements, Physical Activity, and the Risk of
Symptomatic Gallstone Disease in Chinese Women
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Body Mass Index; Gallstone Disease Risk; Physical Activity; Waist-to-Hip
Ratio
ID SHANGHAI BREAST-CANCER; GALLBLADDER-DISEASE; COLON-CANCER; FOLLOW-UP;
OBESITY; HEALTH; EPIDEMIOLOGY; POPULATION; EXERCISE; FAT
AB PURPOSE: Gallstone disease is more common among overweight individuals, particularly in women. We conducted a cross-sectional case-control study of Chinese women nested in the Shanghai Women's Health Study (SWHS) to evaluate the association of gallstone disease with body mass index (BMI), waist to hip ratio (WHR), and physical activity (PA).
METHODS: The study included 8,485 women with self-reported, physician-diagnosed, prevalent gallstone disease and 16,970 frequency-matched controls by birth year and age at gallstone diagnosis (4-year intervals). Information on height, weight history, waist and hip circumferences, physical activities, and other exposures was obtained by in-person interview.
RESULTS: : Usual BMI (p trend < 0.001) and WHR (p trend < 0.001) were both related to a high prevalence of gallstone disease, and a significant interaction between BMI and WHR on gallstone risk was found (odds ratio [OR] = 3.82, 95%CI [95% confidence interval] 2.47-5.23 for those with both highest BMI and WHR relative to those with lowest BMI and WHR, p interaction = 0.03). Gallstone risk was positively associated with cumulative occupational sitting time (P trend = 0.01) and inversely associated with occupational cumulative energy expenditure (p trend = 0.03) as well as with household PA (P trend = 0.02).
CONCLUSIONS: Our findings further support that overall and central excessive adiposity is an independent risk factor for gallstones in women. In addition, regardless of adiposity level, being physically active may ameliorate the risk of this disease. Ann Epidemiol 2009; 19:344-350. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Hou, Lifang] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Hou, Lifang; Ji, Bu-Tian; Weiss, Jocelyn M.; Blair, Aaron; Chow, Wong-Ho] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Shu, Xiao-Ou; Zheng, Wei] Vanderbilt Univ, Ctr Hlth Serv Res, Nashville, TN USA.
[Gao, Yu-Tang; Yang, Gong; Li, Hong-Lan] Shanghai Canc Inst, Shanghai, Peoples R China.
RP Hou, LF (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, 680 N Lake Shore Dr,Suite 1102, Chicago, IL 60611 USA.
EM l-hou@northwestem.edu
FU National Institute of Health (NIH) [R01 CA70867]; Intramural Research
Program, Division of Cancer Epidemiology and Genetics
FX This research was supported by National Institute of Health (NIH)
research grant R01 CA70867 and by the Intramural Research Program,
Division of Cancer Epidemiology and Genetics. The authors express their
appreciation to Shanghai residents who participated in the study and
thank the research staff of the Shanghai Women's Health Study for their
dedication and contributions to the study.
NR 47
TC 13
Z9 17
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1047-2797
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD MAY
PY 2009
VL 19
IS 5
BP 344
EP 350
DI 10.1016/j.annepidem.2008.12.002
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 435IL
UT WOS:000265337500009
PM 19362277
ER
PT J
AU Croswell, JM
Kramer, BS
Kreimer, AR
Prorok, PC
Xu, JL
Baker, SG
Fagerstrom, R
Riley, TL
Clapp, JD
Berg, CD
Gohagan, JK
Andriole, GL
Chia, D
Church, TR
Crawford, ED
Fouad, MN
Gelmann, EP
Lamerato, L
Reding, DJ
Schoen, RE
AF Croswell, Jennifer Miller
Kramer, Barnett S.
Kreimer, Aimee R.
Prorok, Phil C.
Xu, Jian-Lun
Baker, Stuart G.
Fagerstrom, Richard
Riley, Thomas L.
Clapp, Jonathan D.
Berg, Christine D.
Gohagan, John K.
Andriole, Gerald L.
Chia, David
Church, Timothy R.
Crawford, E. David
Fouad, Mona N.
Gelmann, Edward P.
Lamerato, Lois
Reding, Douglas J.
Schoen, Robert E.
TI Cumulative Incidence of False-Positive Results in Repeated, Multimodal
Cancer Screening
SO ANNALS OF FAMILY MEDICINE
LA English
DT Article
DE Mass screening; neoplasms; false Positive reactions; randomized
controlled trial
ID BASE-LINE FINDINGS; COLORECTAL-CANCER; FLEXIBLE SIGMOIDOSCOPY;
RANDOMIZED-TRIAL; BREAST-CANCER; COLON-CANCER; PROSTATE; LUNG; RISK;
PROGRAM
AB PURPOSE Multiple cancer screening tests have been advocated for the general population; however, clinicians and patients are not always well-informed of screening burdens. We sought to determine the cumulative risk of a false-positive screening result and the resulting risk of a diagnostic procedure for an individual participating in a multimodal cancer screening program.
METHODS Data were analyzed from the intervention arm of the ongoing Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, a randomized controlled trial to determine the effects of prostate, lung, colorectal, and ovarian cancer screening on disease-specific mortality. The 68,436 participants, aged 55 to 74 years, were randomized to screening or usual care. Women received serial serum tests to detect cancer antigen 125 (CA-125), transvaginal sonograms, posteroanterior-view chest radiographs, and flexible sigmoidoscopies. Men received serial chest radiographs, flexible sigmoidoscopies, digital rectal examinations, and serum prostate-specific antigen tests. Fourteen screening examinations for each sex were possible during the 3-year screening period.
After 14 tests, the cumulative risk of having at least I false-positive screening test is 60.4% (95% Cl, 59.8%-61.0%) for men, and 48.8% (95% CI, 48.1%-49.4%) for women. The cumulative risk after 14 tests of undergoing an invasive diagnostic procedure prompted by a false-positive test is 28.5% (Cl, 27.8%-29.3%) for men and 22.1% (95% Cl, 21.4%-22.7%) for women.
CONCLUSIONS For an individual in a multimodal cancer screening trial, the risk of a false-positive finding is about 50% or greater by the 14th test. Physicians should educate patients about the likelihood of false positives and resulting diagnostic interventions when counseling about cancer screening. Ann Fam Med 2009;7:212-222. DOI: 10.1370/afm.942.
C1 [Croswell, Jennifer Miller; Kramer, Barnett S.] NIH, Off Director, Off Dis Prevent, Bethesda, MD 20892 USA.
[Kreimer, Aimee R.; Xu, Jian-Lun; Baker, Stuart G.; Fagerstrom, Richard; Berg, Christine D.; Gohagan, John K.] NIH, Natl Canc Inst, Canc Prevent Div, Bethesda, MD 20892 USA.
[Riley, Thomas L.; Clapp, Jonathan D.] IMS Inc, Washington, DC USA.
[Andriole, Gerald L.] Washington Univ, Sch Med, St Louis, MO USA.
[Chia, David] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Church, Timothy R.] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Crawford, E. David] Univ Colorado, Hlth Sci Ctr, Aurora, CO USA.
[Fouad, Mona N.] Univ Alabama, Birmingham, AL USA.
[Gelmann, Edward P.] Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY USA.
[Lamerato, Lois] Henry Ford Hlth Syst, Detroit, MI USA.
[Reding, Douglas J.] Marshfield Clin Res Fdn, Marshfield, WI USA.
[Schoen, Robert E.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
RP Croswell, JM (reprint author), NIH, Off Director, Off Dis Prevent, 6100 Execut Blvd,Suite 2B-03, Bethesda, MD 20892 USA.
EM croswelllj@od.nih.gov
RI Kreimer, Aimee/H-1687-2015;
OI Church, Timothy R./0000-0003-3292-5035
FU US National Cancer Institute
FX Funding for the overall Prostate, Lung, Colorectal, and Ovarian (PLOC)
Cancer Screening Trial was provided by the US National Cancer Institute.
No additional funding was provided for the design and conduct Of this
study.
NR 38
TC 58
Z9 59
U1 1
U2 14
PU ANNALS FAMILY MEDICINE
PI LEAWOOD
PA 11400 TOMAHAWK CREEK PARKWAY, LEAWOOD, KS 66211-2672 USA
SN 1544-1709
J9 ANN FAM MED
JI Ann. Fam. Med.
PD MAY-JUN
PY 2009
VL 7
IS 3
BP 212
EP 222
DI 10.1370/afm.942
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 448QI
UT WOS:000266276700005
PM 19433838
ER
PT J
AU Shi, M
Umbach, DM
Weinberg, CR
AF Shi, Min
Umbach, David M.
Weinberg, Clarice R.
TI Using Case-parent Triads to Estimate Relative Risks Associated with a
Candidate Haplotype
SO ANNALS OF HUMAN GENETICS
LA English
DT Article
DE Log-linear model; candidate haplotype; phase ambiguity; expectation
maximization algorithm; Hardy-Weinberg equilibrium; maternal genetic
effects; Yin-Yang haplotypes
ID CASE/PSEUDOCONTROL ANALYSIS; LINKAGE DISEQUILIBRIUM; GENETIC
ASSOCIATION; GENERAL PEDIGREES; NUCLEAR FAMILIES; LIKELIHOOD; DISEASE;
RECONSTRUCTION; FREQUENCY; GENOTYPE
AB Estimating haplotype relative risks in a family-based study is complicated by phase ambiguity and the many parameters needed to quantify relative risks for all possible diplotypes. This problem becomes manageable if a particular haplotype has been implicated previously as relevant to risk. We fit log-linear models to estimate the risks associated with a candidate haplotype relative to the aggregate of other haplotypes. Our approach uses existing haplotype-reconstruction algorithms but requires assumptions about the distribution of haplotypes among triads in the source population. We consider three levels of stringency for those assumptions: Hardy-Weinberg Equilibrium (HWE), random mating, and no assumptions at all. We assessed our method's performance through simulations encompassing a range of risk haplotype frequencies, missing data patterns, and relative risks for either offspring or maternal genetic effects. The unconstrained model provides robustness to bias from population structure but requires excessively large sample sizes unless there are few haplotypes. Assuming HWE accommodates many more haplotypes but sacrifices robustness. The model assuming random mating is intermediate, both in the number of haplotypes it can handle and in robustness. To illustrate, we reanalyze data from a study of orofacial clefts to investigate a 9-SNP candidate haplotype of the IRF6 gene.
C1 [Shi, Min; Umbach, David M.; Weinberg, Clarice R.] NIEHS, Biostat Branch, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Weinberg, CR (reprint author), NIEHS, Biostat Branch, NIH, DHHS, Mail Drop A3-03 101-A315, Res Triangle Pk, NC 27709 USA.
EM weinber2@niehs.nih.gov
FU Intramural Research Program of the NIH; National Institute of
Environmental Health Sciences [Z01-ES04007-12]
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences
(Z01-ES04007-12). We thank Drs. Jeffrey Murray and Theresa Zucchero for
sharing the genotype data of their orofacial cleft study and Drs. Rolv
Terje Lie and Dmitri Zaykin for helpful comments on the manuscript.
NR 20
TC 6
Z9 6
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0003-4800
J9 ANN HUM GENET
JI Ann. Hum. Genet.
PD MAY
PY 2009
VL 73
BP 346
EP 359
DI 10.1111/j.1469-1809.2009.00515.x
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 440NI
UT WOS:000265706600009
PM 19344450
ER
PT J
AU Luo, Y
Kuo, CC
Shen, H
Chou, J
Greig, NH
Hoffer, BJ
Wang, Y
AF Luo, Yu
Kuo, Chi-Chung
Shen, Hui
Chou, Jenny
Greig, Nigel H.
Hoffer, Barry J.
Wang, Yun
TI Delayed Treatment with a p53 Inhibitor Enhances Recovery in Stroke Brain
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID NEURAL STEM-CELLS; CEREBRAL-ISCHEMIA; ADULT BRAIN; NEUROGENESIS; DEATH;
RAT; EXPRESSION; APOPTOSIS; PROTECTS; NEURONS
AB Objective: Cerebral ischemia can activate endogenous reparative processes, such as proliferation of endogenous neural progenitor cells (NPCs) in the subventricular zone (SVZ). Most of these new cells die shortly after injury. The purpose of this study was to examine a novel strategy for treatment of stroke at 1 week after injury by enhancing the survival of ischemia-induced endogenous NPCs in SVZ.
Methods: Adult rats were subjected to a 90-minutes middle cerebral artery occlusion. A p53 inhibitor pifithrin-alpha (PFT-alpha) was administered to stroke rats from days 6 to 9 after middle cerebral artery occlusion. Locomotor behavior was measured using an activity chamber. Proliferation, survival, migration, and differentiation of endogenous NPCs were examined using quantitative reverse transcription polymerase chain reaction, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, and immunohistochemistry.
Results: PFT-alpha enhanced functional recover), as assessed by a significant increase in multiple behavioral measurements. Delayed PFT-alpha treatment had no effect on the cell death processes in the lesioned cortical region. However, it enhanced the survival of SVZ progenitor cells, and promoted their proliferation and migration. PFT-a inhibited the expression of a p53-dependent proapoptotic gene, termed PUMA (p53-upregulated modulator of apoptosis), within the SVZ of stroke animals. The enhancement of survival/proliferation of NPCs was further found in SVZ neurospheres in tissue culture. PFT-alpha dose-dependently increased the number and size of new neurosphere formation.
Interpretation: Delayed treatment with a p53 inhibitor PFT-alpha is able to modify stroke-induced endogenous neurogenesis and improve the functional recovery in stroke animals.
C1 [Wang, Yun] NIDA, IRP, Neural Protect & Regenerat Sect, Baltimore, MD 21224 USA.
[Greig, Nigel H.] NIA, NIH, Res Program, Baltimore, MD 21224 USA.
RP Wang, Y (reprint author), NIDA, IRP, Neural Protect & Regenerat Sect, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM ywang@intra.nida.nih.gov
RI luo, Yu (Agnes)/E-4446-2010
FU Intramural Research Programs; National Institute on Drug Abuse; National
Institute of Aging
FX This study was supported by the Intramural Research Programs at the NIH
(National Institute on Drug Abuse; National Institute of Aging).
NR 34
TC 53
Z9 54
U1 0
U2 5
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD MAY
PY 2009
VL 65
IS 5
BP 520
EP 530
DI 10.1002/ana.21592
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 453LJ
UT WOS:000266611700008
PM 19475672
ER
PT J
AU Gschwendtner, A
Bevan, S
Cole, JW
Plourde, A
Matarin, M
Ross-Adams, H
Meitinger, T
Wichmann, E
Mitchell, BD
Furie, K
Slowik, A
Rich, SS
Syme, PD
MacLeod, MJ
Meschia, JF
Rosand, J
Kittner, SJ
Markus, HS
Muller-Myhsok, B
Dichgans, M
AF Gschwendtner, Andreas
Bevan, Steve
Cole, John W.
Plourde, Anna
Matarin, Mar
Ross-Adams, Helen
Meitinger, Thomas
Wichmann, Erich
Mitchell, Braxton D.
Furie, Karen
Slowik, Agnieszka
Rich, Stephen S.
Syme, Paul D.
MacLeod, Mary J.
Meschia, James F.
Rosand, Jonathan
Kittner, Steve J.
Markus, Hugh S.
Mueller-Myhsok, Bertram
Dichgans, Martin
CA Int Stroke Genetics Consortium
TI Sequence Variants on Chromosome 9p21.3 Confer Risk for Atherosclerotic
Stroke
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; CORONARY-ARTERY-DISEASE; TRANSIENT ISCHEMIC
ATTACK; SMOOTH-MUSCLE-CELLS; MYOCARDIAL-INFARCTION; CARDIOVASCULAR
EVENTS; PLAQUE VULNERABILITY; MEDIA THICKNESS; METAANALYSIS; REPLICATION
AB Objective: Recent studies have identified a major locus for risk for coronary artery disease and myocardial infiarction on chromosome 9p21.3. Stroke, in particular, ischemic stroke caused by atherosclerotic disease, shares common mechanisms with myocardial infarction. We investigated whether the 9p21 region contributes to ischemic stroke risk.
Methods: In an initial screen, 15 single nucleotide polymorphisms (SNPs) covering the critical genetic interval on 9p21 were genotyped in samples from Southern Germany (1,090 cases, 1,244 control subjects) and the United Kingdom (758 cases, 872 control subjects, 3 SNPs). SNPs significantly associated with ischemic stroke or individual stroke subtypes in either of the screening samples were Subsequently genotyped in 2,528 additional cases and 2,189 additional control Subjects from Europe and North America.
Results: Genotyping of the screening samples demonstrated associations between seven SNPs and atherosclerotic stroke (all p < 0.05). Analysis of the full sample confirmed associations between six SNPs and atherosclerotic stroke in multivariate analyses controlling for demographic variables, coronary, artery disease, myocardial infarction, and vascular risk factors (all p < 0.05). The odds ratios for the lead SNP (rs1537378-C) were similar in the various subsamples with a pooled odds ratio of 1.21 (95% confidence interval, 1.07-1.37) under both fixed- and random-effects models (p = 0.002). The point estimate for the population attributable risk is 20.1% For atherosclerotic stroke.
Interpretation: The chromosome 9p21.3 region represents a major risk locus for atherosclerotic stroke. The effect of this locus on stroke appears to be independent of its relation to coronary artery disease and other stroke risk factors. Our findings support a broad role of the 9p21 region in arterial disease.
C1 [Gschwendtner, Andreas; Dichgans, Martin] Univ Munich, Klinikum Grosshadern, Dept Neurol, Munich, Germany.
[Bevan, Steve; Markus, Hugh S.] Univ London, Ctr Clin Neurosci, London, England.
[Cole, John W.; Mitchell, Braxton D.; Kittner, Steve J.] Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA.
[Cole, John W.; Mitchell, Braxton D.; Kittner, Steve J.] Vet Affairs Med Ctr, Baltimore, MD USA.
[Plourde, Anna; Furie, Karen; Rosand, Jonathan] Massachusetts Gen Hosp, Stroke Serv, Boston, MA 02114 USA.
[Plourde, Anna; Furie, Karen; Rosand, Jonathan] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Matarin, Mar] NIA, Mol Genet Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Ross-Adams, Helen; MacLeod, Mary J.] Univ Aberdeen, Dept Med & Therapeut, Aberdeen, Scotland.
[Meitinger, Thomas] Helmholtz Zentrum Munchen, Inst Human Genet, Munich, Germany.
[Wichmann, Erich] Helmholtz Zentrum Munchen, Inst Epidemiol, Munich, Germany.
[Wichmann, Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Slowik, Agnieszka] Jagiellonian Univ, Coll Med, Dept Neurol, Krakow, Poland.
[Rich, Stephen S.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
[Syme, Paul D.] Univ Edinburgh, Dept Clin & Surg Sci, Edinburgh, Midlothian, Scotland.
[Meschia, James F.] Mayo Clin, Dept Neurol, Jacksonville, FL 32224 USA.
[Mueller-Myhsok, Bertram] Max Planck Inst Psychiat, D-80804 Munich, Germany.
RP Dichgans, M (reprint author), Marchioninistr 15, D-81377 Munich, Germany.
EM martin.dichgans@med.uni-muenchen.de
RI Muller-Myhsok, Bertram/A-3289-2013; Meitinger, Thomas/O-1318-2015;
Matarin, Mar/F-1771-2016;
OI Matarin, Mar/0000-0002-4717-5735; Bevan, Steve/0000-0003-0490-6830;
Mitchell, Braxton/0000-0003-4920-4744; Macleod, Mary
Joan/0000-0003-2115-8184
FU Chief Scientist Office [CZG/4/1/26]; NIDDK NIH HHS [P30 DK072488, P30
DK079637]; NINDS NIH HHS [K23 NS 042720, K23 NS042720-01, K23
NS042720-02, K23 NS042720-03, K23 NS042720-04, K23 NS042720-05, P50 NS
051343, P50 NS051343-01A2, R01 NS 42733, R01 NS042733, R01 NS042733-01,
R01 NS042733-02, R01 NS042733-03, R01 NS042733-04, R01 NS042733-05, R01
NS045012, R01 NS045012-05]
NR 38
TC 127
Z9 129
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD MAY
PY 2009
VL 65
IS 5
BP 531
EP 539
DI 10.1002/ana.21590
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 453LJ
UT WOS:000266611700009
PM 19475673
ER
PT J
AU Qiu, CX
Cotch, MF
Sigurdsson, S
Klein, R
Jonasson, F
Klein, BEK
Garcia, M
Jonsson, PV
Harris, TB
Eiriksdottir, G
Kjartansson, O
van Buchem, MA
Gudnason, V
Launer, LJ
AF Qiu, Chengxuan
Cotch, Mary Frances
Sigurdsson, Sigurdur
Klein, Ronald
Jonasson, Fridbert
Klein, Barbara E. K.
Garcia, Melissa
Jonsson, Palmi V.
Harris, Tamara B.
Eiriksdottir, Gudny
Kjartansson, Olafur
van Buchem, Mark A.
Gudnason, Vilmundur
Launer, Lenore J.
TI Microvascular Lesions in the Brain and Retina: The Age, Gene/Environment
Susceptibility-Reykjavik Study
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID WHITE-MATTER LESIONS; CEREBRAL MRI FINDINGS; ATHEROSCLEROSIS RISK;
CARDIOVASCULAR HEALTH; CEREBROVASCULAR-DISEASE; VESSEL DIAMETERS;
ROTTERDAM SCAN; BLOOD-PRESSURE; OLDER PERSONS; ABNORMALITIES
AB Objective: To investigate whether the severity and location of cerebral white matter hyperintensities (WMHs) and brain infarcts are correlated with the signs of retinal microvascular abnormalities in the elderly.
Methods: The study included 4,176 men and women (mean age, 76 years) who participated in the Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study. Digital retinal images of both dilated eyes were taken and evaluated for the presence of retinal focal arteriolar signs (focal arteriolar narrowing and arteriovenous nicking) and retinopathy lesions (retinal blot hemorrhages and microaneurysms). Brain magnetic resonance imaging scans were acquired and evaluated for the presence and distribution of cerebral infarcts and WMHs. Logistic and multinomial logistic models were constructed to estimate the association of retinal microvascular signs to brain lesions.
Results: Controlling for demographic and major cardiovascular risk factors, We found that retinal focal arteriolar signs, but not retinopathy lesions, were significantly associated with an increasing load of subcortical and periventricular WMHs. The strongest association was found between retinal arteriolar signs and a heavier WMH load, specifically in the subcortical frontal lobe, and periventricular frontal and parietal caps. There was a tendency toward bilateral retinal focal arteriolar narrowing being more strongly associated with the heavier load of subcortical WMHs. Arteriovenous nicking was significantly associated with subcortical infarcts.
Interpretation: In older adults, retinal focal arteriolar signs, but not retinopathy lesions, are correlated with the load of diffuse WMHs, particularly those located in the subcortical frontal lobe, and the periventricular frontal and parietal caps of the brain.
C1 [Qiu, Chengxuan; Garcia, Melissa; Harris, Tamara B.; Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Qiu, Chengxuan] Karolinska Inst, Aging Res Ctr, Dept Neurobiol Care Sci & Soc, Stockholm, Sweden.
[Cotch, Mary Frances] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Sigurdsson, Sigurdur; Eiriksdottir, Gudny; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Klein, Ronald; Klein, Barbara E. K.] Univ Wisconsin, Dept Ophthalmol, Sch Med & Publ Hlth Madison, Madison, WI USA.
[Jonasson, Fridbert; Jonsson, Palmi V.; Gudnason, Vilmundur] Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.
[Jonasson, Fridbert] Natl Univ Hosp Reykjavik, Dept Ophthalmol, Reykjavik, Iceland.
[Jonsson, Palmi V.] Landspitali Univ Hosp, Dept Geriatr, Reykjavik, Iceland.
[Kjartansson, Olafur] Landspitali Univ Hosp, Dept Radiol, Reykjavik, Iceland.
[van Buchem, Mark A.] Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.
RP Launer, LJ (reprint author), NIA, Lab Epidemiol Demog & Biometry, NIH, Gateway Bldg,Suite 3C-309,7201 Wisconsin Ave, Bethesda, MD 20892 USA.
EM launerl@nia.nih.gov
RI Gudnason, Vilmundur/K-6885-2015;
OI Gudnason, Vilmundur/0000-0001-5696-0084; Cotch, Mary
Frances/0000-0002-2046-4350; Qiu, Chengxuan/0000-0003-1922-4912; Klein,
Ronald/0000-0002-4428-6237
FU NIH [N01-AG-1-2100]; National Institute on Aging; National Eye Institute
[Z01-EY00401]; Icelandic Heart Association; Icelandic Parliament;
Swedish Council for Working Life and Social Research
FX This research was supported by the NIH (Intramural Research Program of
the National Institute on Aging and the National Eye Institute,
Z01-EY00401 NIH contract number N01-AG-1-2100), the Icelandic Heart
Association, the Icelandic Parliament, and the Swedish Council for
Working Life and Social Research (C.C.Q)
NR 38
TC 21
Z9 21
U1 0
U2 3
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD MAY
PY 2009
VL 65
IS 5
BP 569
EP 576
DI 10.1002/ana.21614
PG 8
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 453LJ
UT WOS:000266611700013
PM 19475677
ER
PT J
AU Scholz, SW
Houlden, H
Schulte, C
Sharma, M
Li, A
Berg, D
Melchers, A
Paudel, R
Gibbs, JR
Simon-Sanchez, J
Paisan-Ruiz, C
Bras, J
Ding, JH
Chen, H
Traynor, BJ
Arepalli, S
Zonozi, RR
Revesz, T
Holton, J
Wood, N
Lees, A
Oertel, W
Wullner, U
Goldwurm, S
Pellecchia, MT
Illig, T
Riess, O
Fernandez, HH
Rodriguez, RL
Okun, MS
Poewe, W
Wenning, GK
Hardy, JA
Singleton, AB
Gasser, T
AF Scholz, Sonja W.
Houlden, Henry
Schulte, Claudia
Sharma, Manu
Li, Abi
Berg, Daniela
Melchers, Anna
Paudel, Reema
Gibbs, J. Raphael
Simon-Sanchez, Javier
Paisan-Ruiz, Coro
Bras, Jose
Ding, Jinhui
Chen, Honglei
Traynor, Bryan J.
Arepalli, Sampath
Zonozi, Ryan R.
Revesz, Tamas
Holton, Janice
Wood, Nick
Lees, Andrew
Oertel, Wolfgang
Wuellner, Ullrich
Goldwurm, Stefano
Pellecchia, Maria Teresa
Illig, Thomas
Riess, Olaf
Fernandez, Hubert H.
Rodriguez, Ramon L.
Okun, Michael S.
Poewe, Werner
Wenning, Gregor K.
Hardy, John A.
Singleton, Andrew B.
Gasser, Thomas
TI SNCA Variants Are Associated with Increased Risk for Multiple System
Atrophy
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID ALPHA-SYNUCLEIN GENE; PARKINSONS-DISEASE; TRIPLICATION; DIAGNOSIS
C1 [Scholz, Sonja W.; Gibbs, J. Raphael; Simon-Sanchez, Javier; Bras, Jose; Ding, Jinhui; Traynor, Bryan J.; Arepalli, Sampath; Zonozi, Ryan R.; Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Scholz, Sonja W.; Houlden, Henry; Li, Abi; Melchers, Anna; Paudel, Reema; Gibbs, J. Raphael; Paisan-Ruiz, Coro; Revesz, Tamas; Holton, Janice; Wood, Nick; Lees, Andrew; Hardy, John A.] UCL, Dept Mol Neurosci, London, England.
[Scholz, Sonja W.; Houlden, Henry; Li, Abi; Melchers, Anna; Paudel, Reema; Gibbs, J. Raphael; Paisan-Ruiz, Coro; Revesz, Tamas; Holton, Janice; Wood, Nick; Lees, Andrew; Hardy, John A.] UCL, Inst Neurol, Reta Lila Weston Labs, London, England.
[Schulte, Claudia; Sharma, Manu; Berg, Daniela; Gasser, Thomas] Univ Tubingen, Dept Neurodegenerat Dis, Hertie Inst Clin Brain Res, Tubingen, Germany.
[Chen, Honglei] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Oertel, Wolfgang] Univ Marburg, Ctr Nervous Dis, Marburg, Germany.
[Wuellner, Ullrich] Univ Hosp, Bonn Med Ctr, Dept Neurol, Bonn, Germany.
[Goldwurm, Stefano] Ist Clin Perfezionamento, Parkinson Inst, Milan, Italy.
[Pellecchia, Maria Teresa] Univ Naples Federico 2, Dept Neurol Sci, Naples, Italy.
[Illig, Thomas] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol, Munich, Germany.
[Riess, Olaf] Univ Tubingen, Inst Human Genet, Dept Med Genet, Tubingen, Germany.
[Fernandez, Hubert H.; Rodriguez, Ramon L.; Okun, Michael S.] Univ Florida, Dept Neurol & Neurosurg, Gainesville, FL USA.
[Poewe, Werner; Wenning, Gregor K.] Med Univ Innsbruck, Dept Neurol, Innsbruck, Austria.
RP Scholz, SW (reprint author), NIA, Neurogenet Lab, NIH, 35 Convent Dr,Room 1A-1014, Bethesda, MD 20892 USA.
EM scholzs@mail.nih.gov
RI Paisan-Ruiz, Coro/C-2912-2009; Hardy, John/C-2451-2009; Bras,
Jose/D-3366-2009; Bras, Jose/A-1428-2011; Houlden, Henry/C-1532-2008;
Wood, Nicholas/C-2505-2009; Goldwurm, Stefano/Q-8978-2016; Revesz,
Tamas/A-8732-2010; Gibbs, J. Raphael/A-3984-2010; Singleton,
Andrew/C-3010-2009; Holton, Janice/F-6831-2011; Lees,
Andrew/A-6605-2009; Traynor, Bryan/G-5690-2010
OI Okun, Michael/0000-0002-6247-9358; Schulte, Claudia/0000-0003-4006-1265;
Chen, Honglei/0000-0003-3446-7779; Scholz, Sonja/0000-0002-6623-0429;
Houlden, Henry/0000-0002-2866-7777; Wood, Nicholas/0000-0002-9500-3348;
Goldwurm, Stefano/0000-0002-1651-567X; Revesz,
Tamas/0000-0003-2501-0259; Bras, Jose/0000-0001-8186-0333; Holton,
Janice/0000-0002-3882-5249;
FU Intramural NIH HHS [Z01 AG000957-06]; Medical Research Council
[G0701075, G108/638]; NIA NIH HHS [Z01 AG000957, Z01-AG 000957-06];
NIEHS NIH HHS [Z01 ES101986, Z01-ES 101986]; Parkinson's UK [G-0907];
Telethon [GTB07001]
NR 21
TC 131
Z9 138
U1 0
U2 6
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD MAY
PY 2009
VL 65
IS 5
BP 610
EP 614
DI 10.1002/ana.21685
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 453LJ
UT WOS:000266611700018
PM 19475667
ER
PT J
AU Chen, HX
AF Chen, H. X.
TI MONOCLONAL ANTIBODIES (MABS) TARGETING THE TYPE I INSULIN-LIKE GROWTH
FACTOR RECEPTOR (IGF-1R)
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Chen, H. X.] NCI, Invest Drug Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 17
EP 17
PG 1
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100006
ER
PT J
AU Giaccone, G
AF Giaccone, G.
TI BCL-2 INHIBITION
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Giaccone, G.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 19
EP 20
PG 2
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100015
ER
PT J
AU Kummar, S
AF Kummar, S.
TI STATUS OF POLY (ADP-RIBOSE) POLYMERASE (PARP) INHIBITORS IN CLINICAL
DEVELOPMENT
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Kummar, S.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 21
EP 21
PG 1
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100023
ER
PT J
AU Pommier, Y
Dexheimer, TS
Marchand, C
AF Pommier, Y.
Dexheimer, T. S.
Marchand, C.
TI THE DNA REPAIR ENZYME, TYROSYL-DNA PHOSPHODIESTERASE (TDP1) AS A TARGET
FOR ANTICANCER THERAPY
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Pommier, Y.; Dexheimer, T. S.; Marchand, C.] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM pommier@nih.gov
NR 5
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 21
EP 22
PG 2
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100024
ER
PT J
AU Choyke, P
Kurdziel, KA
AF Choyke, P.
Kurdziel, K. A.
TI MOLECULAR IMAGING OF CANCER
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Choyke, P.; Kurdziel, K. A.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 22
EP 22
PG 1
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100025
ER
PT J
AU Setser, A
Lacutoure, ME
Anadkat, MJK
Cotliar, JC
Chen, A
AF Setser, A.
Lacutoure, M. E.
Anadkat, M. J. K.
Cotliar, J. C.
Chen, A.
TI NCI COMMON TERMINOLOGY CRITERIA FOR ADVERSE EVENTS UPDATED TO ENCOMPASS
SKIN TOXICITIES FROM TARGETED THERAPIES
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Setser, A.; Chen, A.] NCI, Rockville, MD USA.
[Lacutoure, M. E.] Robert H Lurie Comprehens Canc Ctr, Chicago, IL USA.
[Anadkat, M. J. K.] Washington Univ, Sch Med, Ctr Adv Med, St Louis, MO 63130 USA.
[Cotliar, J. C.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 23
EP 23
PG 1
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100030
ER
PT J
AU Aryankalayil, M
Palayoor, S
Cerna, D
Coleman, CN
AF Aryankalayil, M.
Palayoor, S.
Cerna, D.
Coleman, C. N.
TI GENE EXPRESSION PROFILING OF PROSTATE CANCER CELLS AFTER SINGLE AND
FRACTIONATED DOSES OF RADIATION FOR MOLECULAR TARGETED THERAPY
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Aryankalayil, M.] NCI, Bethesda, MD 20892 USA.
[Palayoor, S.; Cerna, D.; Coleman, C. N.] NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 24
EP 24
PG 1
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100033
ER
PT J
AU Ivy, SP
Chen, H
AF Ivy, S. P.
Chen, H.
TI MULTI-TARGETED TYROSINE KINASE INHIBITORS PLUS CHEMOTHERAPY
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Ivy, S. P.; Chen, H.] NCI IDB, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 25
EP 25
PG 1
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100037
ER
PT J
AU Kummar, S
Ji, J
Zhang, Y
Simmons, D
Kinders, R
Gutierrez, ME
Allen, D
Homeffer, Y
Juwara, L
Rubinstein, L
Parchment, RE
Murgo, AJ
Chen, A
Tomaszewski, JE
Doroshow, JH
AF Kummar, S.
Ji, J.
Zhang, Y.
Simmons, D.
Kinders, R.
Gutierrez, M. E.
Allen, D.
Homeffer, Y.
Juwara, L.
Rubinstein, L.
Parchment, R. E.
Murgo, A. J.
Chen, A.
Tomaszewski, J. E.
Doroshow, J. H.
TI A PHASE I COMBINATION STUDY OF ABT-888 AND TOPOTECAN HYDROCHLORIDE IN
ADULTS WITH REFRACTORY SOLID TUMORS AND LYMPHOMAS
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Kummar, S.; Gutierrez, M. E.; Allen, D.; Homeffer, Y.; Doroshow, J. H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Rubinstein, L.; Murgo, A. J.; Chen, A.; Tomaszewski, J. E.; Doroshow, J. H.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Ji, J.; Zhang, Y.; Simmons, D.; Kinders, R.; Juwara, L.; Parchment, R. E.] NCI, Lab Human Toxicol & Pharmacol, Appl Dev Res Support Directorate, SAIC Frederick Inc, Frederick, MD 21701 USA.
NR 0
TC 5
Z9 5
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 42
EP 42
PG 1
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100092
ER
PT J
AU Rajan, A
Gutierrez, M
Kummar, S
Yancey, M
Ji, J
Zhang, Y
Simmons, D
Parchment, R
Tomaszewski, J
Doroshow, JH
Giaccone, G
AF Rajan, A.
Gutierrez, M.
Kummar, S.
Yancey, M.
Ji, J.
Zhang, Y.
Simmons, D.
Parchment, R.
Tomaszewski, J.
Doroshow, J. H.
Giaccone, G.
TI A PHASE I COMBINATION STUDY OF AZD2281 AND CISPLATIN PLUS GEMCITABINE IN
ADULTS WITH SOLID TUMORS
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT 7th International Symposium on Targeted Anticancer Therapies
CY MAR 23-25, 2009
CL Amsterdam, NETHERLANDS
C1 [Rajan, A.; Gutierrez, M.; Kummar, S.; Yancey, M.; Ji, J.; Zhang, Y.; Simmons, D.; Parchment, R.; Tomaszewski, J.; Doroshow, J. H.; Giaccone, G.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAY
PY 2009
VL 20
BP 42
EP 43
PG 2
WC Oncology
SC Oncology
GA 451VD
UT WOS:000266498100093
ER
PT J
AU Desai, D
Goldbach-Mansky, R
Milner, JD
Rabin, RL
Hull, K
Pucino, F
Colburn, N
AF Desai, Ditina
Goldbach-Mansky, Raphaela
Milner, Joshua D.
Rabin, Ronald L.
Hull, Keith
Pucino, Frank
Colburn, Nona
TI Anaphylactic Reaction to Anakinra in a Rheumatoid Arthritis Patient
Intolerant to Multiple Nonbiologic and Biologic Disease-Modifying
Antirheumatic Drugs
SO ANNALS OF PHARMACOTHERAPY
LA English
DT Article
DE adverse drug reactions; anakinra; anaphylactic reaction; antirheumatic
drugs; biological therapy; rheumatoid arthritis
ID NECROSIS-FACTOR-ALPHA; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTI-TNF TREATMENT;
CUTANEOUS VASCULITIS; LEUKOCYTOCLASTIC VASCULITIS; ETANERCEPT THERAPY;
CROHNS-DISEASE; INFLIXIMAB; PHARMACOGENETICS; ADALIMUMAB
AB OBJECTIVE: To report a case of probable anaphylaxis due to anakinra in a patient with rheumatoid arthritis and multiple drug allergies.
CASE SUMMARY: A 46-year-old Indian female with rheumatoid arthritis demonstrated distinct adverse reactions to all commercially available anti-tumor necrosis factor therapies, sulfasalazine, and hydroxychloroquine. Over a 4-year period her disease remained active during therapy with methotrexate and prednisone. Biologics were added sequentially, with development of intolerable reactions, first to infliximab (urticarial rash, infusion reactions) after 3 doses, and then to etanercept (autoantibodies, worsening Raynaud's phenomenon, digital microinfarcts) after 1 year. Following 2 months of daily injections of anakinra, she experienced an immediate immunoglobulin E-mediated anaphylactic reaction within 20 minutes of an injection, as evidenced by positive testing to both anakinra and histamine with the skin prick method. The patient subsequently started adalimumab therapy, which was discontinued after the fourth dose due to the development of generalized hives.
DISCUSSION: The Naranjo probability scale demonstrated a probable relationship between anaphylaxis and anakinra in this patient. Although cases of anakinra-related hypersensitivity have been reported in patients in which therapy was interrupted and then reintroduced, to our knowledge, this is the first report of anaphylaxis with continuous therapy.
CONCLUSIONS: This unusual case of a patient with multiple drug allergies presents a difficult clinical scenario, which was unsuccessfully managed with multiple biologic therapies on a trial-and-error basis. In the future, pharmacogenetics may help to better identify individuals at risk for multiple drug reactions and preclude unnecessary exposure to potentially harmful therapeutic options in similar patients.
C1 [Goldbach-Mansky, Raphaela; Colburn, Nona] NIAMSD, Autoinflammatory Dis Sect, NIH, Bethesda, MD 20892 USA.
[Milner, Joshua D.] NIAID, Immunol Lab, NIH, Bethesda, MD USA.
[Rabin, Ronald L.] US FDA, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA.
[Pucino, Frank] NIH, Dept Pharm, Bethesda, MD USA.
[Desai, Ditina] Warehouse Camden Yards, Baltimore, MD USA.
RP Colburn, N (reprint author), NIAMSD, Autoinflammatory Dis Sect, NIH, Bethesda, MD 20892 USA.
EM colburnn@mail.nih.gov
FU Intramural NIH HHS [ZIA AR041138-07]
NR 45
TC 15
Z9 15
U1 1
U2 3
PU HARVEY WHITNEY BOOKS CO
PI CINCINNATI
PA PO BOX 42696, CINCINNATI, OH 45242 USA
SN 1060-0280
J9 ANN PHARMACOTHER
JI Ann. Pharmacother.
PD MAY
PY 2009
VL 43
IS 5
BP 967
EP 972
DI 10.1345/aph.1L573
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 445WR
UT WOS:000266082700021
PM 19417117
ER
PT J
AU Cressey, TR
Van Dyke, R
Jourdain, G
Puthanakit, T
Roongpisuthipong, A
Achalapong, J
Yuthavisuthi, P
Prommas, S
Chotivanich, N
Maupin, R
Smith, E
Shapiro, DE
Mirochnick, M
AF Cressey, Tim R.
Van Dyke, Russell
Jourdain, Gonzague
Puthanakit, Thanyawee
Roongpisuthipong, Anuvat
Achalapong, Jullapong
Yuthavisuthi, Prapap
Prommas, Sinart
Chotivanich, Nantasak
Maupin, Robert
Smith, Elizabeth
Shapiro, David E.
Mirochnick, Mark
CA IMPAACT P1032 Team
TI Early Postpartum Pharmacokinetics of Lopinavir Initiated Intrapartum in
Thai Women
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID NEVIRAPINE; ADULTS; DRUGS
AB Lopinavir (LPV) exposure is reduced during the third trimester of pregnancy. We report the pharmacokinetics of standard LPV-ritonavir dosing (400/100 mg twice daily) in the immediate and early postpartum period when initiated during labor. In 16 human immunodeficiency virus-infected Thai women, the median (range) LPV area under the concentration-time curve and maximum and minimum concentrations in plasma were 99.7 (66.1 to 180.5) mu g.h/ml, 11.2 (8.0 to 17.5) mu g/ml, and 4.6 (1.7 to 12.5) mu g/ml, respectively, at 41 (12 to 74) h after delivery. All of the women attained adequate LPV levels through 30 days postpartum. No serious adverse events were reported.
C1 [Cressey, Tim R.] Chiang Mai Univ, IRD174, Program HIV Prevent & Treatment, IRD,PHPT,Fac Associated Med Sci, Chiang Mai 50205, Thailand.
[Van Dyke, Russell] Tulane Univ, New Orleans, LA 70118 USA.
[Cressey, Tim R.; Jourdain, Gonzague; Shapiro, David E.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Puthanakit, Thanyawee] Chiang Mai Univ, Res Inst Hlth Sci, Chiang Mai 50205, Thailand.
[Roongpisuthipong, Anuvat] Siriraj Hosp, Bangkok, Thailand.
[Achalapong, Jullapong] Chiang Rai Prachanukoh Hosp, Chiang Rai, Thailand.
[Yuthavisuthi, Prapap] Prapokklao Hosp, Chanthaburi, Thailand.
[Prommas, Sinart] Bhumibol Adulyadej Hosp, Bangkok, Thailand.
[Chotivanich, Nantasak] Chonburi Hosp, Chon Buri, Thailand.
[Maupin, Robert] Louisiana State Univ, New Orleans, LA USA.
[Smith, Elizabeth] NIAID, Pediat Med Branch, Div Aids, Bethesda, MD 20892 USA.
[Mirochnick, Mark] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Cressey, TR (reprint author), Chiang Mai Univ, IRD174, Program HIV Prevent & Treatment, IRD,PHPT,Fac Associated Med Sci, 29-7-8 Samlan Rd,Soi 1 Prasing, Chiang Mai 50205, Thailand.
EM tim@phpt.org
FU NIAID NIH HHS [U01AI069512, U01 AI068632, U01 AI069399, U01 AI069512,
U01AI069399]
NR 7
TC 6
Z9 6
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD MAY 1
PY 2009
VL 53
IS 5
BP 2189
EP 2191
DI 10.1128/AAC.01091-08
PG 3
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 438AQ
UT WOS:000265528700070
PM 19237646
ER
PT J
AU Carta, D
McGuigan, C
Margolis, L
Balzarini, J
AF Carta, Davide
McGuigan, Christopher
Margolis, Leonid
Balzarini, Jan
TI Synthesis and Evaluation of Novel Acyclovir Phosphoramidates as Anti-HIV
Agents
SO ANTIVIRAL RESEARCH
LA English
DT Meeting Abstract
CT 22nd International Conference on Antiviral Research
CY MAY 03-07, 2009
CL Miami Beach, FL
C1 [Carta, Davide; McGuigan, Christopher] Cardiff Univ, Welsh Sch Pharm, Cardiff, S Glam, Wales.
[Margolis, Leonid] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Balzarini, Jan] Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium.
RI McGuigan, Chris/P-1580-2014
OI McGuigan, Chris/0000-0001-8409-710X
NR 3
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD MAY
PY 2009
VL 82
IS 2
MA 127
BP A56
EP A56
DI 10.1016/j.antiviral.2009.02.132
PG 1
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA 437RM
UT WOS:000265504600111
ER
PT J
AU Derudas, M
McGuigan, C
Brancale, A
Margolis, L
Balzarini, J
AF Derudas, Marco
McGuigan, Christopher
Brancale, Andrea
Margolis, Leonid
Balzarini, Jan
TI The Application of Phosphoramidate Protide Technology to Acyclovir
confers Novel Anti-HIV Inhibition
SO ANTIVIRAL RESEARCH
LA English
DT Meeting Abstract
CT 22nd International Conference on Antiviral Research
CY MAY 03-07, 2009
CL Miami Beach, FL
C1 [Derudas, Marco; McGuigan, Christopher; Brancale, Andrea] Cardiff Univ, Welsh Sch Pharm, Cardiff, S Glam, Wales.
[Margolis, Leonid] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Balzarini, Jan] Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium.
RI Brancale, Andrea/N-9445-2014; McGuigan, Chris/P-1580-2014
OI Brancale, Andrea/0000-0002-9728-3419; McGuigan,
Chris/0000-0001-8409-710X
NR 2
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD MAY
PY 2009
VL 82
IS 2
MA 129
BP A57
EP A57
DI 10.1016/j.antiviral.2009.02.134
PG 1
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA 437RM
UT WOS:000265504600113
ER
PT J
AU Selvam, P
Maddali, K
Pommier, Y
AF Selvam, Periyasamy
Maddali, Kasthuraiah
Pommier, Yves
TI Indole Derivatives Are Potent Inhibitors of HIV Integrase
SO ANTIVIRAL RESEARCH
LA English
DT Meeting Abstract
CT 22nd International Conference on Antiviral Research
CY MAY 03-07, 2009
CL Miami Beach, FL
C1 [Selvam, Periyasamy] Amrita Sch Pharm, Dept Med Chem, Kochi 26, India.
[Maddali, Kasthuraiah; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD MAY
PY 2009
VL 82
IS 2
MA 84
BP A42
EP A42
DI 10.1016/j.antiviral.2009.02.089
PG 1
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA 437RM
UT WOS:000265504600069
ER
PT J
AU Vercruysse, T
Pavlakis, G
Daelemans, D
AF Vercruysse, Thomas
Pavlakis, George
Daelemans, Dirk
TI High-throughput In Vitro HIV Rev-multimerization Assay
SO ANTIVIRAL RESEARCH
LA English
DT Meeting Abstract
CT 22nd International Conference on Antiviral Research
CY MAY 03-07, 2009
CL Miami Beach, FL
C1 [Vercruysse, Thomas; Daelemans, Dirk] Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium.
[Pavlakis, George] NCI, Human Retrovirus Pathogenesis Sect, Frederick, MD 21702 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD MAY
PY 2009
VL 82
IS 2
MA 96
BP A46
EP A46
DI 10.1016/j.antiviral.2009.02.101
PG 1
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA 437RM
UT WOS:000265504600080
ER
PT J
AU Lamb, ME
Orbach, Y
Sternberg, KJ
Aldridge, J
Pearson, S
Stewart, HL
Esplin, PW
Bowler, L
AF Lamb, Michael E.
Orbach, Yael
Sternberg, Kathleen J.
Aldridge, Jan
Pearson, Sally
Stewart, Heather L.
Esplin, Phillip W.
Bowler, Lynn
TI Use of a Structured Investigative Protocol Enhances the Quality of
Investigative Interviews With Alleged Victims of Child Sexual Abuse in
Britain
SO APPLIED COGNITIVE PSYCHOLOGY
LA English
DT Article
ID ANATOMICALLY DETAILED DOLLS; FORENSIC INTERVIEWS; PEDIATRIC EXAMINATION;
EYEWITNESS TESTIMONY; PRESCHOOL-CHILDREN; AGE-DIFFERENCES; QUESTION
TYPE; RESPONSES; WITNESSES; CONTRADICTIONS
AB One hundred alleged victims of child sexual abuse (aged 4-13: M = 9.3 years) were interviewed by police investigators about their alleged experiences. Half of the children were interviewed using the National Institute of Child Health and Human Development (NICHD) structured interview Protocol, whereas the other children, matched with respect to their age, relationship with the alleged perpetrator, and seriousness of the alleged offenses, were interviewed by investigators following the Memorandum of Good Practice. Protocol-guided interviews elicited more information using freer: call invitations and less information using directive, option-posing and suggestive questions than did standard Memorandum interviews. There were no age differences in the proportion of total information provided in response to open-ended invitations in either condition, but there was a significant increase with age in the proportion of central information provided in response to open-ended invitations. Published in 2008 by John Wiley & Sons, Ltd.
C1 [Lamb, Michael E.] Univ Cambridge, Dept Social & Dev Psychol, Fac Polit Psychol & Sociol, Cambridge CB2 3RQ, England.
[Orbach, Yael; Sternberg, Kathleen J.] NICHHD, Bethesda, MD 20892 USA.
[Aldridge, Jan; Pearson, Sally] Univ Leeds, Leeds LS2 9JT, W Yorkshire, England.
[Stewart, Heather L.] Childrens Justice Ctr, Salt Lake City, UT USA.
[Bowler, Lynn] Derbyshire Constabulary, Ripley, Derby, England.
RP Lamb, ME (reprint author), Univ Cambridge, Dept Social & Dev Psychol, Fac Polit Psychol & Sociol, Free Sch Lane, Cambridge CB2 3RQ, England.
EM mel37@cam.ac.uk
NR 71
TC 26
Z9 26
U1 7
U2 18
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0888-4080
J9 APPL COGNITIVE PSYCH
JI Appl. Cogn. Psychol.
PD MAY
PY 2009
VL 23
IS 4
BP 449
EP 467
DI 10.1002/acp.1489
PG 19
WC Psychology, Experimental
SC Psychology
GA 429SV
UT WOS:000264941300001
ER
PT J
AU Goldman, AL
Pezawas, L
Doz, P
Mattay, VS
Fischl, B
Verchinski, BA
Chen, Q
Weinberger, DR
Meyer-Lindenberg, A
AF Goldman, Aaron L.
Pezawas, Lukas
Doz, Priv
Mattay, Venkata S.
Fischl, Bruce
Verchinski, Beth A.
Chen, Qiang
Weinberger, Daniel R.
Meyer-Lindenberg, Andreas
TI Widespread Reductions of Cortical Thickness in Schizophrenia and
Spectrum Disorders and Evidence of Heritability
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID HUMAN CEREBRAL-CORTEX; MONOZYGOTIC TWINS DISCORDANT; GENETICALLY COMPLEX
TRAITS; 1ST EPISODE SCHIZOPHRENIA; MAGNETIC-RESONANCE IMAGES;
VOXEL-BASED MORPHOMETRY; SURFACE-BASED ANALYSIS; GRAY-MATTER; UNAFFECTED
SIBLINGS; HIPPOCAMPAL VOLUME
AB Context: Schizophrenia is a brain disorder with predominantly genetic risk factors, and previous research has identified heritable cortical and subcortical reductions in local brain volume. To our knowledge, cortical thickness, a measure of particular interest in schizophrenia, has not previously been evaluated in terms of its heritability in relationship to risk for schizophrenia.
Objective: To quantify the distribution and heritability of cortical thickness changes in schizophrenia.
Design: We analyzed a large sample of normal controls, affected patients, and unaffected siblings using a surface-based approach. Cortical thickness was compared between diagnosis groups on a surfacewide node-by-node basis. Heritability related to disease risk was assessed in regions derived from an automated cortical parcellation algorithm by calculating the Risch lambda.
Setting: Research hospital.
Participants: One hundred ninety-six normal controls, 115 affected patients with schizophrenia, and 192 unaffected siblings.
Main Outcome Measure: Regional cortical thickness.
Results: Node-by-node mapping statistics revealed widespread thickness reductions in the patient group, most pronouncedly in the frontal lobe and temporal cortex. Unaffected siblings did not significantly differ from normal controls at the chosen conservative threshold. Risch lambda analysis revealed widespread evidence for heritability for cortical thickness reductions throughout the brain.
Conclusions: To our knowledge, the present study provides the first evidence of broadly distributed and heritable reductions of cortical thickness alterations in schizophrenia. However, since only trend-level reductions of thickness were observed in siblings, cortical thickness per se (at least as measured by this approach) is not a strong intermediate phenotype for schizophrenia. Arch Gen Psychiatry. 2009; 66(5):467-477
C1 [Goldman, Aaron L.; Pezawas, Lukas; Mattay, Venkata S.; Verchinski, Beth A.; Chen, Qiang; Weinberger, Daniel R.; Meyer-Lindenberg, Andreas] NIMH, Neuroimaging Core Facil, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
[Fischl, Bruce] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,Athinoula A Martinos Ctr, Charlestown, MA USA.
[Fischl, Bruce] MIT, Dept Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Fischl, Bruce] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
[Meyer-Lindenberg, Andreas] Cent Inst Mental Hlth, D-6800 Mannheim, Germany.
RP Weinberger, DR (reprint author), NIMH, Neuroimaging Core Facil, Genes Cognit & Psychosis Program, NIH, 10 Ctr Dr,Bldg 10,Room 4S237B, Bethesda, MD 20892 USA.
EM weinberd@mail.nih.gov
RI Meyer-Lindenberg, Andreas/H-1076-2011;
OI Meyer-Lindenberg, Andreas/0000-0001-5619-1123; Pezawas,
Lukas/0000-0002-1329-6352
FU National Center for Research Resources [P41RR14075, R01 RR16594-01A1];
NCRR BIRN Morphometric [BIRN002, U24 RR021382]; National Institute for
Biomedical Imaging and Bioengineering [R01 EB001550]; National Institute
for Neurological Disorders [R01 NS052585-01]; Mental Illness and
Neuroscience Discovery Institute; NIH through the NIH Roadmap for
Medical Research [U54 EB005149]
FX This work was supported by the National Institute of Mental Health
Intramural Research Program and used the high-performance computational
capabilities of the Biowulf Linux cluster at the National Institutes of
Health (NIH) (http://biowulf.nih.gov). Support for this research was
also provided in part by National Center for Research Resources grants
P41RR14075, R01 RR16594-01A1, and NCRR BIRN Morphometric Project
BIRN002, U24 RR021382; National Institute for Biomedical Imaging and
Bioengineering grant R01 EB001550, and National Institute for
Neurological Disorders and Stroke grant R01 NS052585-01 as well as the
Mental Illness and Neuroscience Discovery Institute and is part of the
National Alliance for Medical Image Computing, funded by NIH through the
NIH Roadmap for Medical Research, grant U54 EB005149.
NR 67
TC 140
Z9 144
U1 1
U2 9
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-990X
J9 ARCH GEN PSYCHIAT
JI Arch. Gen. Psychiatry
PD MAY
PY 2009
VL 66
IS 5
BP 467
EP +
PG 14
WC Psychiatry
SC Psychiatry
GA 441RV
UT WOS:000265789100002
PM 19414706
ER
PT J
AU Kaye, J
DeKosky, ST
Williamson, JD
Fitzpatrick, AL
Kronmal, RA
Ives, DG
Saxton, JA
Lopez, OL
Burke, G
Carlson, MC
Fried, LP
Kuller, LH
Robbins, JA
Tracy, RP
Woolard, NF
Dunn, L
Snitz, BE
Nahin, RL
Furberg, CD
AF Kaye, Jeffrey
DeKosky, Steven T.
Williamson, Jeff D.
Fitzpatrick, Annette L.
Kronmal, Richard A.
Ives, Diane G.
Saxton, Judith A.
Lopez, Oscar L.
Burke, Gregory
Carlson, Michelle C.
Fried, Linda P.
Kuller, Lewis H.
Robbins, John A.
Tracy, Russell P.
Woolard, Nancy F.
Dunn, Leslie
Snitz, Beth E.
Nahin, Richard L.
Furberg, Curt D.
CA Ginkgo Evaluation Memory GEM Study
TI Ginkgo biloba for Prevention of Dementia: A Randomized Controlled Trial
SO ARCHIVES OF NEUROLOGY
LA English
DT Editorial Material
ID MILD COGNITIVE IMPAIRMENT; TRANSGENIC MOUSE MODEL; ALZHEIMERS-DISEASE;
EFFICACY
AB Context: Ginkgo biloba is widely used for its potential effects on memory and cognition. To date, adequately powered clinical trials testing the effect of G biloba on dementia incidence are lacking.
Objective: To determine effectiveness of G biloba vs placebo in reducing the incidence of all-cause dementia and Alzheimer disease (AD) in elderly individuals with normal cognition and those with mild cognitive impairment (MCI).
Design, Setting, and Participants: Randomized, double-blind, placebo-controlled clinical trial conducted in 5 academic medical centers in the United States between 2000 and 2008 with a median follow-up of 6.1 years. Three thousand sixtynine community volunteers aged 75 years or older with normal cognition (n = 2587) or MCI (n = 482) at study entry were assessed every 6 months for incident dementia.
Intervention: Twice-daily dose of 120-mg extract of G biloba (n = 1545) or placebo (n = 1524).
Main Outcome Measures: Incident dementia and AD determined by expert panel consensus.
Results: Five hundred twenty-three individuals developed dementia (246 receiving placebo and 277 receiving G biloba) with 92% of the dementia cases classified as possible or probable AD, or AD with evidence of vascular disease of the brain. Rates of dropout and loss to follow-up were low (6.3%), and the adverse effect profiles were similar for both groups. The overall dementia rate was 3.3 per 100 person-years in participants assigned to G biloba and 2.9 per 100 person-years in the placebo group. The hazard ratio (HR) for G biloba compared with placebo for all-cause dementia was 1.12 (95% confidence interval [CI], 0.94-1.33; P = .21) and for AD, 1.16 (95% CI, 0.97-1.39; P = .11). G biloba also had no effect on the rate of progression to dementia in participants with MCI (HR, 1.13; 95% CI, 0.85-1.50; P = .39).
Conclusions: In this study, G biloba at 120 mg twice a day was not effective in reducing either the overall incidence rate of dementia or AD incidence in elderly individuals with normal cognition or those with MCI.
C1 [Kaye, Jeffrey] Oregon Hlth & Sci Univ, NIA, Layton Aging & Alzheimers Dis Ctr, Portland, OR 97239 USA.
RP Kaye, J (reprint author), Oregon Hlth & Sci Univ, NIA, Layton Aging & Alzheimers Dis Ctr, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM kaye@ohsu.edu
FU NIA NIH HHS [AG08017, AG024059, AG024978, AG10483]
NR 20
TC 2
Z9 2
U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD MAY
PY 2009
VL 66
IS 5
BP 652
EP 654
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 444PU
UT WOS:000265993700014
PM 19433666
ER
PT J
AU Klein, AP
Suktitipat, B
Duggal, P
Lee, KE
Klein, R
Bailey-Wilson, JE
Klein, BEK
AF Klein, Alison P.
Suktitipat, Bhoom
Duggal, Priya
Lee, Kristine E.
Klein, Ronald
Bailey-Wilson, Joan E.
Klein, Barbara E. K.
TI Heritability Analysis of Spherical Equivalent, Axial Length, Corneal
Curvature, and Anterior Chamber Depth in the Beaver Dam Eye Study
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID HIGH MYOPIA MAPS; TANJONG-PAGAR SURVEY; HIGH-GRADE MYOPIA; GENOME-WIDE
SCAN; OCULAR REFRACTION; VISUAL-ACUITY; CLINICAL RESEARCH; POPULATION;
LINKAGE; LOCUS
AB Objective: To examine genetic influences for quantitative refraction. Spherical equivalent and its related binary traits of myopia and hyperopia are highly correlated within families. Many linkage regions have been reported for myopia, high myopia, and quantitative refraction. However, the measured phenotype of spherical equivalent is in large part dictated by the relationship between the underlying optical components of axial length, corneal curvature, and anterior chamber depth.
Methods: Using data from the fourth visit of the Beaver Dam Eye Study, we conducted familial correlation and heritability analysis of quantitative spherical equivalent, axial length, anterior chamber depth, and corneal curvature using data from 7.15 individuals in 189 pedigrees.
Results: Overall, every trait was highly heritable. Heritability estimates were 0.58 (SE 0.13) for spherical equivalent after adjustment for age, education, and nuclear sclerosis; 0.95 (SE 0.11) for corneal curvature after adjustment for height; 0.67 (SE 0.14) for axial length after adjustment for height and education; and 0.78 (SE 0.14) for anterior chamber depth after adjustment for age, education, height, and nuclear sclerosis.
Conclusion: Refraction and the underlying traits of axial length, corneal curvature, and anterior chamber depth are highly heritable. Genetic analysis of these traits may provide greater insight into the development of refractive errors.
C1 [Klein, Alison P.] Johns Hopkins Sch Med, Dept Oncol, Baltimore, MD USA.
[Klein, Alison P.] Johns Hopkins Sch Med, Dept Pathol, Baltimore, MD USA.
[Klein, Alison P.; Suktitipat, Bhoom] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Duggal, Priya; Bailey-Wilson, Joan E.] NHGRI, Stat Genet Sect, Inherited Dis Res Branch, NIH, Baltimore, MD USA.
[Suktitipat, Bhoom] Mahidol Univ, Dept Biochem, Fac Med, Siriraj Hosp, Bangkok 10700, Thailand.
[Lee, Kristine E.; Klein, Ronald; Klein, Barbara E. K.] Univ Wisconsin, Dept Ophthalmol & Visual Sci, Sch Med & Publ Hlth, Madison, WI 53706 USA.
RP Klein, AP (reprint author), Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, 1550 Orleans St, Baltimore, MD 21231 USA.
EM aklein1@jhmi.edu
OI Bailey-Wilson, Joan/0000-0002-9153-2920; Suktitipat,
Bhoom/0000-0001-8034-7757
FU National Eye Institute [EY017237, EY06594, EY015286]; Research to
Prevent Blindness; National Human Genome Research Institute; National
Center for Research Resources [RR03655]
FX This work was supported by grants EY017237 (Dr A. P. Klein), EY06594
(Drs R. Klein and B. E. K. Klein), and EY015286 (Dr B. E. K. Klein) from
the National Eye Institute; grants from Research to Prevent Blindness
(Drs R. Klein and B. E. K. Klein); and by the Intramural Research
Program of the National Human Genome Research Institute. Some of the
results of this article were obtained by using the program package
S.A.G.E., which is supported by US Public Health Service Resource Grant
RR03655 from the National Center for Research Resources.
NR 49
TC 42
Z9 43
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD MAY
PY 2009
VL 127
IS 5
BP 649
EP 655
PG 7
WC Ophthalmology
SC Ophthalmology
GA 442NK
UT WOS:000265847700010
PM 19433716
ER
PT J
AU Cao, DJ
Igboeli, B
Yuan, LJ
Kapikian, AZ
Ayers, JL
Abinanti, FR
Hoshino, Y
AF Cao, Dianjun
Igboeli, Blessing
Yuan, Lijuan
Kapikian, Albert Z.
Ayers, Jess L.
Abinanti, Francis R.
Hoshino, Yasutaka
TI A longitudinal cohort study in calves evaluated for rotavirus infections
from 1 to 12 months of age by sequential serological assays
SO ARCHIVES OF VIROLOGY
LA English
DT Article
ID GROUP-A ROTAVIRUS; NEONATAL CALF DIARRHEA; SERUM NEUTRALIZING ANTIBODY;
FED COLOSTRUM SUPPLEMENTS; BOVINE ROTAVIRUS; GNOTOBIOTIC CALVES;
MOLECULAR CHARACTERIZATION; P-TYPE; MONOCLONAL-ANTIBODIES; PORCINE
ROTAVIRUS
AB Using an immunocytochemical staining assay involving six different recombinant baculoviruses with each expressing one of the major bovine rotavirus VP7 (G6, G8 and G10) and VP4 (P6[1], P7[5] and P8[11]) serotypes, we analyzed IgG antibody responses to individual proteins in archival serum samples collected from 31 calves monthly from 1 to 12 months of age during 1974-1975 in Higley, Arizona. Seroresponses to VP7 and VP4, as determined by a fourfold or greater antibody response, were not always elicited concurrently following infection: in some calves, (1) seroresponses to VP7 were detected earlier than to VP4 or vice versa; and (2) a subsequent second seroresponse was detected for VP7 or VP4 only. In addition, a second infection was more likely to be caused by different G and/or P types. Analyses of serum samples showed that the most frequent G-P combination was G8P6[1], followed by G8P7[5], G8P8[11] and G6P6[1].
C1 [Cao, Dianjun; Igboeli, Blessing; Kapikian, Albert Z.; Hoshino, Yasutaka] NIAID, Epidemiol Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Yuan, Lijuan] Virginia Maryland Reg Coll Vet Med, Virol & Immunol Dept Biomed Sci & Pathobiol, Blacksburg, VA 24061 USA.
[Ayers, Jess L.; Abinanti, Francis R.] Univ Arizona, Dept Vet Sci, Tucson, AZ 85721 USA.
RP Hoshino, Y (reprint author), NIAID, Epidemiol Sect, Infect Dis Lab, NIH, Bldg 50,Room 6308, Bethesda, MD 20892 USA.
EM thoshino@niaid.nih.gov
RI Yuan, Lijuan/A-2468-2008
OI Yuan, Lijuan/0000-0003-0709-5228
FU Intramural Research Program of the National Institute of Allergy and
Infectious Disease, National Institutes of Health, USA
FX This work was supported in part by the Intramural Research Program of
the National Institute of Allergy and Infectious Disease, National
Institutes of Health, USA. There is no conflict of interest to declare.
NR 76
TC 4
Z9 5
U1 0
U2 2
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0304-8608
J9 ARCH VIROL
JI Arch. Virol.
PD MAY
PY 2009
VL 154
IS 5
BP 755
EP 763
DI 10.1007/s00705-009-0331-y
PG 9
WC Virology
SC Virology
GA 443MW
UT WOS:000265915300003
PM 19343476
ER
PT J
AU Liu, YP
Gutterman, DD
AF Liu, Yanping
Gutterman, David D.
TI Vascular control in humans: focus on the coronary microcirculation
SO BASIC RESEARCH IN CARDIOLOGY
LA English
DT Review
DE coronary circulation; myogenic response; flow-mediated dilation; EDHF;
reactive oxygen species; diabetes; K(+) channels
ID SENSITIVE POTASSIUM CHANNELS; EPOXYGENASE-DERIVED EICOSANOIDS;
CA2+-ACTIVATED K+ CHANNELS; MESENTERIC SMALL ARTERIES; FLOW-INDUCED
DILATION; SMOOTH-MUSCLE-CELLS; ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION;
LEFT-VENTRICULAR HYPERTROPHY; INTERNAL MAMMARY ARTERY; CAMP-MEDIATED
DILATION
AB Myocardial perfusion is regulated by a variety of factors that influence arteriolar vasomotor tone. An understanding of the physiological and pathophysiological factors that modulate coronary blood flow provides the basis for the judicious use of medications for the treatment of patients with coronary artery disease. Vasomotor properties of the coronary circulation vary among species. This review highlights the results of recent studies that examine the mechanisms by which the human coronary microcirculation is regulated in normal and disease states, focusing on diabetes. Multiple pathways responsible for myogenic constriction and flow-mediated dilation in human coronary arterioles are addressed. The important role of endothelium-derived hyperpolarizing factors, their interactions in mediating dilation, as well as speculation regarding the clinical significance are emphasized. Unique properties of coronary arterioles in human vs. other species are discussed.
C1 [Gutterman, David D.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Liu, Yanping] NIH, Natl Ctr Res Resources, Bethesda, MD 20892 USA.
[Gutterman, David D.] Med Coll Wisconsin, Dept Med & Cardiovasc Ctr, Vet Adm Med Ctr, Milwaukee, WI 53226 USA.
RP Gutterman, DD (reprint author), Med Coll Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
EM dgutt@mcw.edu
FU NIH-NHLBI [R01HL067968, R01HL080704]; American Heart Association
Fellowship; VA Merit Review Program
FX This review was supported by funding from NIH-NHLBI (R01HL067968 and
R01HL080704), an American Heart Association Fellowship, and the VA Merit
Review Program.
NR 156
TC 42
Z9 44
U1 1
U2 7
PU DR DIETRICH STEINKOPFF VERLAG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, 69121 HEIDELBERG, GERMANY
SN 0300-8428
J9 BASIC RES CARDIOL
JI Basic Res. Cardiol.
PD MAY
PY 2009
VL 104
IS 3
BP 211
EP 227
DI 10.1007/s00395-009-0775-y
PG 17
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 431UB
UT WOS:000265088400001
PM 19190954
ER
PT J
AU Chan, SSL
Copeland, WC
AF Chan, Sherine S. L.
Copeland, William C.
TI DNA polymerase gamma and mitochondrial disease: Understanding the
consequence of POLG mutations
SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
LA English
DT Article; Proceedings Paper
CT International Symposium on Mitchondrial Physiology and Pathology
CY JUN, 2008
CL Bari, ITALY
DE Mitochondria; Mitochondrial disease; DNA polymerase gamma; Mitochondrial
DNA replication; Oxidative stress
ID PROGRESSIVE EXTERNAL OPHTHALMOPLEGIA; ALPERS-SYNDROME; CAG REPEAT;
SACCHAROMYCES-CEREVISIAE; MALE-INFERTILITY; ACCESSORY SUBUNIT; W748S
MUTATION; GENE POLG; POLYMORPHISM; DEFECTS
AB DNA polymerase gamma is the only known DNA polymerase in human mitochondria and is essential for mitochondrial DNA replication and repair. It is well established that defects in mtDNA replication lead to mitochondrial dysfunction and disease. Over 160 coding variations in the gene encoding the catalytic subunit of DNA polymerase gamma (POLG) have been identified. Our group and others have characterized a number of the more common and interesting mutations, as well as those disease mutations in the DNA polymerase gamma accessory subunit. We review the results of these studies, which provide clues to the mechanisms leading to the disease state. Published by Elsevier B.V.
C1 [Chan, Sherine S. L.; Copeland, William C.] Natl Inst Environm Hlth Sci, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Chan, SSL (reprint author), Natl Inst Environm Hlth Sci, Mol Genet Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM sherine.s.l.chan@gmail.com; copelan1@niehs.nih.gov
FU Intramural NIH HHS [Z01 ES065078-14, Z01 ES065080-13]; NIEHS NIH HHS
[1K99-ES015555-01, K99 ES015555, K99 ES015555-01, R00 ES015555]
NR 52
TC 76
Z9 76
U1 1
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0005-2728
J9 BBA-BIOENERGETICS
JI Biochim. Biophys. Acta-Bioenerg.
PD MAY
PY 2009
VL 1787
IS 5
BP 312
EP 319
DI 10.1016/j.bbabio.2008.10.007
PG 8
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 451MX
UT WOS:000266475400005
PM 19010300
ER
PT J
AU Fung, KL
Gottesman, MM
AF Fung, King Leung
Gottesman, Michael M.
TI A synonymous polymorphism in a common MDR1 (ABCB1) haplotype shapes
protein function
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Review
DE ABCB1; MDR1; Polymorphism; Haplotype; Ribosome stalling
ID HUMAN P-GLYCOPROTEIN; MULTIDRUG-RESISTANCE GENE; HEALTHY JAPANESE
SUBJECTS; VIRUS EXPRESSION SYSTEM; CF-1 MICE DEFICIENT; HAMSTER OVARY
CELLS; DRUG-RESISTANCE; CATALYTIC CYCLE; ATPASE ACTIVITY;
SUBSTRATE-SPECIFICITY
AB The MDR1 (ABCB1) gene encodes a membrane-bound transporter that actively effluxes a wide range of compounds from cells. The overexpression of MDR1 by multidrug-resistant cancer cells is a serious impediment to chemotherapy. MDR1 is expressed in various tissues to protect them from the adverse effect of toxins. The pharmacokinetics of drugs that are also MDR1 substrates also influence disease outcome and treatment efficacy. Although MDR1 is a well-conserved gene, there. is increasing evidence that its polymorphisms affect substrate specificity. Three single nucleotide polymorphisms (SNPs) occur frequently and have strong linkage, creating a common haplotype at positions 1236C>T (G412G), 2677G>T (A893S) and 3435C>T (111451). The frequency of the synonymous 3435C>T polymorphism has been shown to vary significantly according to ethnicity. Existing literature suggests that the haplotype plays a role in response to drugs and disease susceptibility. This review summarizes recent findings on the 3435C>T polymorphism of MDR1 and the haplotype to which it belongs. A possible molecular mechanism of action by ribosome stalling that can change protein structure and function by altering protein folding is discussed. Published by Elsevier B.V.
C1 [Fung, King Leung; Gottesman, Michael M.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Room 2108, Bethesda, MD 20892 USA.
EM mgottesman@nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute. We thank Mr.
George Leiman for editorial assistance.
NR 136
TC 155
Z9 167
U1 1
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-9639
J9 BBA-PROTEINS PROTEOM
JI BBA-Proteins Proteomics
PD MAY
PY 2009
VL 1794
IS 5
BP 860
EP 871
DI 10.1016/j.bbapap.2009.02.014
PG 12
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 444CD
UT WOS:000265956800015
PM 19285158
ER
PT J
AU Nayak, TK
Brechbiel, MW
AF Nayak, Tapan K.
Brechbiel, Martin W.
TI Radioimmunoimaging with Longer-Lived Positron-Emitting Radionuclides:
Potentials and Challenges
SO BIOCONJUGATE CHEMISTRY
LA English
DT Review
ID RADIOLABELING MONOCLONAL-ANTIBODIES; BIFUNCTIONAL CHELATING AGENT;
RECEPTOR-POSITIVE TUMORS; EMISSION-TOMOGRAPHY PET; IN-VIVO
BIODISTRIBUTION; XENOGRAFT-BEARING MICE; NON-HODGKINS-LYMPHOMA; HUMAN
GROWTH HORMONE; ANTI-CEA ANTIBODIES; CARRIER-FREE GA-66
AB Radioimmunoimaging and therapy has been an area of interest for several decades. Steady progress has been made toward clinical translation of radiolabeled monoclonal antibodies for diagnosis and treatment of diseases. Tremendous advances have been made in imaging technologies such as positron emission tomography (PET). However, these advances have so far eluded routine translation into clinical radioimmunoimaging applications due to the mismatch between the short half-lives of routinely used positron-emitting radionuclides such as (18)F versus the pharmacokinetics of most intact monoclonal antibodies of interest. The lack of suitable positron-emitting radionuclides that match the pharmacokinetics of intact antibodies has generated interest in exploring the use of longer-lived positron emitters that are more suitable for radioimmunoimaging and dosimetry applications with intact monoclonal antibodies. In this review, we examine the opportunities and challenges of radioimmunoimaging with select longer-lived positron-emitting radionuclides such as (124)I, (89)Zr, and (86)Y with respect to radionuclide production, ease of radiolabeling intact antibodies, imaging characteristics, radiation dosimetry, and clinical translation potential.
C1 [Nayak, Tapan K.; Brechbiel, Martin W.] NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Brechbiel, MW (reprint author), NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bldg 10,Room IB40, Bethesda, MD 20892 USA.
EM martinwb@mail.nih.gov
OI Nayak, Tapan/0000-0002-3706-6092
FU NIH; NCI; Center for Cancer Research; United States Department of Health
and Human Services
FX This report was supported by the Intramural Research Program of the NIH,
NCI, Center for Cancer Research, and the United States Department of
Health and Human Services. Gratitude is expressed to Mike Slackenerny
for constant encouragement and support.
NR 182
TC 89
Z9 90
U1 1
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD MAY
PY 2009
VL 20
IS 5
BP 825
EP 841
DI 10.1021/bc800299f
PG 17
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 448WK
UT WOS:000266292500001
PM 19125647
ER
PT J
AU Guo, YJ
Ribeiro, JMC
Anderson, JM
Bour, S
AF Guo, Yongjian
Ribeiro, Jose M. C.
Anderson, Jennifer M.
Bour, Stephan
TI dCAS: a desktop application for cDNA sequence annotation
SO BIOINFORMATICS
LA English
DT Article
ID SIALOME; INSIGHT; TOOL
AB Motivation: Understanding gene regulation and expression is the key to the advancement of biology. EST sequence assembly and analysis provide unique benefits in this regard. We have developed a standalone application, dCAS (Desktop cDNA Annotation System), which performs automated EST cleaning, clustering, assembly and annotation on a desktop computer. Compared with other available tools, dCAS provides a more convenient and user-friendly solution to biologists for extracting biological meaning from sequence data.
C1 [Guo, Yongjian; Bour, Stephan] Off Cyber Infrastruct & Computat Biol, Bioinformat & Computat Biosci Branch, Bethesda, MD 20892 USA.
[Ribeiro, Jose M. C.; Anderson, Jennifer M.] NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA.
RP Guo, YJ (reprint author), Off Cyber Infrastruct & Computat Biol, Bioinformat & Computat Biosci Branch, Bethesda, MD 20892 USA.
OI Ribeiro, Jose/0000-0002-9107-0818
NR 11
TC 35
Z9 36
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD MAY 1
PY 2009
VL 25
IS 9
BP 1195
EP 1196
DI 10.1093/bioinformatics/btp129
PG 2
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 437YR
UT WOS:000265523300018
PM 19318425
ER
PT J
AU Wahlberg, K
Ghatan, PH
Modell, S
Nygren, A
Ingvar, M
Asberg, M
Heilig, M
AF Wahlberg, Kristina
Ghatan, Per Hamid
Modell, Sieglinde
Nygren, Ake
Ingvar, Martin
Asberg, Marie
Heilig, Markus
TI Suppressed Neuroendocrine Stress Response in Depressed Women on
Job-Stress-Related Long-Term Sick Leave: A Stable Marker Potentially
Suggestive of Preexisting Vulnerability
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE ACTH; burnout; cortisol; depression; Dex-CRH-test; stress; vulnerability
ID PITUITARY-ADRENAL AXIS; HIGH FAMILIAL RISK; AFFECTIVE-DISORDERS; BODILY
DISORDERS; MOOD DISORDERS; ACTH RESPONSE; CRH TEST; DEXAMETHASONE;
PATHOPHYSIOLOGY; STIMULATION
AB Background: We recently reported marked hyporeactivity of the hypothalamo-pituitary-adrenal (HPA) axis in depressed women on job-stress-related long-term sick leave (LTSL). This unexpected finding prompted the question of whether HPA axis hypofunction in this group results from stress exposure or reflects preexisting vulnerability. Here, as a first step toward addressing this question, we assessed temporal stability of HPA axis reactivity in these subjects.
Method: We used the combined dexamethasone/corticotropin-releasing hormone (DEX-CRH) test to retest HPA axis reactivity in 29 patients and 27 control subjects after 12 months of follow-up. Clinical status and cognitive performance was also retested.
Results: Despite marked clinical improvement and normalization of initially observed impairments in attention and working memory, marked HPA axis hyporeactivity persisted in patients. A high test-retest correlation was found both at the level of corticotropin (R = .85, p < .001) and cortisol (R = .76, p < .001) responses.
Conclusions: Hyporeactivity of the HPA was stable over 12 months in LTSL subjects, independent of clinical improvement and normalized cognitive function. The stability of this response over time suggests that decreased DEX-CRH responses in this group may be a trait rather than a state marker. This finding is compatible with a hypothesis that HPA axis hyporeactivity may reflect a preexisting vulnerability in these subjects.
C1 [Wahlberg, Kristina; Ghatan, Per Hamid; Ingvar, Martin; Heilig, Markus] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Nygren, Ake; Asberg, Marie] Danderyd Hosp, Dept Clin Sci, Stockholm, Sweden.
[Modell, Sieglinde] Bristol Myers Squibb Co, Munich, Germany.
[Heilig, Markus] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
RP Heilig, M (reprint author), NIAAA, Lab Clin & Translat Studies, NIH, 10 Ctr Dr,10-1E-5334, Bethesda, MD 20892 USA.
EM markus.heilig@mail.nih.gov
OI Heilig, Markus/0000-0003-2706-2482; Ingvar, Martin/0000-0002-9041-5714
FU Swedish insurance company AFA
FX The authors report no biomedical financial interests or Potential
conflicts of interest.
NR 33
TC 41
Z9 41
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2009
VL 65
IS 9
BP 742
EP 747
DI 10.1016/j.biopsych.2008.10.035
PG 6
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 433XP
UT WOS:000265239400004
PM 19058782
ER
PT J
AU Akimov, SA
Hlaponin, EA
Bashkirov, PV
Boldyrev, IA
Mikhalyov, II
Telford, WG
Molotkovskaya, IM
AF Akimov, S. A.
Hlaponin, E. A.
Bashkirov, P. V.
Boldyrev, I. A.
Mikhalyov, I. I.
Telford, W. G.
Molotkovskaya, I. M.
TI GANGLIOSIDE GM1 INCREASES LINE TENSION AT RAFT BOUNDARY IN MODEL
MEMBRANES
SO BIOLOGICHESKIE MEMBRANY
LA English
DT Article
DE raft; ganglioside; apoptosis; line tension
ID LIPID RAFTS; FLUORESCENCE MICROSCOPY; DOMAINS; MONOLAYERS; CERAMIDE;
SEPARATION; CURVATURE; APOPTOSIS; VESICLES; PROBES
AB Gangliosides are significant participants in suppression of immune system during tumor processes. It was shown that they can induce apoptosis of T-lymphocytes in a raft-dependent manner. Fluorescence confocal microscopy was used to study distribution and influence of ganglioside GM1 on raft properties in giant unilamellar vesicles. Both raft and non-raft phase markers were utilized. No visible phase separation was observed without GM1 unless lateral tension was applied to the membrane. At 2 mol % of GM1 large domains appeared indicating macroscopic phase separation. Increase of GM1 content to 5 mol % resulted in shape transformation of the domains consistent with growth of line tension at the domain boundary. At 10 mol % of GM1 almost all domains were pinched out from vesicles, forming their own homogeneous liposomes. Estimations showed that the change of the GM1 content from 2 to 5-10 mol % resulted in a several-fold increase of line tension. This finding provides a possible mechanism of apoptosis induction by GM1. Incorporation of GM1 into a membrane leads to an increase of the line tension. This results in a growth of the average size of rafts due to coalescence or merger of small domains. Thus, necessary proteins can find themselves in one common raft and start the corresponding cascade of reactions.
C1 [Akimov, S. A.; Hlaponin, E. A.; Bashkirov, P. V.] Russian Acad Sci, Frumkin Inst Phys Chem & Electrochem, Moscow 119991, Russia.
[Boldyrev, I. A.; Mikhalyov, I. I.; Molotkovskaya, I. M.] Russian Acad Sci, Shemyakin Ovchinnikov Inst Bioorgan Chem, Moscow 117997, Russia.
[Telford, W. G.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Akimov, SA (reprint author), Russian Acad Sci, Frumkin Inst Phys Chem & Electrochem, Leninsky Pr 3115, Moscow 119991, Russia.
EM megakrot@mail.ru
RI Akimov, Sergey/L-2001-2013; Akimov, Sergey/I-6432-2015
FU ISTC [2654]; BTEP; Russian Academy of Sciences; Russian Foundation
[07-04-01145, 06-04-48666]; National Institutes of Health; USA
Department of Health and Human Services [R01 GM066837]; National Cancer
Institute intramural research funds; Leading Scientific Schools of
Russian Federation Program [4181.2008.4, 5946.2008.4]
FX We are grateful to Yu.A. Chizmadzhev, Jul.G. Molotkovsky, D.G. Knyazev,
and O.V. Batishchev for careful reading the manuscript and fruitful
discussions. The work was supported by ISTC (no. 2654)/BTEP/(no. 57)
program, the Program for Molecular and Cellular Biology of Presidium of
Russian Academy of Sciences, Russian Foundation for Basic Research (nos.
07-04-01145 and 06-04-48666), National Institutes of Health, USA
Department of Health and Human Services (R01 GM066837 and National
Cancer Institute intramural research funds), President of Russian
Federation for State Support of Leading Scientific Schools of Russian
Federation Program (nos. 4181.2008.4 and 5946.2008.4).
NR 31
TC 3
Z9 3
U1 0
U2 3
PU MEZHDUNARODNAYA KNIGA
PI MOSCOW
PA 39 DIMITROVA UL., 113095 MOSCOW, RUSSIA
SN 0233-4755
J9 BIOL MEMBRANY
JI Biol. Membr.
PD MAY-JUN
PY 2009
VL 26
IS 3
BP 234
EP 239
PG 8
WC Cell Biology
SC Cell Biology
GA 454QN
UT WOS:000266697500009
ER
PT J
AU Rossi, M
Bang, JK
Mazur, S
Iera, JA
Phillips, DC
Zambetti, GP
Appella, DH
AF Rossi, Matteo
Bang, Jeong-Kyu
Mazur, Sharlyn
Iera, Jaclyn A.
Phillips, Darren C.
Zambetti, Gerard P.
Appella, Daniel H.
TI Induction of apoptosis promoted by Bang52; a small molecule that
downregulates Bcl-x(L)
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Cancer; Apoptosis; Bcl-xL
ID BCL-2 FAMILY-MEMBERS; PRIMA-1 INDUCES APOPTOSIS; THYMIDINE KINASE LOCUS;
MUTANT P53; CELL-DEATH; WILD-TYPE; CYTOFLUOROMETRIC ANALYSIS;
PROTEIN-INTERACTION; X-L; CANCER
AB Cancer cells evade death by over-producing specific proteins that inhibit apoptosis. One such group of proteins is the Bcl-2 family, of which Bcl-x(L) is an important member. This protein binds and inhibits BAK, another protein that promotes apoptosis. While the development of chemical inhibitors that block Bcl-x(L)-BAK association have been the focus of intense research efforts, we demonstrate in this manuscript an alternative strategy to downregulate Bcl-x(L). We have identified a small molecule (Bang52) that induces apoptosis in a lymphoblast-derived cell line by lowering levels of Bcl-x(L). Since Bang52 bears no resemblance to any chemical binder of Bcl-x(L) we believe that degradation of the protein is stimulated by a new type of pathway. These findings highlight a novel approach to the development of small molecules that promote apoptosis. (c) 2009 Elsevier Ltd. All rights reserved.
C1 [Iera, Jaclyn A.; Appella, Daniel H.] NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Rossi, Matteo; Bang, Jeong-Kyu; Mazur, Sharlyn] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Phillips, Darren C.; Zambetti, Gerard P.] St Jude Childrens Hosp, Dept Biochem, Memphis, TN 38105 USA.
RP Appella, DH (reprint author), NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM appellad@niddk.nih.gov
FU NIH [CA6320]; NIH/NCI Cancer Center [CA21765]
FX The authors gratefully acknowledge financial support from the Intramural
Research Program of NIH, CA6320 and NIH/NCI Cancer Center Support Grant
CA21765. We are also grateful for the support of the American Lebanese
Syrian Associated Charities (ALSAC) of St. Jude Children's Research
Hospital. We also want to thank Tom Chittenden (Apoptosis Technology,
Inc., Boston, MA) for providing the HeLa-xL cells, and Dr.
Ana Robles (NCI) for providing the WTK1, NH32, and TK6 cells.
NR 47
TC 0
Z9 0
U1 1
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD MAY 1
PY 2009
VL 19
IS 9
BP 2429
EP 2434
DI 10.1016/j.bmcl.2009.03.067
PG 6
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 432MA
UT WOS:000265137100011
PM 19349174
ER
PT J
AU Yuan, PX
Salvadore, G
Li, XX
Zhang, L
Du, J
Chen, G
Manji, HK
AF Yuan, Peixiong
Salvadore, Giacomo
Li, Xiaoxia
Zhang, Lei
Du, Jing
Chen, Guang
Manji, Husseini K.
TI Valproate activates the Notch3/c-FLIP signaling cascade: a strategy to
attenuate white matter hyperintensities in bipolar disorder in late
life?
SO BIPOLAR DISORDERS
LA English
DT Article
DE apoptosis; bipolar disorder; FLIP; hyperintensity; Notch3; VPA; VSMC
ID SMOOTH-MUSCLE-CELLS; AUTOSOMAL-DOMINANT ARTERIOPATHY; FLICE-INHIBITORY
PROTEIN; HISTONE DEACETYLASE; SUBCORTICAL INFARCTS; DOWN-REGULATION;
C-FLIP; CHROMATIN CONDENSATION; MULTIPLE-SCLEROSIS; ENDOTHELIAL-CELLS
AB Increased prevalence of deep white matter hyperintensities (DWMHs) has been consistently observed in patients with geriatric depression and bipolar disorder. DMWHs are associated with chronicity, disability, and poor quality of life. They are thought to be ischemic in their etiology and may be related to the underlying pathophysiology of mood disorders in the elderly. Notably, these lesions strikingly resemble radiological findings related to the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephelopathy (CADASIL) syndrome. CADASIL arises from mutations in Notch3, resulting in impaired signaling via cellular Fas-associated death domain-like interleukin-1-beta-converting enzyme-inhibitory protein (c-FLIP) through an extracellular signal-regulated kinase (ERK)-dependent pathway. These signaling abnormalities have been postulated to underlie the progressive degeneration of vascular smooth muscle cells (VSMC). This study investigates the possibility that the anticonvulsant valproate (VPA), which robustly activates the ERK mitogen-activated protein kinase (MAPK) cascade, may exert cytoprotective effects on VSMC through the Notch3/c-FLIP pathway.
Human VSMC were treated with therapeutic concentrations of VPA subchronically. c-FLIP was knocked down via small interfering ribonucleic acid transfection. Cell survival, apoptosis, and protein levels were measured.
VPA increased c-FLIP levels dose- and time-dependently and promoted VSMC survival in response to Fas ligand-induced apoptosis in VSMC. The anti-apoptotic effect of VPA was abolished by c-FLIP knockdown. VPA also produced similar in vivo effects in rat brain.
These results raise the intriguing possibility that VPA may be a novel therapeutic agent for the treatment of CADASIL and related disorders. They also suggest that VPA might decrease the liability of patients with late-life mood disorders to develop DWMHs.
C1 [Yuan, Peixiong; Salvadore, Giacomo; Du, Jing; Chen, Guang; Manji, Husseini K.] NIMH, NIH, Mol Pathophysiol Lab, Bethesda, MD 20892 USA.
[Li, Xiaoxia; Zhang, Lei] Uniformed Serv Univ Hlth Sci, Dept Psychiat, Bethesda, MD 20814 USA.
RP Manji, HK (reprint author), NIMH, NIH, Mol Pathophysiol Lab, 35 Convent Dr,Room 1C-912, Bethesda, MD 20892 USA.
EM manji@nih.gov
RI Du, Jing/A-9023-2012; Chen, Guang/A-2570-2017
FU Intramural NIH HHS [, NIH0010733956]; PHS HHS [NIH0010733956]
NR 59
TC 10
Z9 10
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD MAY
PY 2009
VL 11
IS 3
BP 256
EP 269
DI 10.1111/j.1399-5618.2009.00675.x
PG 14
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 433DR
UT WOS:000265185000002
PM 19419383
ER
PT J
AU Romero, R
AF Romero, R.
TI The Role of Infection and Inflammation in Preterm Labor and Fetal Injury
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Romero, R.] NICHHD, Perinatol Res Branch, Intramural Div, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD MAY
PY 2009
VL 85
IS 5
BP 381
EP 381
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 454PX
UT WOS:000266695900010
ER
PT J
AU Gohlke, JM
Stockton, P
Sieber, S
Foley, J
Portier, CJ
AF Gohlke, J. M.
Stockton, P.
Sieber, S.
Foley, J.
Portier, C. J.
TI AhR-Mediated Gene Expression in the Developing Mouse Telencephalon
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Gohlke, J. M.; Portier, C. J.] NIEHS, Environm Syst Biol Grp, Mol Toxicol Lab, Res Triangle Pk, NC 27709 USA.
[Stockton, P.; Foley, J.] NIEHS, Lab Environm Pathol, Res Triangle Pk, NC 27709 USA.
[Sieber, S.] NIEHS, Microarray Grp, Mol Toxicol Lab, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD MAY
PY 2009
VL 85
IS 5
BP 405
EP 405
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 454PX
UT WOS:000266695900054
ER
PT J
AU Oz, OK
Ford, J
Umetami, M
Hajibeigi, A
Rodriguez, K
Korach, K
AF Oz, O. K.
Ford, J.
Umetami, M.
Hajibeigi, A.
Rodriguez, K.
Korach, K.
TI Estradiol regulates renal klotho through estrogen receptor alpha
SO BONE
LA English
DT Meeting Abstract
CT 2nd Joint Meeting of the
International-Bone-and-Mineral-Society/Australian-New-Zealand-Bone-and-M
ineral-Society
CY MAR 21-25, 2009
CL Sydney, AUSTRALIA
SP Int Bone & Mineral Soc, Australian & New Zealand Bone & Mineral Soc
C1 [Oz, O. K.; Ford, J.; Umetami, M.; Hajibeigi, A.] Univ Texas SW Med Ctr Dallas, Dallas, TX, Australia.
[Rodriguez, K.; Korach, K.] NIEHS, NIH, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 8756-3282
J9 BONE
JI Bone
PD MAY
PY 2009
VL 44
MA 476
BP S171
EP S171
DI 10.1016/j.bone.2009.01.364
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 436SP
UT WOS:000265436200380
ER
PT J
AU Yang, Y
Mak, KK
Guo, X
Day, TF
AF Yang, Y.
Mak, K. K.
Guo, X.
Day, T. F.
TI Wnt and Hh signaling in skeletal development and homeostasis
SO BONE
LA English
DT Meeting Abstract
CT 2nd Joint Meeting of the
International-Bone-and-Mineral-Society/Australian-New-Zealand-Bone-and-M
ineral-Society
CY MAR 21-25, 2009
CL Sydney, AUSTRALIA
SP Int Bone & Mineral Soc, Australian & New Zealand Bone & Mineral Soc
C1 [Yang, Y.; Mak, K. K.; Guo, X.; Day, T. F.] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 8756-3282
J9 BONE
JI Bone
PD MAY
PY 2009
VL 44
MA 066
BP S41
EP S41
DI 10.1016/j.bone.2009.01.104
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 436SP
UT WOS:000265436200062
ER
PT J
AU Barazany, D
Basser, PJ
Assaf, Y
AF Barazany, Daniel
Basser, Peter J.
Assaf, Yaniv
TI In vivo measurement of axon diameter distribution in the corpus callosum
of rat brain
SO BRAIN
LA English
DT Article
DE MRI; brain; corpus callosum; axon diameter distribution; diffusion
ID MYELINATED NERVE-FIBERS; DIFFUSION-TENSOR; WHITE-MATTER; RESTRICTED
DIFFUSION; CONDUCTION-VELOCITY; MRI; DEMYELINATION; SPECTROSCOPY;
MORPHOLOGY; HUMANS
AB Here, we present the first in vivo non-invasive measurement of the axon diameter distribution in the rat corpus callosum. Previously, this measurement was only possible using invasive histological methods. The axon diameter, along with other physical properties, such as the intra-axonal resistance, membrane resistance and capacitance etc. helps determine many important functional properties of nerves, such as their conduction velocity. In this work, we provide a novel magnetic resonance imaging method called AxCaliber, which can resolve the distinct signatures of trapped water molecules diffusing within axons as well as water molecules diffusing freely within the extra-axonal space. Using a series of diffusion weighted magnetic resonance imaging brain scans, we can reliably infer both the distribution of axon diameters and the volume fraction of these axons within each white matter voxel. We were able to verify the known microstructural variation along the corpus callosum of the rat from the anterior (genu) to posterior (splenium) regions. AxCaliber yields a narrow distribution centered 1 m in the genu and splenium and much broader distributions centered 3 m in the body of the corpus callosum. The axon diameter distribution found by AxCaliber is generally broader than those usually obtained by histology. One factor contributing to this difference is the significant tissue shrinkage that results from histological preparation. To that end, AxCaliber might provide a better estimate of the in vivo morphology of white matter. Being a magnetic resonance imaging based methodology, AxCaliber has the potential to be used in human scanners for morphological studies of white matter in normal and abnormal development, and white matter related diseases.
C1 [Barazany, Daniel; Assaf, Yaniv] Tel Aviv Univ, George S Wise Fac Life Sci, Dept Neurobiol, IL-69978 Tel Aviv, Israel.
[Basser, Peter J.] NICHHD, Sect Tissue Biophys & Biomimet, NIH, Bethesda, MD 20892 USA.
RP Assaf, Y (reprint author), Tel Aviv Univ, George S Wise Fac Life Sci, Dept Neurobiol, IL-69978 Tel Aviv, Israel.
EM asafyan@zahav.net.il
RI Basser, Peter/H-5477-2011
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development; National Institutes of
Health; The Israel Science Foundation [994/08]
FX Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (to P.J.B.); National
Institutes of Health (to P.J.B.). The Israel Science Foundation grant
no. 994/08 (to Y.A.).
NR 40
TC 167
Z9 168
U1 0
U2 15
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD MAY
PY 2009
VL 132
BP 1210
EP 1220
DI 10.1093/brain/awp042
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 444AB
UT WOS:000265950900010
PM 19403788
ER
PT J
AU Krasnova, IN
Cadet, JL
AF Krasnova, Irina N.
Cadet, Jean Lud
TI Methamphetamine toxicity and messengers of death
SO BRAIN RESEARCH REVIEWS
LA English
DT Review
DE Methamphetamine; Neurotoxicity; Dopamine; Oxidative stress; Serotonin;
Cell death
ID INDUCED DOPAMINERGIC NEUROTOXICITY; BLOOD-BRAIN-BARRIER; VESICULAR
MONOAMINE TRANSPORTER-2; INDUCED NEURONAL APOPTOSIS; DISMUTASE
TRANSGENIC MICE; NITRIC-OXIDE SYNTHASE; TYROSINE-HYDROXYLASE ACTIVITY;
MAGNETIC-RESONANCE-SPECTROSCOPY; POSITRON-EMISSION-TOMOGRAPHY;
NERVE-TERMINAL DEGENERATION
AB Methamphetamine (METH) is an illicit psychostimulant that is widely abused in the world. Several lines of evidence suggest that chronic METH abuse leads to neurodegenerative changes in the human brain. These include damage to dopamine and serotonin axons, loss of gray matter accompanied by hypertrophy of the white matter and microgliosis in different brain areas. in the present review, we summarize data on the animal models of METH neurotoxicity which include degeneration of monoaminergic terminals and neuronal apoptosis. In addition, we discuss molecular and cellular bases of METH-induced neuropathologies. The accumulated evidence indicates that multiple events, including oxidative stress, excitotoxicity, hyperthermia, neuroinflammatory responses, mitochondrial dysfunction, and endoplasmic reticulum stress converge to mediate METH-induced terminal degeneration and neuronal apoptosis. When taken together, these findings suggest that pharmacological strategies geared towards the prevention and treatment of the deleterious effects of this drug will need to attack the various pathways that form the substrates of METH toxicity, Published by Elsevier B.V
C1 [Krasnova, Irina N.; Cadet, Jean Lud] NIDA, Mol Neuropsychiat Res Branch, Intramural Res Program, NIH DHHS, Baltimore, MD 21224 USA.
RP Cadet, JL (reprint author), NIDA, Mol Neuropsychiat Res Branch, Intramural Res Program, NIH DHHS, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM jcadet@intra.nida.nih.gov
FU Intramural Research Program of the National Institute on Drug Abuse;
NIH; DHHS
FX This paper is Supported by the Intramural Research Program of the
National Institute on Drug Abuse, NIH, DHHS. The authors recognize and
thank wholeheartedly two reviewers for their helpful comments on an
original version of this review.
NR 354
TC 227
Z9 233
U1 8
U2 46
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0173
J9 BRAIN RES REV
JI Brain Res. Rev.
PD MAY
PY 2009
VL 60
IS 2
BP 379
EP 407
DI 10.1016/j.brainresrev.2009.03.002
PG 29
WC Neurosciences
SC Neurosciences & Neurology
GA 453YV
UT WOS:000266649700008
PM 19328213
ER
PT J
AU Rebbeck, TR
Antoniou, AC
Llopis, TC
Nevanlinna, H
Aittomaki, K
Simard, J
Spurdle, AB
Couch, FJ
Pereira, LHM
Greene, MH
Andrulis, IL
Pasche, B
Kaklamani, V
Hamann, U
Szabo, C
Peock, S
Cook, M
Harrington, PA
Donaldson, A
Male, AM
Gardiner, CA
Gregory, H
Side, LE
Robinson, AC
Emmerson, L
Ellis, I
Peyrat, JP
Fournier, J
Vennin, P
Adenis, C
Muller, D
Fricker, JP
Longy, M
Sinilnikova, OM
Stoppa-Lyonnet, D
Schmutzler, RK
Versmold, B
Engel, C
Meindl, A
Kast, K
Schaefer, D
Froster, UG
Chenevix-Trench, G
Easton, DF
AF Rebbeck, Timothy R.
Antoniou, Antonis C.
Caldes Llopis, Trinidad
Nevanlinna, Heli
Aittomaki, Kristiina
Simard, Jacques
Spurdle, Amanda B.
Couch, Fergus J.
Pereira, Lutecia H. Mateus
Greene, Mark H.
Andrulis, Irene L.
Pasche, Boris
Kaklamani, Virginia
Hamann, Ute
Szabo, Csilla
Peock, Susan
Cook, Margaret
Harrington, Patricia A.
Donaldson, Alan
Male, Allison M.
Gardiner, Carol Anne
Gregory, Helen
Side, Lucy E.
Robinson, Anne C.
Emmerson, Louise
Ellis, Ian
Peyrat, Jean-Philippe
Fournier, Joelle
Vennin, Philippe
Adenis, Claude
Muller, Daniele
Fricker, Jean-Pierre
Longy, Michel
Sinilnikova, Olga M.
Stoppa-Lyonnet, Dominique
Schmutzler, Rita K.
Versmold, Beatrix
Engel, Christoph
Meindl, Alfons
Kast, Karin
Schaefer, Dieter
Froster, Ursula G.
Chenevix-Trench, Georgia
Easton, Douglas F.
CA KConFab
Ontario Canc Genetics Network
Breast Canc Family Registry
EMBRACE
GEMO
TI No association of TGFB1 L10P genotypes and breast cancer risk in BRCA1
and BRCA2 mutation carriers: a multi-center cohort study
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE BRCA1; BRCA2; Risk modifiers; Hereditary cancer
ID TRANSFORMING-GROWTH-FACTOR-BETA-1 GENE; POLYMORPHISMS; BETA;
SUSCEPTIBILITY; CONSORTIUM; TGF-BETA-1; VARIANT
AB Background The transforming growth factor beta-1 gene (TGFB1) is a plausible candidate for breast cancer susceptibility. The L10P variant of TGFB1 is associated with higher circulating levels and secretion of TGF-beta, and recent large-scale studies suggest strongly that this variant is associated with breast cancer risk in the general population. Methods To evaluate whether TGFB1 L10P also modifies the risk of breast cancer in BRCA1 or BRCA2 mutation carriers, we undertook a multi-center study of 3,442 BRCA1 and 2,095 BRCA2 mutation carriers. Results We found no evidence of association between TGFB1 L10P and breast cancer risk in either BRCA1 or BRCA2 mutation carriers. The per-allele HR for the L10P variant was 1.01 (95%CI: 0.92-1.11) in BRCA1 carriers and 0.92 (95%CI: 0.81-1.04) in BRCA2 mutation carriers. Conclusions These results do not support the hypothesis that TGFB1 L10P genotypes modify the risk of breast cancer in BRCA1 or BRCA2 mutation carriers.
C1 Univ Pennsylvania Sch Med, Dept Biostatist & Epidemiol, Ctr Clin Epidemiol & Biostatist, Philadelphia, PA 19104 USA.
Hosp Clinico San Carlos HCSC, Med Oncol Branch, Martin 28040, TN, Spain.
Helsinki Univ Cent Hosp, Dept Obstet & Gynecol, Helsinki, Finland.
Helsinki Univ Cent Hosp, Dept Clin Genet, Helsinki, Finland.
[Rebbeck, Timothy R.] Univ Penn, Sch Med, Dept Epidemiol & Biostat, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Antoniou, Antonis C.; Peock, Susan; Cook, Margaret; Easton, Douglas F.; EMBRACE] Univ Cambridge, Dept Publ Hlth & Primary Care, Genet Epidemiol Unit, Canc Res UK, Cambridge, England.
[Caldes Llopis, Trinidad] HCSC, Med Oncol Branch, Madrid 28040, Spain.
[Nevanlinna, Heli] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland.
[Aittomaki, Kristiina] Univ Helsinki, Cent Hosp, Dept Clin Genet, Helsinki, Finland.
[Simard, Jacques] Univ Quebec, Ctr Hosp, Canc Genom Lab, Oncol & Mol Endocrinol Res Ctr, Quebec City, PQ, Canada.
[Simard, Jacques] Univ Laval, Quebec City, PQ, Canada.
[Spurdle, Amanda B.; Chenevix-Trench, Georgia] Queensland Inst Med Res, Brisbane, Qld 4029, Australia.
[KConFab] Peter MacCallum Canc Inst, Melbourne, Vic 3002, Australia.
[Couch, Fergus J.; Szabo, Csilla] Mayo Clin, Coll Med, Dept Lab Med & Pathol, Rochester, MN USA.
[Pereira, Lutecia H. Mateus] NCI, Lab Populat Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
[Greene, Mark H.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Andrulis, Irene L.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Fred A Litwin Ctr Canc Genet, Toronto, ON M5G 1X5, Canada.
[Andrulis, Irene L.] Canc Care Ontario, Toronto, ON, Canada.
[Ontario Canc Genetics Network] Ontario Canc Genet Network, Toronto, ON, Canada.
[Pasche, Boris; Kaklamani, Virginia] Northwestern Univ, Feinberg Sch Med, Div Hematol Oncol, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Breast Canc Family Registry] Breast Canc Family Registry, Toronto, ON, Canada.
[Hamann, Ute] Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany.
[Donaldson, Alan] St Michaels Hosp, S Western Reg Genet Serv, Cambridge, England.
[Male, Allison M.] Inst Child Hlth, Clin & Mol Genet Unit, London, England.
[Male, Allison M.] Great Ormond St Hosp Sick Children, London, England.
[Gardiner, Carol Anne] Nottingham Univ Hosp NHS Trust, Nottingham Ctr Med Genet, Nottingham, England.
[Gregory, Helen] NHS Grampian, N Scotland Reg Genet Serv, Aberdeen, Scotland.
[Gregory, Helen] Univ Aberdeen, Aberdeen, Scotland.
[Side, Lucy E.] Churchill Hosp, Oxford Reg Genet Serv, Oxford OX3 7LJ, England.
[Robinson, Anne C.] Southend Univ Hosp NHS Fdn Trust, S Essex Canc Res Network, Southend On Sea, England.
[Emmerson, Louise] Glan Clwyd Gen Hosp, All Wales Med Genet Serv, Rhyl, England.
[Ellis, Ian] Alder Hey Childrens Hosp, Dept Clin Genet, Liverpool L12 2AP, Merseyside, England.
[Peyrat, Jean-Philippe; Fournier, Joelle; Vennin, Philippe; Adenis, Claude] Ctr Oscar Lambret, F-59020 Lille, France.
[Muller, Daniele; Fricker, Jean-Pierre] Ctr Paul Strauss, Strasbourg, France.
[Longy, Michel] Inst Bergonie, Bordeaux, France.
[Sinilnikova, Olga M.; GEMO] Univ Lyon 1, Unite Mixte Genet Constitut Canc Frequents, Hosp Civils Lyon, Ctr Leon Berard,CNRS,UMR5201, F-69365 Lyon, France.
[Sinilnikova, Olga M.] Univ Lyon 1, Genet Mol Lab, CNRS, UMR5201, F-69365 Lyon, France.
[Stoppa-Lyonnet, Dominique] Inst Curie, INSERM, U509, Serv Genet Oncol, Paris, France.
[Schmutzler, Rita K.; Versmold, Beatrix] Univ Cologne, Div Mol Gynecooncol, Dept Obstet & Gynecol, Cologne, Germany.
[Engel, Christoph] Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany.
[Meindl, Alfons] Tech Univ, Dept Obstet & Gynaecol, Munich, Germany.
[Kast, Karin] Tech Univ, Dept Obstet & Gynaecol, Dresden, Germany.
[Schaefer, Dieter] Univ Frankfurt, Inst Human Genet, Frankfurt, Germany.
[Froster, Ursula G.] Univ Leipzig, Inst Human Genet, Leipzig, Germany.
RP Rebbeck, TR (reprint author), Univ Penn, Sch Med, Dept Epidemiol & Biostat, Ctr Clin Epidemiol & Biostat, 904 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM rebbeck@mail.med.upenn.edu
RI Spurdle, Amanda/A-4978-2011; Andrulis, Irene/E-7267-2013;
OI Spurdle, Amanda/0000-0003-1337-7897; Eeles,
Rosalind/0000-0002-3698-6241; Nevanlinna, Heli/0000-0002-0916-2976;
Burn, John/0000-0002-9823-2322; Evans, Gareth/0000-0002-8482-5784
FU Cancer Research - UK; [R01-CA102776]; [R01-CA112520]
FX ACA, HAP and the CIMBA data management are funded by Cancer Research -
UK. Douglas F. Easton is a Principal Research Fellow of Cancer Research
- UK. Timothy R. Rebbeck is supported by R01-CA102776. Boris Pasche is
supported by R01-CA112520.
NR 28
TC 11
Z9 11
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD MAY
PY 2009
VL 115
IS 1
BP 185
EP 192
DI 10.1007/s10549-008-0064-8
PG 8
WC Oncology
SC Oncology
GA 436UA
UT WOS:000265440400021
PM 18523885
ER
PT J
AU Basu, MK
Poliakov, E
Rogozin, IB
AF Basu, Malay Kumar
Poliakov, Eugenia
Rogozin, Igor B.
TI Domain mobility in proteins: functional and evolutionary implications
SO BRIEFINGS IN BIOINFORMATICS
LA English
DT Article
DE mobile domain; promiscuous domain; domain network; domain architecture;
domain evolution
ID MULTIDOMAIN PROTEINS; GENOME EVOLUTION; NETWORKS; GENES; DATABASE;
CLASSIFICATION; FAMILY; ORGANIZATION; SEQUENCES; BEHAVIOR
AB A substantial fraction of eukaryotic proteins contains multiple domains, some of which show a tendency to occur in diverse domain architectures and can be considered mobile (or promiscuous). These promiscuous domains are typically involved in proteinprotein interactions and play crucial roles in interaction networks, particularly those contributing to signal transduction. They also play a major role in creating diversity of protein domain architecture in the proteome. It is now apparent that promiscuity is a volatile and relatively fast-changing feature in evolution, and that only a few domains retain their promiscuity status throughout evolution. Many such domains attained their promiscuity status independently in different lineages. Only recently, we have begun to understand the diversity of protein domain architectures and the role the promiscuous domains play in evolution of this diversity. However, many of the biological mechanisms of protein domain mobility remain shrouded in mystery. In this review, we discuss our present understanding of protein domain promiscuity, its evolution and its role in cellular function.
C1 [Poliakov, Eugenia] NEI, Retinal Cell & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Rogozin, Igor B.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Basu, MK (reprint author), J Craig Venter Inst, 9704 Med Ctr Dr, Rockville, MD 20850 USA.
EM malaykbasu@gmail.com
FU National Institutes of Health/DHHS
FX We thank Kasturi Mitra, Dr Susan Gentleman and Charlie Shenitz for
carefully reading and proof-reading the manuscript. This work was
supported in part by the Intramural Research Program of the National
Institutes of Health/DHHS.
NR 60
TC 30
Z9 30
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1467-5463
J9 BRIEF BIOINFORM
JI Brief. Bioinform.
PD MAY
PY 2009
VL 10
IS 3
BP 205
EP 216
DI 10.1093/bib/bbn057
PG 12
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 437YG
UT WOS:000265522200001
PM 19151098
ER
PT J
AU Tuncbag, N
Kar, G
Keskin, O
Gursoy, A
Nussinov, R
AF Tuncbag, Nurcan
Kar, Gozde
Keskin, Ozlem
Gursoy, Attila
Nussinov, Ruth
TI A survey of available tools and web servers for analysis of
protein-protein interactions and interfaces
SO BRIEFINGS IN BIOINFORMATICS
LA English
DT Review
DE protein-protein interactions; protein-protein interfaces; binding site
prediction; docking; web servers; databases
ID MOLECULAR INTERACTION DATABASE; BINDING SITE PREDICTION; HOT-SPOTS;
SHAPE COMPLEMENTARITY; RECOGNITION SITES; QUATERNARY STRUCTURE; DOMAIN
INTERACTIONS; CRYSTAL CONTACTS; PDB STRUCTURES; 3D STRUCTURE
AB The unanimous agreement that cellular processes are (largely) governed by interactions between proteins has led to enormous community efforts culminating in overwhelming information relating to these proteins; to the regulation of their interactions, to the way in which they interact and to the function which is determined by these interactions. These data have been organized in databases and servers. However, to make these really useful, it is essential not only to be aware of these, but in particular to have a working knowledge of which tools to use for a given problem; what are the tool advantages and drawbacks; and no less important how to combine these for a particular goal since usually it is not one tool, but some combination of tool-modules that is needed. This is the goal of this review.
C1 [Nussinov, Ruth] NCI, Ctr Canc Res, Nanobiol Program, SAIC, Frederick, MD 21702 USA.
[Tuncbag, Nurcan] Koc Univ, Computat Sci & Engn Program, Istanbul, Turkey.
[Kar, Gozde] Koc Univ, Chem & Biol Engn Program, Istanbul, Turkey.
[Keskin, Ozlem] Koc Univ, Chem & Biol Engn Dept, Istanbul, Turkey.
[Keskin, Ozlem; Gursoy, Attila] Koc Univ, Ctr Computat Biol & Bioinformat, Istanbul, Turkey.
[Gursoy, Attila] Koc Univ, Dept Comp Engn, Istanbul, Turkey.
[Nussinov, Ruth] Tel Aviv Univ, Sch Med, Dept Human Genet, Tel Aviv, Israel.
RP Nussinov, R (reprint author), NCI, Ctr Canc Res, Nanobiol Program, SAIC, Bldg 469,Rm 151, Frederick, MD 21702 USA.
EM ruthnu@helix.nih.gov
RI Tuncbag, Nurcan/D-3383-2011; Gursoy, Attila/E-9565-2015
OI Gursoy, Attila/0000-0002-2297-2113
FU Turkish Academy of Sciences Distinguished Young Investigator Award;
Scientific and Technological Research Council of Turkey; National Cancer
Institute; National Institutes of Health [N01-CO-12400]; Center for
Cancer Research (partial)
FX Turkish Academy of Sciences Distinguished Young Investigator Award (to
O.K.); the Scientific and Technological Research Council of Turkey
Fellowship (to N.T.). Federal funds from the National Cancer Institute;
National Institutes of Health; (under contract number N01-CO-12400).
Intramural Research Program of the National Institutes of Health;
National Cancer Institute; Center for Cancer Research (partial).
NR 158
TC 88
Z9 89
U1 2
U2 22
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1467-5463
J9 BRIEF BIOINFORM
JI Brief. Bioinform.
PD MAY
PY 2009
VL 10
IS 3
BP 217
EP 232
DI 10.1093/bib/bbp001
PG 16
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 437YG
UT WOS:000265522200002
PM 19240123
ER
PT J
AU Kato, GJ
Wang, ZN
Machado, RF
Blackwelder, WC
Taylor, JG
Hazen, SL
AF Kato, Gregory J.
Wang, Zeneng
Machado, Roberto F.
Blackwelder, William C.
Taylor, James G.
Hazen, Stanley L.
TI Endogenous nitric oxide synthase inhibitors in sickle cell disease:
abnormal levels and correlations with pulmonary hypertension,
desaturation, haemolysis, organ dysfunction and death
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE sickle cell disease; asymmetric dimethylarginine; symmetric
dimethylarginine; arginine; pulmonary hypertension
ID STAGE RENAL-DISEASE; ASYMMETRIC DIMETHYLARGININE; RISK-FACTOR;
ENDOTHELIAL DYSFUNCTION; ARTERIAL-HYPERTENSION; ARGININE METABOLISM;
MORTALITY; HEMOGLOBIN; ADMA; BIOAVAILABILITY
AB Pulmonary hypertension (PH) in patients with sickle cell disease (SCD) is linked to intravascular haemolysis, impaired nitric oxide bioavailability, renal dysfunction, and early mortality. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthases (NOS), is associated with vascular disease in other populations. We determined the plasma concentrations for several key arginine metabolites and their relationships to clinical variables in 177 patients with SCD and 29 control subjects: ADMA, symmetric dimethylarginine (SDMA), NG-monomethyl L-arginine (L-NMMA), N-omega-hydroxy-L-arginine (NOHA), arginine and citrulline. The median ADMA was significantly higher in SCD than controls (0.94 mu mol/l vs. 0.31 mu mol/l, P < 0.001). Patients with homozygous SCD had a remarkably lower ratio of arginine to ADMA (50 mu mol/l vs. 237, P < 0.001). ADMA correlated with markers of haemolysis, low oxygen saturation and soluble adhesion molecules. PH was associated with high levels of ADMA and related metabolites. Higher ADMA level was associated with early mortality, remaining significant in a multivariate analysis. Subjects with homozygous SCD have high systemic levels of ADMA, associated with PH and early death, implicating ADMA as a functional NOS inhibitor in these patients. These defects and others converge on the nitric oxide pathway in homozygous SCD with vasculopathy.
C1 [Kato, Gregory J.; Machado, Roberto F.; Taylor, James G.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Kato, Gregory J.; Machado, Roberto F.; Blackwelder, William C.] NHLBI, Dept Crit Care Med, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Wang, Zeneng; Hazen, Stanley L.] Cleveland Clin, Dept Cell Biol, Cleveland, OH 44106 USA.
[Wang, Zeneng; Hazen, Stanley L.] Cleveland Clin, Dept Cardiovasc Med, Cleveland, OH 44106 USA.
[Wang, Zeneng; Hazen, Stanley L.] Cleveland Clin, Ctr Cardiovasc Diagnost & Prevent, Cleveland, OH 44106 USA.
RP Kato, GJ (reprint author), NHLBI, Pulm & Vasc Med Branch, NIH, 10 Ctr Dr,MSC 1476,Bldg 10 CRC,Room 5-5140, Bethesda, MD 20892 USA.
EM gkato@mail.nih.gov
RI Kato, Gregory/I-7615-2014;
OI Kato, Gregory/0000-0003-4465-3217; Taylor, James/0000-0002-4421-1809
FU National Institutes of Health [P01HL087018, P01 HL076491, P01 HL077107]
FX The authors gratefully acknowledge intellectual support from Mark
Gladwin, protocol management support by Mary K. Hall, and research
nursing support from Wynona Coles, James Nichols, and Lori Hunter. This
research was supported by intramural research funds from the National
Institutes of Health (G.J.K., R.F.M., W.C.B. and J.G.T.) and by National
Institutes of Health grants P01HL087018, P01 HL076491 and P01 HL077107
(S.L.H.).
NR 43
TC 44
Z9 45
U1 1
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD MAY
PY 2009
VL 145
IS 4
BP 506
EP 513
DI 10.1111/j.1365-2141.2009.07658.x
PG 8
WC Hematology
SC Hematology
GA 437IP
UT WOS:000265480900007
PM 19344390
ER
PT J
AU Patel, KV
Longo, DL
Ershler, WB
Yu, BB
Semba, RD
Ferrucci, L
Guralnik, JM
AF Patel, Kushang V.
Longo, Dan L.
Ershler, William B.
Yu, Binbing
Semba, Richard D.
Ferrucci, Luigi
Guralnik, Jack M.
TI Haemoglobin concentration and the risk of death in older adults:
differences by race/ethnicity in the NHANES III follow-up
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE anaemia; haemoglobin concentration; race; ethnicity; ageing; National
Health and Nutrition Examination Survey
ID IRON-DEFICIENCY; PHYSICAL PERFORMANCE; SERUM CREATININE;
NATIONAL-HEALTH; UNITED-STATES; ANEMIA; MORTALITY; NUTRITION; BLACKS;
WHITES
AB Mildly low haemoglobin concentration is associated with increased mortality in older adults. However, this relationship has not been well characterized in racial/ethnic minorities. Therefore, this study determined the haemoglobin threshold below which risk of death is significantly increased in older non-Hispanic whites, non-Hispanic blacks, and Mexican Americans. Data on 4089 participants of the 1988-94 US National Health and Nutrition Examination Survey who were >= 65 years of age were analyzed with mortality follow-up through December 31, 2000. Mean haemoglobin in non-Hispanic whites (n = 2686) and Mexican Americans (n = 663) was 140 g/l, while in non-Hispanic blacks (n = 740) the mean was 10 g/l lower. A total of 1944 (47.5%) participants died. Among non-Hispanic whites and Mexican Americans, age- and sex-adjusted models showed that the haemoglobin thresholds below which mortality risk was significantly increased were 4 and 2 g/l respectively, above the World Health Organization (WHO) cut-off points for anaemia. In contrast, the threshold for non-Hispanic blacks was 7 g/l below the WHO criteria. Similar threshold effects were observed when analyzing haemoglobin in categories and adjusting for multiple confounders. In conclusion, the haemoglobin threshold below which mortality rises significantly is a full g/dl lower in non-Hispanic blacks than in non-Hispanic whites and Mexican Americans.
C1 [Patel, Kushang V.; Yu, Binbing; Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Longo, Dan L.; Ershler, William B.; Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Semba, Richard D.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RP Patel, KV (reprint author), NIA, Lab Epidemiol Demog & Biometry, 7201 Wisconsin Ave,Gateway Bldg,Suite 3C309, Bethesda, MD 20892 USA.
EM patelku@mail.nih.gov
FU US National Institute on Aging; National Institutes of Health
FX This study was supported by the Intramural Research Program of the US
National Institute on Aging, National Institutes of Health.
NR 40
TC 28
Z9 29
U1 2
U2 3
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD MAY
PY 2009
VL 145
IS 4
BP 514
EP 523
DI 10.1111/j.1365-2141.2009.07659.x
PG 10
WC Hematology
SC Hematology
GA 437IP
UT WOS:000265480900008
PM 19344387
ER
PT J
AU Ferrada, C
Moreno, E
Casado, V
Bongers, G
Cortes, A
Mallol, J
Canela, EI
Leurs, R
Ferre, S
Lluis, C
Franco, R
AF Ferrada, Carla
Moreno, Estefania
Casado, Vicent
Bongers, Gerold
Cortes, Antoni
Mallol, Josefa
Canela, Enric I.
Leurs, Rob
Ferre, Sergi
Lluis, Carme
Franco, Rafael
TI Marked changes in signal transduction upon heteromerization of dopamine
D-1 and histamine H-3 receptors
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE dopaminergic transmission; histaminergic transmission; receptor
heteromers; signal transduction; dopamine D-1 receptor; histamine H-3
receptor; MAPK pathway; bioluminescent resonance energy transfer
ID MC NEUROBLASTOMA-CELLS; PROTEIN-COUPLED RECEPTORS; RAT STRIATAL SLICES;
ADENOSINE RECEPTOR; OPIOID RECEPTORS; DRUG DISCOVERY; ACTIVATION; BRAIN;
D1; HETERODIMERIZATION
AB Functional interactions between the G protein-coupled dopamine D-1 and histamine H-3 receptors have been described in the brain. In the present study we investigated the existence of D-1-H-3 receptor heteromers and their biochemical characteristics.
D-1-H-3 receptor heteromerization was studied in mammalian transfected cells with Bioluminescence Resonance Energy Transfer and binding assays. Furthermore, signalling through mitogen-activated protein kinase (MAPK) and adenylyl cyclase pathways was studied in co-transfected cells and compared with cells transfected with either D-1 or H-3 receptors.
Bioluminescence Resonance Energy Transfer and binding assays confirmed that D-1 and H-3 receptors can heteromerize. Activation of histamine H-3 receptors did not lead to signalling towards the MAPK pathway unless dopamine D-1 receptors were co-expressed. Also, dopamine D-1 receptors, usually coupled to G(s) proteins and leading to increases in cAMP, did not couple to G(s) but to G(i) in co-transfected cells. Furthermore, signalling via each receptor was blocked not only by a selective antagonist but also by an antagonist of the partner receptor.
D-1-H-3 receptor heteromers constitute unique devices that can direct dopaminergic and histaminergic signalling towards the MAPK pathway in a G(s)-independent and G(i)-dependent manner. An antagonist of one of the receptor units in the D-1-H-3 receptor heteromer can induce conformational changes in the other receptor unit and block specific signals originating in the heteromer. This gives rise to unsuspected therapeutic potentials for G protein-coupled receptor antagonists.
C1 [Ferrada, Carla; Moreno, Estefania; Casado, Vicent; Cortes, Antoni; Mallol, Josefa; Canela, Enric I.; Lluis, Carme; Franco, Rafael] Univ Barcelona, Mol Neurobiol Unit, Dept Biochem & Mol Biol, Sch Biol,IDIBAPS,CIBERNED, Barcelona, Spain.
[Bongers, Gerold; Leurs, Rob] Vrije Univ Amsterdam, VU Drug Discovery Ctr, Div Med Chem, Leiden Amsterdam Ctr Drug Res,Fac Sci, Amsterdam, Netherlands.
[Franco, Rafael] Univ Navarra, Ctr Invest Med Aplicada, Pamplona 31008, Spain.
[Ferre, Sergi] NIDA, IRP, NIH, DHHS, Baltimore, MD USA.
RP Franco, R (reprint author), Univ Navarra, Ctr Invest Med Aplicada, Ave Pio 12 55, Pamplona 31008, Spain.
EM rfranco@unav.es
RI Bongers, Gerold/B-6503-2013; Canela, Enric I./M-8726-2013; Ferre,
Sergi/K-6115-2014; Franco, Rafael/C-3694-2015; Casado,
Vicent/K-1660-2014
OI Bongers, Gerold/0000-0002-3187-120X; Canela, Enric
I./0000-0003-4992-7440; Ferre, Sergi/0000-0002-1747-1779; Moreno,
Estefania/0000-0002-2491-5753; Casado, Vicent/0000-0002-1764-3825;
Franco, Rafael/0000-0003-2549-4919;
FU Spanish Ministerio de Ciencia y Tecnologia [SAF2005-00170,
SAF2006-05481]; Fundacio La Marato de TV3 [060110]; National Institute
on Drug Abuse
FX This work was supported by Grants from Spanish Ministerio de Ciencia y
Tecnologia (SAF2005-00170 to E.I.C. SAF2006-05481 to R.F), Grant 060110
from Fundacio La Marato de TV3 (RF) and by the intramural funds of the
National Institute on Drug Abuse (SF). We acknowledge Dr Timothy A
Esbenshade (Abbott Laboratories) for the kind gift of
[3H]-A-349821. Sergi FerrE is employed by NIDA-NIH. No claim
to US government work.
NR 60
TC 60
Z9 61
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1188
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD MAY
PY 2009
VL 157
IS 1
BP 64
EP 75
DI 10.1111/j.1476-5381.2009.00152.x
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 430ZV
UT WOS:000265032000008
PM 19413572
ER
PT J
AU De Angelis, R
Tavilla, A
Verdecchia, A
Scoppa, S
Hachey, M
Feuer, EJ
Mariotto, AB
AF De Angelis, Roberta
Tavilla, Andrea
Verdecchia, Arduino
Scoppa, Steve
Hachey, Mark
Feuer, Eric J.
Mariotto, Angela B.
TI Breast Cancer Survivors in the United States Geographic Variability and
Time Trends, 2005-2015
SO CANCER
LA English
DT Article
DE breast neoplasms; prevalence; registries; forecasting; regional health
planning
ID CHRONIC DISEASE MORBIDITY; REGISTRY DATA; PREVALENCE; MORTALITY
AB BACKGROUND: Breast cancer continues to place a significant burden on the healthcare system. Regional prevalence measures are instrumental in the development of cancer control policies. Very few population-based cancer registries are able to provided local, long-term incidence and follow-up information that permits the direct calculation of prevalence. Model-based prevalence estimates are an alternative when this information is lacking or incomplete. The current work represents a comprehensive collection of female breast cancer prevalence from 2005 to 2015 in the United States and the District of Columbia (DC). METHODS: Breast cancer prevalence estimates were derived from state-specific cancer mortality and survival data using a statistical package called the Mortality-incidence Analysis Model or MIAMOD. Cancer survival models were derived from the Surveillance, Epidemiology, and End Results Program data and were adjusted to represent state-specific survival. Comparisons with reported incidence for 39 states and DC had validated estimates. RESULTS: By the year 2010, 2.9 million breast cancer survivors are predicted in the US, equaling 1.85% of the female population. Large variability in prevalent percentages was reported between states, ranging from 1.4% to 2.4% in 2010. Geographic variability was reduced when calculating age-standardized prevalence proportions or cancer survivors by disease duration, including 0 to 2 years and 2 to 5 years. The residual variability in age-adjusted prevalence was explained primarily by the state-specific, age-adjusted breast cancer incidence rates. State-specific breast cancer survivors are expected to increase from 16% to 51% in the decennium from 2005 to 2015 and by 31% at the national level. CONCLUSIONS: To the authors' knowledge, the current study is the first to provide systematic estimations of breast cancer prevalence in all US states through 2015. The estimated levels and time trends were consistent with the available population-based data on breast cancer incidence, prevalence, and population aging. Cancer 2009;115:1954-66. (C) 2009 American Cancer Society.
C1 [De Angelis, Roberta; Tavilla, Andrea; Verdecchia, Arduino] Italian Natl Inst Hlth, Natl Ctr Epidemiol, Rome, Italy.
[Scoppa, Steve; Hachey, Mark] Informat Management Serv Inc, Silver Spring, MD USA.
[Feuer, Eric J.; Mariotto, Angela B.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP De Angelis, R (reprint author), Ist Super Sanita, Ctr Nazl Epidemiol, Viale Regina Elena 299, I-00161 Rome, Italy.
EM roberta.deangelis@iss.it
FU National Institutes of Health [263-MQ-514300, 263-MQ-320101]
FX Supported by grants 263-MQ-514300 (to A.T.) and 263-MQ-320101 (to A.T.)
from the National Institutes of Health.
NR 22
TC 31
Z9 33
U1 0
U2 3
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD MAY 1
PY 2009
VL 115
IS 9
BP 1954
EP 1966
DI 10.1002/cncr.24217
PG 13
WC Oncology
SC Oncology
GA 435OZ
UT WOS:000265354500020
PM 19248047
ER
PT J
AU Newcomb, PA
Chia, VM
Hampton, JM
Doria-Rose, VP
Dietz, AT
AF Newcomb, Polly A.
Chia, Victoria M.
Hampton, John M.
Doria-Rose, V. Paul
Dietz, Amy Trentham
TI Hormone therapy in relation to survival from large bowel cancer
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Hormone therapy; Colorectal cancer; Mortality
ID ESTROGEN PLUS PROGESTIN; RANDOMIZED CONTROLLED-TRIAL; COLORECTAL-CANCER;
REPLACEMENT THERAPY; POSTMENOPAUSAL WOMEN; COLON-CANCER; BODY-MASS;
RISK; DIAGNOSIS; MORTALITY
AB Epidemiologic studies of hormone therapy (HT) and colorectal cancer incidence consistently show an inverse association; however, few studies have considered prediagnostic use of HT on mortality among colorectal cancer patients. We evaluated the relationship of HT and survival among a population-based cohort of women with large bowel cancer. Cases (n = 1,297) were newly diagnosed with invasive cancer of the colon or rectum, aged 40-74 years at diagnosis, who were identified by Wisconsin's statewide registry (1988-1991; 1997-2001) for two case-control studies. Information on HT use and other colorectal cancer risk factors was collected by standardized interview. There were 507 deaths (274 of these attributable to colorectal cancer) over 8.4 years of follow-up through December 2005. Hormone use was not associated with colorectal cancer mortality (adjusted hazard rate ratio = 1.09, confidence interval = 0.81-1.47). Colorectal cancer specific mortality was not associated with HT when considered separately by preparation type. Stage did not modify this relationship. Long-term HT was weakly positively associated with increased mortality after diagnosis of proximal colon, but not distal colon cancer. Because we detected no differences in survival among users of HT compared to non-users, the results suggest that HT use may affect only the incidence of some colorectal tumors.
C1 [Newcomb, Polly A.; Chia, Victoria M.; Doria-Rose, V. Paul] Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA 98109 USA.
[Newcomb, Polly A.; Hampton, John M.; Dietz, Amy Trentham] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Madison, WI USA.
[Doria-Rose, V. Paul] NCI, Biometry Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
RP Newcomb, PA (reprint author), Fred Hutchinson Canc Res Ctr, Canc Prevent Program, 1100 Fairview Ave N,Mailstop M4-B402, Seattle, WA 98109 USA.
EM pnewcomb@fhcrc.org
OI Doria-Rose, Vincent/0000-0002-8802-5143
FU Alcoholic Beverage Medical Research Foundation and National Institute of
Health [CA47147]
FX Financial support: This work was supported in part by the Alcoholic
Beverage Medical Research Foundation and National Institute of Health
grant CA47147.
NR 28
TC 5
Z9 5
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD MAY
PY 2009
VL 20
IS 4
BP 409
EP 416
DI 10.1007/s10552-008-9255-1
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 430VV
UT WOS:000265018900001
PM 18998219
ER
PT J
AU Clegg, LX
Reichman, ME
Miller, BA
Hankey, BF
Singh, GK
Lin, YD
Goodman, MT
Lynch, CF
Schwartz, SM
Chen, VW
Bernstein, L
Gomez, SL
Graff, JJ
Lin, CC
Johnson, NJ
Edwards, BK
AF Clegg, Limin X.
Reichman, Marsha E.
Miller, Barry A.
Hankey, Benjamin F.
Singh, Gopal K.
Lin, Yi Dan
Goodman, Marc T.
Lynch, Charles F.
Schwartz, Stephen M.
Chen, Vivien W.
Bernstein, Leslie
Gomez, Scarlett L.
Graff, John J.
Lin, Charles C.
Johnson, Norman J.
Edwards, Brenda K.
TI Impact of socioeconomic status on cancer incidence and stage at
diagnosis: selected findings from the surveillance, epidemiology, and
end results: National Longitudinal Mortality Study
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE SEER; NLMS; Cancer incidence; Stage; Education; Income; Poverty;
Unemployment; SES; Race/ethnicity; Rural/urban; Health disparities;
Record linkage
ID BREAST-CANCER; UNITED-STATES; CERVICAL-CANCER; SOCIAL-CLASS;
RACIAL-DIFFERENCES; COLORECTAL-CANCER; PROSTATE-CANCER; RESULTS PROGRAM;
DEATH INDEX; US WOMEN
AB Population-based cancer registry data from the Surveillance, Epidemiology, and End Results (SEER) Program at the National Cancer Institute (NCI) are mainly based on medical records and administrative information. Individual-level socioeconomic data are not routinely reported by cancer registries in the United States because they are not available in patient hospital records. The U.S. representative National Longitudinal Mortality Study (NLMS) data provide self-reported, detailed demographic and socioeconomic data from the Social and Economic Supplement to the Census Bureau's Current Population Survey (CPS). In 1999, the NCI initiated the SEER-NLMS study, linking the population-based SEER cancer registry data to NLMS data. The SEER-NLMS data provide a new unique research resource that is valuable for health disparity research on cancer burden. We describe the design, methods, and limitations of this data set. We also present findings on cancer-related health disparities according to individual-level socioeconomic status (SES) and demographic characteristics for all cancers combined and for cancers of the lung, breast, prostate, cervix, and melanoma.
Records of cancer patients diagnosed in 1973-2001 when residing 1 of 11 SEER registries were linked with 26 NLMS cohorts. The total number of SEER matched cancer patients that were also members of an NLMS cohort was 26,844. Of these 26,844 matched patients, 11,464 were included in the incidence analyses and 15,357 in the late-stage diagnosis analyses. Matched patients (used in the incidence analyses) and unmatched patients were compared by age group, sex, race, ethnicity, residence area, year of diagnosis, and cancer anatomic site. Cohort-based age-adjusted cancer incidence rates were computed. The impact of socioeconomic status on cancer incidence and stage of diagnosis was evaluated.
Men and women with less than a high school education had elevated lung cancer rate ratios of 3.01 and 2.02, respectively, relative to their college educated counterparts. Those with family annual incomes less than $12,500 had incidence rates that were more than 1.7 times the lung cancer incidence rate of those with incomes $50,000 or higher. Lower income was also associated with a statistically significantly increased risk of distant-stage breast cancer among women and distant-stage prostate cancer among men.
Socioeconomic patterns in incidence varied for specific cancers, while such patterns for stage were generally consistent across cancers, with late-stage diagnoses being associated with lower SES. These findings illustrate the potential for analyzing disparities in cancer outcomes according to a variety of individual-level socioeconomic, demographic, and health care characteristics, as well as by area measures available in the linked database.
C1 [Clegg, Limin X.] US Dept Vet Affairs, Off Healthcare Inspect, Off Inspector Gen, Washington, DC 20420 USA.
[Reichman, Marsha E.; Miller, Barry A.; Edwards, Brenda K.] NCI, Surveillance Res Program, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Hankey, Benjamin F.] Informat Management Serv Inc, Silver Spring, MD USA.
[Singh, Gopal K.] US Hlth Resources & Serv Adm, Rockville, MD 20857 USA.
[Lin, Yi Dan] Monash Univ, Sch Med, Melbourne, Vic 3004, Australia.
[Goodman, Marc T.] Univ Hawaii, Canc Res Ctr, Honolulu, HI 96813 USA.
[Lynch, Charles F.] Univ Iowa, State Hlth Registry Iowa, Iowa City, IA USA.
[Schwartz, Stephen M.] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Chen, Vivien W.] LSU Sch Publ Hlth, Louisiana Tumor Registry, New Orleans, LA USA.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Duarte, CA 91010 USA.
[Gomez, Scarlett L.] No Calif Canc Ctr, Fremont, CA USA.
[Graff, John J.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Lin, Charles C.; Johnson, Norman J.] US Bur Census, Suitland, MD USA.
RP Clegg, LX (reprint author), US Dept Vet Affairs, Off Healthcare Inspect, Off Inspector Gen, 54AA,810 Vermont Ave NW, Washington, DC 20420 USA.
EM Lin.Clegg@va.gov
FU National Cancer Institute
FX We thank Marie-Josephe Horner, epidemiologist from the National Cancer
Institute, for technical and editorial assistance in the preparation of
this manuscript.
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PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD MAY
PY 2009
VL 20
IS 4
BP 417
EP 435
DI 10.1007/s10552-008-9256-0
PG 19
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 430VV
UT WOS:000265018900002
PM 19002764
ER
PT J
AU Berndt, SI
Huang, WY
Yeager, M
Weissfeld, JL
Chanock, SJ
Hayes, RB
AF Berndt, Sonja I.
Huang, Wen-Yi
Yeager, Meredith
Weissfeld, Joel L.
Chanock, Stephen J.
Hayes, Richard B.
TI Genetic variants in frizzled-related protein (FRZB) and the risk of
colorectal neoplasia
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Colorectal adenoma; Colorectal cancer; Polymorphism; Wnt signaling
pathway
ID CANCER
AB The Wnt/APC/beta-catenin signaling pathway, which includes frizzled-related protein (FRZB), plays a critical role in the development of colorectal cancer, and recent evidence suggests that the functional polymorphism, FRZB Arg324Gly, may be associated with risk for this disease. To determine if this finding could be replicated, we investigated the association between two FRZB polymorphisms (Arg324Gly and Arg200Trp) and the risk of colorectal adenoma and cancer in nested case-control studies.
Participants consisted of 1,709 adenoma cases, 620 cancer cases, and 1,849 controls within the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CI) for the associations with colorectal neoplasia.
No association was observed for either polymorphism or any haplotypes with colorectal adenoma or colorectal cancer (p > 0.05 for all).
Our study does not support the previously observed association between the FRZB 324Gly variant and colorectal cancer risk. However, further study of additional genetic variants within this pathway is still warranted, given the important role of the Wnt signaling pathway in colorectal carcinogenesis.
C1 [Berndt, Sonja I.; Huang, Wen-Yi; Yeager, Meredith; Chanock, Stephen J.; Hayes, Richard B.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Weissfeld, Joel L.] Univ Pittsburgh, Pittsburgh, PA USA.
[Yeager, Meredith] NCI, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Berndt, SI (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 8116,MSC 7240, Bethesda, MD 20892 USA.
EM berndts@mail.nih.gov
OI Hayes, Richard/0000-0002-0918-661X
FU Intramural Research Program of the Division of Cancer Epidemiology and
Genetics; National Cancer Institute; National Institutes of Health (NIH)
FX This study was supported by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute,
acknowledge the study participants for donating their time and making
this study possible.National Institutes of Health (NIH). The authors
thank Drs. Christine Berg and Philip Prorok, Division of Cancer
Prevention, NCI, the screening center investigators and staff of the
PLCO Cancer Screening Trial, Mr. Thomas Riley and staff at Information
Management Services, Inc., and Ms. Barbara O'Brien and staff at Westat,
Inc. for their contributions to the PLCO Cancer Screening Trial.
Finally, we
NR 9
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U1 0
U2 0
PU SPRINGER
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PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD MAY
PY 2009
VL 20
IS 4
BP 487
EP 490
DI 10.1007/s10552-008-9274-y
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 430VV
UT WOS:000265018900007
PM 19067193
ER
PT J
AU Olson, SH
Chen, C
De Vivo, I
Doherty, JA
Hartmuller, V
Horn-Ross, PL
Lacey, JV
Lynch, SM
Sansbury, L
Setiawan, VW
Schouten, LJ
Shu, XO
AF Olson, Sara H.
Chen, Chu
De Vivo, Immaculata
Doherty, Jennifer A.
Hartmuller, Virginia
Horn-Ross, Pamela L.
Lacey, James V., Jr.
Lynch, Shannon M.
Sansbury, Leah
Setiawan, V. Wendy
Schouten, Leo J.
Shu, Xiao Ou
TI Maximizing resources to study an uncommon cancer: E2C2-Epidemiology of
Endometrial Cancer Consortium
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Endometrial cancer; Epidemiology
ID GENETIC POLYMORPHISMS; POSTMENOPAUSAL WOMEN; MULTIETHNIC COHORT;
STEROID-HORMONES; RISK; CYP19A1; ASSOCIATION; CONSUMPTION; SOY
AB Endometrial cancer affects more than 40,000 women a year in the U.S. While the association of this disease with high body mass index and sex steroid hormones is well known, there are many questions about etiology that have not been resolved. Little is known about the genetic basis for risk associated with hormones or obesity, other common genetic factors associated with risk, or gene-environment interactions. E2C2, the Epidemiology of Endometrial Cancer Consortium, was formed in 2006 to provide a collaborative environment for addressing these questions by pooling data from existing studies. This allows for investigations of uncommon risk factors, risk for rare histologic subtypes, and associations within strata that cannot be achieved in individual studies. This report describes the establishment of the consortium, ongoing projects that demonstrate the advantages of collaborative efforts, and challenges faced. Overall, the consortium promises to provide an important means of furthering our knowledge about this cancer.
C1 [Olson, Sara H.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10065 USA.
[Chen, Chu; Doherty, Jennifer A.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA 98104 USA.
[Chen, Chu] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA.
[Chen, Chu] Univ Washington, Dept Otolaryngol Head & Neck Surg, Sch Med, Seattle, WA 98195 USA.
[De Vivo, Immaculata] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA.
[De Vivo, Immaculata] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Hartmuller, Virginia; Lynch, Shannon M.; Sansbury, Leah] NCI, Epidemiol & Genet Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Horn-Ross, Pamela L.] No Calif Canc Ctr, Fremont, CA USA.
[Lacey, James V., Jr.] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Setiawan, V. Wendy] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Schouten, Leo J.] Maastricht Univ, Sch Oncol & Dev Biol, GROW, Dept Epidemiol, Maastricht, Netherlands.
[Shu, Xiao Ou] Vanderbilt Inst Med & Publ Hlth, Vanderbilt Epidemiol Ctr, Nashville, TN USA.
[Shu, Xiao Ou] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN USA.
[Shu, Xiao Ou] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
RP Olson, SH (reprint author), Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, 307 E 63 St, New York, NY 10065 USA.
EM olsons@mskcc.org
RI Schouten, Leo/G-3713-2012
FU NCI NIH HHS [R01 CA092585, K05 CA092002, K05 CA092002-04, N01 PC035137,
P01 CA033619, P01 CA033619-209003, P01 CA077596, P01 CA077596-03, P01
CA087969, P01 CA087969-10, P30 CA016087, P30 CA016087-29S2, R01
CA047749, R01 CA047749-06, R01 CA049449, R01 CA049449-19, R01 CA058598,
R01 CA058598-10, R01 CA063446, R01 CA063446-04, R01 CA063464, R01
CA063464-10, R01 CA070867, R01 CA070867-11, R01 CA074877-04, R01
CA075977, R01 CA075977-04, R01 CA077398, R01 CA083918, R01 CA083918-05,
R01 CA087538, R01 CA087538-05, R01 CA092585-05, R01 CA098346, R01
CA098346-05, R01 CA098661, R01 CA098661-05, R01 CA105212, R01
CA105212-04, R03 CA080636, R03 CA080636-01, R35 CA039779, R35
CA039779-14, R37 CA054281, R37 CA054281-17]; NICHD NIH HHS [N01
HD923166]; NIEHS NIH HHS [P30 ES000260, P30 ES000260-46]
NR 20
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U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD MAY
PY 2009
VL 20
IS 4
BP 491
EP 496
DI 10.1007/s10552-008-9290-y
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 430VV
UT WOS:000265018900008
PM 19132539
ER
PT J
AU Sen, M
Tosca, PJ
Zwayer, C
Ryan, MJ
Johnson, JD
Knostman, KAB
Giclas, PC
Peggins, JO
Tomaszewski, JE
McMurray, TP
Li, CY
Leibowitz, MS
Ferris, RL
Gooding, WE
Thomas, SM
Johnson, DE
Grandis, JR
AF Sen, Malabika
Tosca, Patricia J.
Zwayer, Christa
Ryan, Michael J.
Johnson, Jerry D.
Knostman, Katherine A. B.
Giclas, Patricia C.
Peggins, James O.
Tomaszewski, Joseph E.
McMurray, Timothy P.
Li, Changyou
Leibowitz, Michael S.
Ferris, Robert L.
Gooding, William E.
Thomas, Sufi M.
Johnson, Daniel E.
Grandis, Jennifer R.
TI Lack of toxicity of a STAT3 decoy oligonucleotide
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE STAT3 decoy; Toxicity
ID TRANSCRIPTION FACTOR DECOY; IN-VIVO; CANCER-THERAPY; NECK-CANCER;
CONSTITUTIVE ACTIVATION; SIGNAL TRANSDUCER; PROSTATE-CANCER;
BREAST-CANCER; INHIBITION; APOPTOSIS
AB Background STAT3 overexpression has been detected in several cancers including head and neck squamous cell carcinoma (HNSCC). Previous studies using intratumoral administration of a STAT3 decoy oligonucleotide that abrogates STAT3- mediated gene transcription in preclinical cancer models have demonstrated antitumor efficacy. This study was conducted to observe the toxicity and biologic effects of the STAT3 decoy in a non-human primate model, in anticipation of initiating a clinical trial in HNSCC patients.
Methods Three study groups (two monkeys/sex/group) were administered a single intramuscular injection of low dose of STAT3 decoy (0.8 mg total dose/monkey), high dose of STAT3 decoy (3.2 mg total dose/monkey) or vehicle control (PBS alone) on day 1 and necropsies were performed on days 2 and 15 (one monkey/sex/group/day). Low and high doses of the decoy were administered in the muscle in a volume of 0.9 ml. Tissue and blood were harvested for toxicology and biologic analyses.
Results Upon observation, the STAT3 decoy-treated animals exhibited behavior that was similar to the vehicle control group. Individual animal body weights remained within 1% of pretreatment weights throughout the study. Hematological parameters were not significantly different between the control and the treatment groups. Clinical chemistry fluctuations were considered within normal limits and were not attributed to the STAT3 decoy. Assessment of complement activation breakdown product (Bb) levels demonstrated no activation of the alternative pathway of complement in any animal at any dose level. At necropsy, there were no gross or microscopic findings attributed to STAT3 decoy in any organ examined. STAT3 target gene expression at the injection site revealed decreased Bcl-X-L and cyclin D1 expression levels in the animals treated with high dose of STAT3 decoy compared to the animals injected with low dose of STAT3 decoy or the vehicle as control.
Conclusion Based on these findings, the no-observablead-verse-effect-level ( NOAEL) was greater than 3.2 mg/kg when administered as a single dose to male and female Cynomolgus monkeys. Plans are underway to test the safety and biologic effects of intratumoral administration of the STAT3 decoy in HNSCC patients.
C1 [Grandis, Jennifer R.] Univ Pittsburgh, Inst Eye & Ear, Pittsburgh, PA 15213 USA.
[Sen, Malabika; McMurray, Timothy P.; Leibowitz, Michael S.; Ferris, Robert L.; Thomas, Sufi M.; Grandis, Jennifer R.] Univ Pittsburgh, Dept Otolaryngol, Pittsburgh, PA 15213 USA.
[Johnson, Daniel E.; Grandis, Jennifer R.] Univ Pittsburgh, Dept Pharmacol, Pittsburgh, PA 15213 USA.
[Tosca, Patricia J.; Zwayer, Christa; Ryan, Michael J.; Johnson, Jerry D.; Knostman, Katherine A. B.] Battelle Toxicol, Columbus, OH 43201 USA.
[Leibowitz, Michael S.; Ferris, Robert L.] Univ Pittsburgh, Dept Immunol, Pittsburgh, PA 15213 USA.
[Gooding, William E.] Univ Pittsburgh, Dept Biostat, Pittsburgh, PA 15213 USA.
[Li, Changyou; Johnson, Daniel E.] Univ Pittsburgh, Dept Med, Pittsburgh, PA 15213 USA.
[Giclas, Patricia C.] Natl Jewish Med & Res Ctr, Denver, CO 80206 USA.
[Peggins, James O.; Tomaszewski, Joseph E.] NCI, Bethesda, MD 20892 USA.
[Sen, Malabika; Tosca, Patricia J.; Zwayer, Christa; Ryan, Michael J.; Johnson, Jerry D.; Knostman, Katherine A. B.; Giclas, Patricia C.; Peggins, James O.; Tomaszewski, Joseph E.; McMurray, Timothy P.; Li, Changyou; Leibowitz, Michael S.; Ferris, Robert L.; Gooding, William E.; Thomas, Sufi M.; Johnson, Daniel E.; Grandis, Jennifer R.] Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15213 USA.
RP Grandis, JR (reprint author), Univ Pittsburgh, Inst Eye & Ear, Suite 500,200 Lothrop St, Pittsburgh, PA 15213 USA.
EM jgrandis@pitt.edu
OI Thomas, Sufi/0000-0001-5370-0842
FU NCI RAID [P50 CA097190, R01 CA101840-01]
FX This work was supported by the NCI RAID program, P50 CA097190, and R01
CA101840-01 (to JRG).
NR 31
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U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD MAY
PY 2009
VL 63
IS 6
BP 983
EP 995
DI 10.1007/s00280-008-0823-6
PG 13
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 434EF
UT WOS:000265257300002
PM 18766340
ER
PT J
AU Lin, CC
Calvo, E
Papadopoulos, KP
Patnaik, A
Sarantopoulos, J
Mita, AC
Preston, GG
Mita, MM
Rodon, J
Mays, T
Yeh, IT
O'Rourke, P
Takimoto, CH
Dancey, JE
Chen, H
Tolcher, AW
AF Lin, Chia-Chi
Calvo, Emiliano
Papadopoulos, Kyriakos P.
Patnaik, Amita
Sarantopoulos, John
Mita, Alain C.
Preston, Glenn G.
Mita, Monica M.
Rodon, Jordi
Mays, Theresa
Yeh, I-Tien
O'Rourke, Pat
Takimoto, Chris H.
Dancey, Janet E.
Chen, Helen
Tolcher, Anthony W.
TI Phase I study of cetuximab, erlotinib, and bevacizumab in patients with
advanced solid tumors
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article; Proceedings Paper
CT 18th AACR/EORTC/NCI International Conference on Molecular Targets and
Cancer Therapeutics
CY NOV 07-10, 2006
CL Prague, CZECH REPUBLIC
SP AACR, EORTC, NCI
DE Epidermal growth factor receptor; Vascular endothelial growth factor;
Renal cell carcinoma
ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE INHIBITOR; CELL LUNG-CANCER;
MONOCLONAL-ANTIBODY; COLORECTAL-CANCER; GEFITINIB; COMBINATION;
MUTATIONS; TRIAL; CARCINOMA
AB Background Complex interrelationships exist between the epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) receptor pathways. EGFR activation elicits cell proliferation and increased VEGF expression. To maximally inhibit EGFR and then downstream VEGF activity, this phase I study was initiated to determine the maximum tolerated dose (MTD) of erlotinib with fixed-dose cetuximab, and then combine with bevacizumab in patients with advanced malignancies.
Patients and methods Patients with advanced malignancies likely to express EGFR were treated with a full dose of cetuximab intravenous weekly, combined with various doses of oral erlotinib daily (Part 1). Once the MTD was determined in Part 1, escalating doses of bevacizumab were administered intravenously biweekly (Part 2).
Results Forty patients were enrolled and received 155 courses over four dose levels. In Part 1, dose-limiting grade 3 rash occurred in two patients administered with erlotinib at 100 mg daily, and the MTD of erlotinib for this combination was 50 mg daily with standard-dose cetuximab (11 patients treated). Other adverse events included rash, diarrhea, fatigue, and hypomagnesemia. In Part 2, bevacizumab at 10 mg/kg intravenous every 2 weeks was safely added, with additional nondose-limiting headache, proteinuria, and hypertension. There was one partial response in a patient with renal cell carcinoma. Durable stable disease was observed in five patients for 6-11 months.
Conclusions The MTD for Part 1 was 50 mg daily of erlotinib combined with standard cetuximab. Bevacizumab at 10 mg/kg biweekly can be safely administered with the MTD for erlotinib and cetuximab combination.
C1 [Lin, Chia-Chi; Calvo, Emiliano; Papadopoulos, Kyriakos P.; Patnaik, Amita; Sarantopoulos, John; Mita, Alain C.; Mita, Monica M.; Rodon, Jordi; Mays, Theresa; O'Rourke, Pat; Takimoto, Chris H.; Tolcher, Anthony W.] Canc Therapy & Res Ctr S Texas, Inst Drug Dev, San Antonio, TX 78229 USA.
[Preston, Glenn G.] Brooke Army Med Ctr, Ft Sam Houston, TX 78234 USA.
[Yeh, I-Tien] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Dancey, Janet E.; Chen, Helen] NCI, Canc Therapy Evaluat Program, Rockville, MD USA.
RP Tolcher, AW (reprint author), S Texas Accelerated Res Therapeut, 4319 Med Dr,Suite 205, San Antonio, TX 78229 USA.
EM atolcher@start.stoh.com
FU NCI NIH HHS [U01-CA069853]
NR 36
TC 10
Z9 12
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD MAY
PY 2009
VL 63
IS 6
BP 1065
EP 1071
DI 10.1007/s00280-008-0811-x
PG 7
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 434EF
UT WOS:000265257300009
PM 18795291
ER
PT J
AU Schelman, WR
Morgan-Meadows, S
Marnocha, R
Lee, F
Eickhoff, J
Huang, W
Pomplun, M
Jiang, ZS
Alberti, D
Kolesar, JM
Ivy, P
Wilding, G
Traynor, AM
AF Schelman, William R.
Morgan-Meadows, Sherry
Marnocha, Rebecca
Lee, Fred
Eickhoff, Jens
Huang, Wei
Pomplun, Marcia
Jiang, Zhisheng
Alberti, Dona
Kolesar, Jill M.
Ivy, Percy
Wilding, George
Traynor, Anne M.
TI A phase I study of Triapine (R) in combination with doxorubicin in
patients with advanced solid tumors
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Triapine (R); 3-Aminopyridine-2-carboxaldehyde thiosemicarbazone
Doxorubicin; Phase I; Ribonucleotide reductase
ID RIBONUCLEOTIDE REDUCTASE-ACTIVITY; 3-AMINOPYRIDINE-2-CARBOXALDEHYDE
THIOSEMICARBAZONE 3-AP; CELL LUNG-CANCER; HYDROXYUREA RESISTANCE;
ANTITUMOR-ACTIVITY; INHIBITOR; POTENT; DRUG; CARDIOTOXICITY; GEMCITABINE
AB Purpose To assess the maximum-tolerated dose (MTD), dose-limiting toxicity (DLT), pharmacokinetics and antitumor activity of Triapine (R) administered in combination with doxorubicin.
Study design Patients were treated with doxorubicin intravenously (IV) on day 1 and Triapine (R) IV on days 1-4 of a 21-day cycle. The starting dose (level 1) was doxorubicin 60 mg/m(2) and Triapine (R) 25 mg/m(2). PK analysis was performed at various time-points before and after treatment.
Results Twenty patients received a total of 49 courses of treatment on study. At dose level 2 (doxorubicin 60 mg/m(2), Triapine (R) 45 mg/m(2)), two patients experienced DLTs (febrile neutropenia, grade 4 thrombocytopenia). An additional three patients were enrolled at dose level 1 without initial toxicity. Enrollment then resumed at dose level 2a with a decreased dose of doxorubicin (45 mg/m(2)) with Triapine (R) 45 mg/m(2). The two patients enrolled on this level had two DLTs (diarrhea, CVA). Enrollment was planned to resume at dose level 1; however, the sixth patient enrolled to this cohort developed grade 5 heart failure (ejection fraction 20%, pretreatment EF 62%) after the second course. Thus, doxorubicin and Triapine (R) were reduced to 45 and 25 mg/m(2), respectively (level 1a), prior to resuming enrollment at dose level 1, the MTD. The main drug-related toxicity was myelosuppression. Non-hematologic toxicities included mild-to-moderate fatigue, grade 3 diarrhea and grade 4 CVA. There was one treatment-related death due to heart failure. While no objective responses were observed, subjective evidence of clinical activity was observed in patients with refractory melanoma and prostate cancer.
Conclusions Pretreated patients with advanced malignancies can tolerate the combination of Triapine (R) and doxorubicin at doses that achieve subjective clinical benefit with the main treatment-related toxicities being myelosuppression and fatigue. The MTD was determined to be doxorubicin 60 mg/m(2) on day 1 and Triapine (R) 25 mg/m2 on days 1-4 of a 21-day cycle.
C1 [Schelman, William R.; Marnocha, Rebecca; Lee, Fred; Eickhoff, Jens; Huang, Wei; Pomplun, Marcia; Jiang, Zhisheng; Alberti, Dona; Kolesar, Jill M.; Wilding, George; Traynor, Anne M.] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Madison, WI 53792 USA.
[Morgan-Meadows, Sherry] So Canc Ctr, Mobile, AL USA.
[Ivy, Percy] NCI, Clin Trials Evaluat Program, Bethesda, MD 20892 USA.
RP Traynor, AM (reprint author), Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, 600 Highland Ave,K6-568, Madison, WI 53792 USA.
EM amt@medicine.wisc.edu
FU Early Clinical Trials of Anti-Cancer Agents with PhaseI Emphasis, NCI
[UO1 CA062491]; CTEP Translational Research Initiative [24XS090];
Clinical and Translational Science Award, National Center for
ResearchResources, NIH [1UL1RR025011]
FX The authors would like to thank the University of Wisconsin Paul P.
Carbone Comprehensive Cancer Center (UWCCC) Analytical Instrumentation
Laboratory for Pharmacokinetics, Pharmacodynamics, and Pharmacogenetics
(3P Lab) for support in the acquisition of pharmacokinetic data for this
research. The authors also would like to thank the patients who
participated in this clinical trial, and the nurses and research
specialist of the UWCCC phase I program for their efforts in conducting
and managing this trial. UO1 CA062491, Early Clinical Trials of
Anti-Cancer Agents with PhaseI Emphasis, NCI; CTEP Translational
Research Initiative, Contract 24XS090; and 1UL1RR025011, Clinical and
Translational Science Award, National Center for ResearchResources, NIH.
NR 32
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U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD MAY
PY 2009
VL 63
IS 6
BP 1147
EP 1156
DI 10.1007/s00280-008-0890-8
PG 10
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 434EF
UT WOS:000265257300019
PM 19082825
ER
PT J
AU Wentzensen, N
Gravitt, PE
Solomon, D
Wheeler, CM
Castle, PE
AF Wentzensen, Nicolas
Gravitt, Patti E.
Solomon, Diane
Wheeler, Cosette M.
Castle, Philip E.
TI A Study of Amplicor Human Papillomavirus DNA Detection in the Atypical
Squamous Cells of Undetermined Significance-Low-Grade Squamous
Intraepithelial Lesion Triage Study
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID HYBRID CAPTURE 2; ABNORMAL PAP-SMEAR; CERVICAL-CANCER; RANDOMIZED-TRIAL;
CYTOLOGY INTERPRETATIONS; HYBRID-CAPTURE-2 ASSAY; COST-EFFECTIVENESS;
SCREENING-TESTS; ROCHE AMPLICOR; HPV GENOTYPES
AB We analyzed the performance of Amplicor for detecting carcinogenic human papillomavirus (HPV) infections and cervical precancer in women with an atypical squamous cells of undetermined significance (ASCUS) Pap and compared the results with Hybrid Capture 2 (hc2) in the ASCUS and low-grade squamous intraepithelial lesion (LSIL) triage study (ALTS). Baseline specimens collected from women referred into ALTS based on an ASCUS Pap result were prospectively tested by hc2 and retrospectively tested by Amplicor (n = 3,277). Following receiver-operator-characteristics curve analysis, Amplicor performance was analyzed at three cutoffs (0.2, 1.0, and 1.5). Paired Amplicor and hc2 results were compared for the detection of 2-year cumulative cervical intraepithelial neoplasia (CIN) grade 3 and more severe disease outcomes (CIN3+) and for the detection of 13 targeted carcinogenic HPV types. Amplicor at the 0.2 cutoff had a higher sensitivity for the detection of CIN3+ (95.8% versus 92.6%, P = 0.01) but a much lower specificity (38.9% versus 50.6%, P < 0.001) than hc2. Amplicor at the 1.5 cutoff had an identical sensitivity for the detection of CIN3+ (92.6%) and a slightly lower specificity (47.5%; P < 0.001). The positive predictive value of hc2 was higher at all Amplicor cutoffs, whereas referral rates were significantly lower (53.2% for hc2 versus 64.1% at the 0.2 cutoff and 56.0% at the 1.5 cutoff, P < 0.001). Amplicor was more analytically specific for detecting targeted carcinogenic HPV types than hc2. Amplicor at the 1.5 cutoff had comparable performance with hc2. Whereas Amplicor missed more disease related to nontargeted types, hc2 was more likely to miss disease related to targeted types. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1341-9)
C1 [Wentzensen, Nicolas; Castle, Philip E.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20854 USA.
[Solomon, Diane] NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, Rockville, MD 20854 USA.
[Gravitt, Patti E.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Gravitt, Patti E.] Johns Hopkins Univ, Dept Mol Microbiol & Immunol, Baltimore, MD USA.
[Wheeler, Cosette M.] Univ New Mexico, Hlth Sci Ctr, Dept Mol Genet & Microbiol, Albuquerque, NM 87131 USA.
[Wheeler, Cosette M.] Univ New Mexico, Hlth Sci Ctr, Dept Obstet & Gynecol, Albuquerque, NM 87131 USA.
RP Wentzensen, N (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Room 5012,6120 Execut Blvd, Rockville, MD 20854 USA.
EM wentzenn@mail.nih.gov
FU NIH; National Cancer Institute
FX Grant support: Intramural Research Program of the NIH and the National
Cancer Institute.
NR 40
TC 16
Z9 17
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2009
VL 18
IS 5
BP 1341
EP 1349
DI 10.1158/1055-9965.EPI-08-1180
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 445WF
UT WOS:000266081500002
PM 19423515
ER
PT J
AU Han, XS
Zheng, TZ
Lan, Q
Zhang, YQ
Kilfoy, BA
Qin, Q
Rothman, N
Zahm, SH
Holford, TR
Leaderer, B
Zhang, YW
AF Han, Xuesong
Zheng, Tongzhang
Lan, Qing
Zhang, Yaqun
Kilfoy, Briseis A.
Qin, Qin
Rothman, Nathaniel
Zahm, Shelia H.
Holford, Theodore R.
Leaderer, Brian
Zhang, Yawei
TI Genetic Polymorphisms in Nitric Oxide Synthase Genes Modify the
Relationship between Vegetable and Fruit Intake and Risk of Non-Hodgkin
Lymphoma
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID ANTIOXIDANT-RELATED NUTRIENTS; OXIDATIVE STRESS GENES; DIETARY FACTORS;
DNA-DAMAGE; NOS1 GENE; EXPRESSION; CANCER; CARCINOGENESIS; ASSOCIATION;
CELLS
AB Oxidative damage caused by reactive oxygen species and other free radicals is involved in carcinogenesis. it has been suggested that high vegetable and fruit intake may reduce the risk of non-Hodgkin lymphoma (NHL) as vegetables and fruit are rich in antioxidants. The aim of this study is to evaluate the interaction of vegetable and fruit intake with genetic polymorphisms in oxidative stress pathway genes and NHL risk. This hypothesis was investigated in a population-based case-control study of NHL and NHL histologic subtypes in women from Connecticut, including 513 histologically confirmed incident cases and 591 randomly selected controls. Gene-vegetable/fruit joint effects were estimated using unconditional logistic regression model. The false discovery rate method was applied to adjust for multiple comparisons. Significant interactions with vegetable and fruit intake were mainly found for genetic polymorphisms on nitric oxide synthase (NOS) genes among those with diffuse large B-cell lymphoma and follicular lymphoma. Two single nucleotide polymorphisms in the NOS1 gene were found to significantly modify the association between total vegetable and fruit intake and risk of NHL overall, as well as the risk of follicular lymphoma. When vegetables, bean vegetables, cruciferous vegetables, green leafy vegetables, red vegetables, yellow/orange vegetables, fruit, and citrus fruits were examined separately, strong interaction effects were narrowed to vegetable intake among patients with diffuse large B-cell lymphoma. Our results suggest that genetic polymorphisms in oxidative stress pathway genes, especially in the NOS genes, modify the association between vegetable and fruit intake and risk of NHL. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1429-38)
C1 [Han, Xuesong; Zheng, Tongzhang; Kilfoy, Briseis A.; Holford, Theodore R.; Leaderer, Brian; Zhang, Yawei] Yale Univ, Sch Publ Hlth, New Haven, CT 06520 USA.
[Lan, Qing; Rothman, Nathaniel; Zahm, Shelia H.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
[Zhang, Yaqun] Gansu Prov Design & Res Inst Environm, Lanzhou, Gansu, Peoples R China.
[Qin, Qin] Univ So Maine, Ctr Toxicol & Environm Hlth, Portland, ME 04103 USA.
RP Zhang, YW (reprint author), Yale Univ, Sch Publ Hlth, 60 Coll St,LEPH 440,POB 208034, New Haven, CT 06520 USA.
EM yawei.zhang@yale.edu
RI Aschebrook-Kilfoy, Briseis/A-2537-2012; Zahm, Shelia/B-5025-2015
FU NIH [CA62006, 1D43TW007864-01]
FX Grant support: NIH grant CA62006, the Intramural Research Program of the
NIH, National Cancer Institute, and the NIH Fogarty Training Grant
1D43TW007864-01. This publication was made possible by CTSA grant no.
UL1 RR024139 from the National Center for Research Resources, a
component of the NIH, and the NHL Roadmap for Medical Research. Its
contents are solely the responsibility of the authors and do not
necessarily represent the official view of the National Center for
Research Resources.
NR 68
TC 6
Z9 6
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2009
VL 18
IS 5
BP 1429
EP 1438
DI 10.1158/1055-9965.EPI-09-0001
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 445WF
UT WOS:000266081500014
PM 19423521
ER
PT J
AU Rohrmann, S
Sutcliffe, CG
Bienstock, JL
Monsegue, D
Akereyeni, F
Bradwin, G
Rifai, N
Pollak, MN
Agurs-Collins, T
Platz, EA
AF Rohrmann, Sabine
Sutcliffe, Catherine G.
Bienstock, Jessica L.
Monsegue, Deborah
Akereyeni, Folasade
Bradwin, Gary
Rifai, Nader
Pollak, Michael N.
Agurs-Collins, Tanya
Platz, Elizabeth A.
TI Racial Variation in Sex Steroid Hormones and the Insulin-Like Growth
Factor Axis in Umbilical Cord Blood of Male Neonates
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SERUM TESTOSTERONE LEVELS; BONE-MINERAL DENSITY; PROSTATE-CANCER; WHITE
MEN; BINDING GLOBULIN; AFRICAN-AMERICAN; FACTOR-I; BIRTH-WEIGHT;
AMNIOTIC-FLUID; INCREASED RISK
AB Background: To address whether umbilical cord blood concentrations of sex steroid hormones and the insulin-like growth factor (IGF) axis differ between African-American and White male neonates.
Methods: In 2004 and 2005, venous cord blood samples were collected from 75 African-American and 38 White male full-term uncomplicated births along with birth weight, placental weight, mother's age and parity, and time of birth. Testosterone, androstanediol glucuronide, estradiol, and sex hormone binding globulin (SHBG) were measured by immunoassay, and IGF-I, IGF-2, and IGF binding protein (BP)-3 by ELISA. Crude and multivariable-adjusted geometric mean concentrations were computed.
Results: Androstanediol glucuronide, estradiol, and SHBG concentrations did not differ by race; however, the molar ratio of testosterone to SHBG was higher in African-American than White male babies after adjustment (P = 0.01). Both before and after adjustment, Whites had higher concentrations of IGF-I (adjusted; White, African-American, 93.1, 71.9 ng/mL), IGF-2 (537.3-474.8 ng/mL), and IGFBP-3 (1,673-1,482 ng/mL) than African-Americans (P < 0.05), although the molar ratio of IGF-I plus IGF-2 to IGFBP-3 did not differ by race.
Conclusion: The higher cord blood testosterone to SHBG ratio in African-American compared with White male babies after taking into account maternal and birth factors is compatible with the hypothesis that differences in androgen levels in utero contribute to their higher prostate cancer risk, although we would have expected crude differences as well. Lower cord blood IGF-I and IGF-2 levels in African-American compared with White male babies are not consistent with the hypothesis that differences in growth factor levels contribute to their higher prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1484-91)
C1 [Rohrmann, Sabine] German Canc Res Ctr, Div Canc Epidemiol, D-6900 Heidelberg, Germany.
[Sutcliffe, Catherine G.; Platz, Elizabeth A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Bienstock, Jessica L.] Johns Hopkins Univ, Sch Med, Dept Gynecol & Obstet, Baltimore, MD 21205 USA.
[Platz, Elizabeth A.] Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Platz, Elizabeth A.] Johns Hopkins Med Inst, James Buchanan Brady Urol Inst, Baltimore, MD 21205 USA.
[Monsegue, Deborah; Agurs-Collins, Tanya] Howard Univ, Ctr Canc, Washington, DC 20059 USA.
[Akereyeni, Folasade] Howard Univ, Ctr Human Genome, Washington, DC 20059 USA.
[Bradwin, Gary; Rifai, Nader] Harvard Univ, Sch Med, Dept Lab Med, Boston, MA USA.
[Bradwin, Gary; Rifai, Nader] Childrens Hosp, Boston, MA 02115 USA.
[Pollak, Michael N.] McGill Univ, Jewish Gen Hosp, Dept Med & Oncol, Montreal, PQ H3T 1E2, Canada.
[Agurs-Collins, Tanya] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Platz, EA (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, 615 N Wolfe St,Rm E6132, Baltimore, MD 21205 USA.
EM eplatz@jhsph.edu
RI Perez , Claudio Alejandro/F-8310-2010; Pollak, Michael/G-9094-2011;
Rohrmann, Sabine/D-2113-2012
OI Perez , Claudio Alejandro/0000-0001-9688-184X; Pollak,
Michael/0000-0003-3047-0604;
FU National Cancer institute [U54 (Hopkins CA091409), U54 (Howard
CA091431)]
FX Grant support: National Cancer institute grant U54 (Hopkins CA091409)
and U54 (Howard CA091431).
NR 45
TC 20
Z9 21
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2009
VL 18
IS 5
BP 1484
EP 1491
DI 10.1158/1055-9965.EPI-08-0817
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 445WF
UT WOS:000266081500021
PM 19423525
ER
PT J
AU Moolchan, ET
Parzynski, CS
Jaszyna-Gasior, M
Collins, CC
Leff, MK
Zimmerman, DL
AF Moolchan, Eric T.
Parzynski, Craig S.
Jaszyna-Gasior, Maria
Collins, Charles C.
Leff, Michelle K.
Zimmerman, Debra L.
TI A Link between Adolescent Nicotine Metabolism and Smoking Topography
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID REPLACEMENT THERAPY; DEPENDENT SMOKERS; TOBACCO SMOKING; CYP2A6;
ASSOCIATION; CIGARETTES; COTININE; SEX
AB Adult slow nicotine metabolizers have lower smoke exposure, carbon monoxide levels, and plasma nicotine levels than normal and fast metabolizers. Emerging evidence suggests nicotine metabolism influences smoking topography. This study investigated the association of nicotine metabolism (the ratio of plasma 3-hydroxycotinine to cotinine; 3OHCOT/COT) with smoking topography in adolescent smokers (n = 85; 65% female, 68% European American; mean age, 15.3 +/- 1.2 years; mean cigarettes per day, 18.5 +/- 8.5; mean Fagerstrom Test for Nicotine Dependence, 7.0 +/- 1.2) presenting for a nicotine replacement therapy trial. Measures obtained included puff volume, interpuff interval, number of puffs, puff duration, and puff velocity. Linear regression analysis controlling for hormonal contraception use showed that 30HCOT/COT ratios predicted mean puff volume in the overall sample (t = 2.126; P = 0.037; adjusted R(2) = 0.067). After gender stratification, faster metabolism predicted higher mean puff volume (t = 2.81; P = 0.009; adjusted R(2) = 0.192) but fewer puffs (t = -3.160; P = 0.004; adjusted R(2) = 0.237) and lower mean puff duration (t = -2.06; P = 0.048; adjusted R(2) = 0.101) among boys only, suggesting that as nicotine metabolism increases, puff volume increases but puffing frequency decreases. No significant relationships were found between nicotine metabolism and total puff volume, mean puff duration, interpuff interval, or puff velocity. If confirmed in a broader sample of adolescent smokers, these findings suggest that as among dependent adult smokers, rate of metabolism among adolescent boys is linked to select parameters of puffing behavior that may affect cessation ability. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1578-83)
C1 [Moolchan, Eric T.; Parzynski, Craig S.; Jaszyna-Gasior, Maria; Collins, Charles C.; Leff, Michelle K.; Zimmerman, Debra L.] NIDA, Intramural Res Program, NIH, Biomed Res Ctr, Baltimore, MD USA.
RP Moolchan, ET (reprint author), Alkermes Inc, 88 Sidney St, Cambridge, MA 02139 USA.
EM eric.moolchan@alkermes.com
FU NIDA
FX NIDA intramural research funds.
NR 29
TC 10
Z9 10
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2009
VL 18
IS 5
BP 1578
EP 1583
DI 10.1158/1055-9965.EPI-08-0592
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 445WF
UT WOS:000266081500033
PM 19423535
ER
PT J
AU Gaudet, MM
Milne, RL
Cox, A
Camp, NJ
Goode, EL
Humphreys, MK
Dunning, AM
Morrison, J
Giles, GG
Severi, G
Baglietto, L
English, DR
Couch, FJ
Olson, JE
Wang, XS
Chang-Claude, J
Flesch-Janys, D
Abbas, S
Salazar, R
Mannermaa, A
Kataja, V
Kosma, VM
Lindblom, A
Margolin, S
Heikkinen, T
Kampjarvi, K
Aaltonen, K
Nevanlinna, H
Bogdanova, N
Coinac, I
Schurmann, P
Dork, T
Bartram, CR
Schmutzler, RK
Tchatchou, S
Burwinkel, B
Brauch, H
Torres, D
Hamann, U
Justenhoven, C
Ribas, G
Arias, JI
Benitez, J
Bojesen, SE
Nordestgaard, BG
Flyger, HL
Peto, J
Fletcher, O
Johnson, N
Silva, ID
Fasching, PA
Beckmann, MW
Strick, R
Ekici, AB
Broeks, A
Schmidt, MK
van Leeuwen, FE
Van't Veer, LJ
Southey, MC
Hopper, JL
Apicella, C
Haiman, CA
Henderson, BE
Le Marchand, L
Kolonel, LN
Kristensen, V
Alnae, GG
Hunter, DJ
Kraft, P
Cox, DG
Hankinson, SE
Seynaeve, C
Vreeswijk, MPG
Tollenaar, RAEM
Devilee, P
Chanock, S
Lissowska, J
Brinton, L
Peplonska, B
Czene, K
Hall, P
Li, YQ
Liu, JJ
Balasubramanian, S
Rafii, S
Reed, MWR
Pooley, KA
Conroy, D
Baynes, C
Kang, D
Yoo, KY
Noh, DY
Ahn, SH
Shen, CY
Wang, HC
Yu, JC
Wu, PE
Anton-Culver, H
Ziogoas, A
Egan, K
Newcomb, P
Titus-Ernstoff, L
Dietz, AT
Sigurdson, AJ
Alexander, BH
Bhatti, P
Allen-Brady, K
Cannon-Albright, LA
Wong, J
Spurdle, AB
Beesley, J
Pharoah, PDP
Easton, DF
Garcia-Closas, M
AF Gaudet, Mia M.
Milne, Roger L.
Cox, Angela
Camp, Nicola J.
Goode, Ellen L.
Humphreys, Manjeet K.
Dunning, Alison M.
Morrison, Jonathan
Giles, Graham G.
Severi, Gianluca
Baglietto, Laura
English, Dallas R.
Couch, Fergus J.
Olson, Janet E.
Wang, Xianshu
Chang-Claude, Jenny
Flesch-Janys, Dieter
Abbas, Sascha
Salazar, Ramona
Mannermaa, Arto
Kataja, Vesa
Kosma, Veli-Matti
Lindblom, Annika
Margolin, Sara
Heikkinen, Tuomas
Kampjarvi, Kati
Aaltonen, Kirsimari
Nevanlinna, Heli
Bogdanova, Natalia
Coinac, Irina
Schuermann, Peter
Doerk, Thilo
Bartram, Claus R.
Schmutzler, Rita K.
Tchatchou, Sandrine
Burwinkel, Barbara
Brauch, Hiltrud
Torres, Diana
Hamann, Ute
Justenhoven, Christina
Ribas, Gloria
Arias, Jose I.
Benitez, Javier
Bojesen, Stig E.
Nordestgaard, Borge G.
Flyger, Henrik L.
Peto, Julian
Fletcher, Olivia
Johnson, Nichola
Silva, Isabel dos Santos
Fasching, Peter A.
Beckmann, Matthias W.
Strick, Reiner
Ekici, Arif B.
Broeks, Annegien
Schmidt, Marjanka K.
van Leeuwen, Flora E.
Van't Veer, Laura J.
Southey, Melissa C.
Hopper, John L.
Apicella, Carmel
Haiman, Christopher A.
Henderson, Brian E.
Le Marchand, Loic
Kolonel, Laurence N.
Kristensen, Vessela
Alnaes, Grethe Grenaker
Hunter, David J.
Kraft, Peter
Cox, David G.
Hankinson, Susan E.
Seynaeve, Caroline
Vreeswijk, Maaike P. G.
Tollenaar, Rob A. E. M.
Devilee, Peter
Chanock, Stephen
Lissowska, Jolanta
Brinton, Louise
Peplonska, Beata
Czene, Kamila
Hall, Per
Li, Yuqing
Liu, Jianjun
Balasubramanian, Sabapathy
Rafii, Saeed
Reed, Malcolm W. R.
Pooley, Karen A.
Conroy, Don
Baynes, Caroline
Kang, Daehee
Yoo, Keun-Young
Noh, Dong-Young
Ahn, Sei-Hyun
Shen, Chen-Yang
Wang, Hui-Chun
Yu, Jyh-Cherng
Wu, Pei-Ei
Anton-Culver, Hoda
Ziogoas, Argyrios
Egan, Kathleen
Newcomb, Polly
Titus-Ernstoff, Linda
Dietz, Amy Trentham
Sigurdson, Alice J.
Alexander, Bruce H.
Bhatti, Parveen
Allen-Brady, Kristina
Cannon-Albright, Lisa A.
Wong, Jathine
Spurdle, Amanda B.
Beesley, Jonathan
Pharoah, Paul D. P.
Easton, Doug F.
Garcia-Closas, Montserrat
CA Australian Ovarian Canc Study Grp
Georgia Chenevix-Trench
Breast Canc Assoc Consortium
TI Five Polymorphisms and Breast Cancer Risk: Results from the Breast
Cancer Association Consortium
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID PROGESTERONE-RECEPTOR GENE; TUMOR-NECROSIS-FACTOR; VARIANT; CASP8;
APOPTOSIS; ERCC4
AB Previous studies have suggested that minor alleles for ERCC4 rs744154, TNF rs361525, CASP10 rs13010627, PGR rs1042838, and BID rs8190315 may influence breast cancer risk, but the evidence is inconclusive due to their small sample size. These polymorphisms were genotyped in more than 30,000 breast cancer cases and 30,000 controls, primarily of European descent, from 30 studies in the Breast Cancer Association Consortium. We calculated odds ratios (OR) and 95% confidence intervals (95% CI) as a measure of association. We found that the minor alleles for these polymorphisms were not related to invasive breast cancer risk overall in women of European descent: ECCR4 per-allele OR (95% CI) = 0.99 (0.97-1.02), minor allele frequency = 27.5%; TNF 1.00 (0.95-1.06), 5.0%; CASP10 1.02 (0.98-1.07), 6.5%; PGR 1.02 (0.99-1.06), 15.3%; and BID 0.98 (0.86-1.12), 1.7%. However, we observed significant between-study heterogeneity for associations with risk for single-nucleotide polymorphisms (SNP) in CASP10, PGR, and BID. Estimates were imprecise for women of Asian and African descent due to small numbers and lower minor allele frequencies (with the exception of BID SNP). The ORs for each copy of the minor allele were not significantly different by estrogen or progesterone receptor status, nor were any significant interactions found between the polymorphisms and age or family history of breast cancer. In conclusion, our data provide persuasive evidence against an overall association between invasive breast cancer risk and ERCC4 rs744154, TNF rs361525, CASPIO rs13010627, PGR rs1042838, and BID rs8190315 genotypes among women of European descent. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1610-6)
C1 [Gaudet, Mia M.] Mem Sloan Kettering Canc Ctr, Polish Breast Canc Study, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Chanock, Stephen; Brinton, Louise; Garcia-Closas, Montserrat] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Chanock, Stephen; Brinton, Louise; Garcia-Closas, Montserrat] NCI, Core Genotyping Facil, Adv Technol Ctr, Gaithersburg, MD USA.
[Peplonska, Beata] Ctr Canc, Warsaw, Poland.
[Peplonska, Beata] M Sklodowska Curie Inst Oncol, Warsaw, Poland.
[Peplonska, Beata] Nofer Inst Occupat Med, Lodz, Poland.
[Milne, Roger L.; Ribas, Gloria; Benitez, Javier] CNIO, Spanish Natl Canc Ctr Breast Canc Study BCS, Madrid, Spain.
[Arias, Jose I.] Monte Naranco Hosp, Oviedo, Spain.
[Cox, Angela; Balasubramanian, Sabapathy; Rafii, Saeed; Reed, Malcolm W. R.] Univ Sheffield, Sch Med, Sheffield Breast Canc Study, Sheffield, S Yorkshire, England.
[Camp, Nicola J.; Allen-Brady, Kristina; Cannon-Albright, Lisa A.; Wong, Jathine] Univ Utah, Sch Med, Utah Breast Canc Study, Div Genet Epidemiol,Dept Biomed Informat, Salt Lake City, UT USA.
[Goode, Ellen L.; Couch, Fergus J.; Olson, Janet E.; Wang, Xianshu] Mayo Clin, Coll Med, Mayo Clin Breast Canc Study, Rochester, MI USA.
[Humphreys, Manjeet K.; Dunning, Alison M.; Morrison, Jonathan; Pooley, Karen A.; Conroy, Don; Baynes, Caroline; Pharoah, Paul D. P.; Easton, Doug F.] Univ Cambridge, Dept Oncol, Studies Epidemiol & Risk Factors Canc Hered, Cambridge, England.
[Humphreys, Manjeet K.; Dunning, Alison M.; Morrison, Jonathan; Pooley, Karen A.; Conroy, Don; Baynes, Caroline; Pharoah, Paul D. P.; Easton, Doug F.] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
[Giles, Graham G.; Severi, Gianluca; Baglietto, Laura; English, Dallas R.] German Canc Res Ctr, Melbourne Collaborat Cohort Study, Canc Epidemiol Ctr, D-6900 Heidelberg, Germany.
[Chang-Claude, Jenny; Abbas, Sascha] German Canc Res Ctr, Mammary Carcinoma Risk Factor Invest MARIE, Div Canc Epidemiol, D-6900 Heidelberg, Germany.
[Flesch-Janys, Dieter] Univ Clin Hamburg Eppendorf, Inst Med Biometr & Epidemiol, Hamburg, Germany.
[Salazar, Ramona] Bioglobe GmbH, Hamburg, Germany.
[Mannermaa, Arto; Kosma, Veli-Matti] Kuopio Univ Hosp, Kuopio Breast Canc Project, Dept Pathol, SF-70210 Kuopio, Finland.
[Kataja, Vesa] Kuopio Univ Hosp, Dept Oncol, SF-70210 Kuopio, Finland.
[Mannermaa, Arto; Kosma, Veli-Matti] Univ Kuopio, Inst Clin Med Pathol & Forens Med, FIN-70211 Kuopio, Finland.
[Kataja, Vesa] Vaasa Cent Hosp, Dept Oncol, Vaasa, Finland.
[Lindblom, Annika] Karolinska Inst, Karolinska Breast Canc Study, Dept Mol Med & Surg, Stockholm, Sweden.
[Margolin, Sara] Karolinska Inst, Dept Oncol, Stockholm, Sweden.
[Heikkinen, Tuomas; Kampjarvi, Kati; Aaltonen, Kirsimari; Nevanlinna, Heli] Univ Helsinki, Cent Hosp, Helsinki Breast Canc Study, Dept Obstet & Gynecol, Helsinki, Finland.
[Kampjarvi, Kati] Univ Helsinki, Cent Hosp, Dept Oncol, Helsinki, Finland.
[Bogdanova, Natalia; Coinac, Irina; Schuermann, Peter; Doerk, Thilo] Hannover Med Sch, Hannover Breast Canc Study, Clin Obstet & Gynecol, D-3000 Hannover, Germany.
[Bogdanova, Natalia; Coinac, Irina; Schuermann, Peter; Doerk, Thilo] Hannover Med Sch, Hannover Breast Canc Study, Clin Radiat Oncol, D-3000 Hannover, Germany.
[Bartram, Claus R.] Univ Heidelberg, Inst Human Genet, German Consortium Hereditary Breast & Ovarian Can, Heidelberg, Germany.
[Schmutzler, Rita K.] Univ Cologne, Ctr Clin, Div Mol Gynaecooncol, Dept Obstet & Gynaecol, Cologne, Germany.
[Schmutzler, Rita K.] Univ Hosp Cologne, Ctr Mol Med Cologne, Cologne, Germany.
[Tchatchou, Sandrine; Burwinkel, Barbara] German Canc Res Ctr, Helmholtz Univ Grp Mol Epidemiol, D-6900 Heidelberg, Germany.
[Brauch, Hiltrud; Justenhoven, Christina] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-7000 Stuttgart, Germany.
[Brauch, Hiltrud; Justenhoven, Christina] Univ Tubingen, Tubingen, Germany.
[Torres, Diana; Hamann, Ute] Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany.
[Bojesen, Stig E.; Nordestgaard, Borge G.] Herlev Univ Hosp, Copenhagen Breast Canc Study, Copenhagen, Denmark.
[Bojesen, Stig E.; Nordestgaard, Borge G.] Herlev Univ Hosp, Copenhagen City Heart Study, Dept Clin Biochem, Copenhagen, Denmark.
[Bojesen, Stig E.; Flyger, Henrik L.] Herlev Univ Hosp, Dept Breast Surg, Copenhagen, Denmark.
[Nordestgaard, Borge G.] Univ Copenhagen, Copenhagen Gen Populat Study, Copenhagen, Denmark.
[Peto, Julian; Fletcher, Olivia; Johnson, Nichola; Silva, Isabel dos Santos] Breakthrough Res Ctr, British Breast Canc Study, London, England.
[Peto, Julian; Fletcher, Olivia; Johnson, Nichola; Silva, Isabel dos Santos] London Sch Hyg & Trop Med, London WC1, England.
[Fasching, Peter A.; Beckmann, Matthias W.; Strick, Reiner] Univ Hosp Erlangen, Dept Gynecol & Obstet, Erlangen, Germany.
[Ekici, Arif B.] Univ Hosp Erlangen, Dept Human Genet, Erlangen, Germany.
[Broeks, Annegien; Schmidt, Marjanka K.; van Leeuwen, Flora E.; Van't Veer, Laura J.] Netherlands Canc Inst, Amsterdam Breast Canc Study, Dept Expt Therapy, Amsterdam, Netherlands.
[Broeks, Annegien; Schmidt, Marjanka K.; van Leeuwen, Flora E.; Van't Veer, Laura J.] Netherlands Canc Inst, Dept Epidemiol, Amsterdam, Netherlands.
[Broeks, Annegien; Schmidt, Marjanka K.; van Leeuwen, Flora E.; Van't Veer, Laura J.] Netherlands Canc Inst, Dept Mol Pathol, Amsterdam, Netherlands.
[Southey, Melissa C.; Hopper, John L.; Apicella, Carmel] Univ Melbourne, Genet Epidemiol Lab, Dept Pathol, Australian Breast Canc Family Study, Melbourne, Vic, Australia.
[Hopper, John L.; Apicella, Carmel] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
Univ Otago, Dept Prevent & Social Med, Dunedin, New Zealand.
[Haiman, Christopher A.; Henderson, Brian E.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Le Marchand, Loic; Kolonel, Laurence N.] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
[Kristensen, Vessela; Alnaes, Grethe Grenaker] Norwegian Radium Hosp, Inst Canc Res, Dept Genet, Norwegian Breast Canc Study, Oslo, Norway.
[Hunter, David J.; Kraft, Peter; Cox, David G.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol,Nurses Hlth Study, Boston, MA 02115 USA.
[Hunter, David J.; Hankinson, Susan E.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Seynaeve, Caroline] Leiden Univ, Med Ctr Breast Canc Study ORIGO, Dept Med Oncol, Family Canc Clin,Erasmus MC Daniel den Hoed Canc, Rotterdam, Netherlands.
[Vreeswijk, Maaike P. G.] Leiden Univ, Dept Human Genet, Med Ctr, NL-2300 RA Leiden, Netherlands.
[Tollenaar, Rob A. E. M.] Leiden Univ, Dept Surg, Med Ctr, NL-2300 RA Leiden, Netherlands.
[Devilee, Peter] Leiden Univ, Dept Pathol, Med Ctr, NL-2300 RA Leiden, Netherlands.
[Devilee, Peter] Leiden Univ, Dept Human Genet, Med Ctr, NL-2300 RA Leiden, Netherlands.
[Czene, Kamila; Hall, Per] Karolinska Inst, Dept Med Epidemiol & Biostat, Singapore & Swedish Breast Canc Study, Stockholm, Sweden.
[Li, Yuqing; Liu, Jianjun] Genome Inst Singapore, Singapore, Singapore.
[Kang, Daehee; Yoo, Keun-Young; Noh, Dong-Young; Ahn, Sei-Hyun] Seoul Natl Univ, Coll Med, Seoul Breast Canc Study, Seoul, South Korea.
[Kang, Daehee; Yoo, Keun-Young; Noh, Dong-Young; Ahn, Sei-Hyun] Natl Canc Ctr, Seoul, South Korea.
[Kang, Daehee; Yoo, Keun-Young; Noh, Dong-Young; Ahn, Sei-Hyun] Univ Ulsan, Coll Med, Dept Surg, Ulsan 680749, South Korea.
[Shen, Chen-Yang; Wang, Hui-Chun; Wu, Pei-Ei] Acad Sinica, Inst Biomed Sci, Taiwanese Breast Canc Study, Taipei, Taiwan.
[Shen, Chen-Yang] China Med Univ, Grad Inst Environm Sci, Taichong, Taiwan.
[Yu, Jyh-Cherng] Triserv Gen Hosp, Dept Surg, Taipei, Taiwan.
[Anton-Culver, Hoda; Ziogoas, Argyrios; Garcia-Closas, Montserrat] Univ Calif Irvine, Sch Med, Dept Epidemiol, Univ Calif Irvine Breast Canc Study, Irvine, CA 92717 USA.
[Egan, Kathleen] H Lee Moffitt Canc Ctr & Res Inst, US Three State Study, Tampa, FL USA.
[Newcomb, Polly] Fred Hutchinson Canc Res Ctr, Canc Prevent Res Grp, Seattle, WA 98104 USA.
[Newcomb, Polly; Dietz, Amy Trentham] Univ Wisconsin, Ctr Comprehens Canc, Madison, WI USA.
[Titus-Ernstoff, Linda] Dartmouth Med Ctr, Lebanon, NH USA.
[Titus-Ernstoff, Linda] Norris Cotton Canc Ctr, Lebanon, NH USA.
[Sigurdson, Alice J.; Bhatti, Parveen] NCI, US Radiol Technol Study, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Alexander, Bruce H.] Univ Minnesota, Div Environm Hlth Sci, Minneapolis, MN USA.
[Spurdle, Amanda B.; Beesley, Jonathan; Georgia Chenevix-Trench] Queensland Inst Med Res, Kathleen Cuningham Fdn Consortium Res Familial Br, Brisbane, Qld 4006, Australia.
RP Gaudet, MM (reprint author), Mem Sloan Kettering Canc Ctr, Polish Breast Canc Study, Dept Epidemiol & Biostat, 3rd Floor,307 E 63rd St, New York, NY 10021 USA.
EM gaudetm@mskcc.org
RI Yoo, Keun-Young/J-5548-2012; Ekici, Arif/C-3971-2013; Peplonska,
Beata/F-6004-2010; Garcia-Closas, Montserrat /F-3871-2015; Brinton,
Louise/G-7486-2015; Dork, Thilo/J-8620-2012; Cox, David/A-2023-2009;
Spurdle, Amanda/A-4978-2011; Wang, Hui-Chun/C-5680-2009; Noh,
Dong-Young/G-5531-2011; Shen, CY/F-6271-2010; Kang, Dae Hee/E-8631-2012;
Bowtell, David/H-1007-2016;
OI Garcia-Closas, Montserrat /0000-0003-1033-2650; Brinton,
Louise/0000-0003-3853-8562; Cox, David/0000-0002-2152-9259; Spurdle,
Amanda/0000-0003-1337-7897; Bowtell, David/0000-0001-9089-7525; Czene,
Kamila/0000-0002-3233-5695; Lissowska, Jolanta/0000-0003-2695-5799;
Dunning, Alison Margaret/0000-0001-6651-7166; Nevanlinna,
Heli/0000-0002-0916-2976; dos Santos Silva, Isabel/0000-0002-6596-8798;
albright, lisa/0000-0003-2602-3668; Cox, Angela/0000-0002-5138-1099;
Giles, Graham/0000-0003-4946-9099; English, Dallas/0000-0001-7828-8188
FU Australian National Health and Medical Research Council [209057, 251533,
396414, 504711]; The Cancer Council Victoria; National Institutes of
Health [CA98364]; U.S. medical research and materiel command breast
cancer IDEA award [W81XWH-04-1-0588]; Eagles Cancer Research Fellow;
Deutsche Krebshilfe e.V. [70-2892-Br 1]; Government Funding (EVO) of
Kuopio University Hospital; Finnish Cancer Organisations; Cancer Fund of
North Savo; Swedish Cancer Society; Gustav the V Jubilee Foundation; FoU
Foundation; Bert von Kantzows Foundation; The Academy of Finland
[110663]; Helsinki University Central Hospital; Sigrid Juselius
Foundation; The Finnish Cancer Society; Hannover Medical School; Friends
of Hannover Medical School; Deutsche Krebshilfe [107054]; Center of
Molecular Medicine, Cologne; Helmholtz society; German Human Genome
Project; Federal Ministry of Education and Research (BMBF) Germany
[01KW9975/5, 01KW9976/8, 01KW9977/0, 01KW0114]; Deutsches
Krebsforschungszentrum, Heidelberg; Robert Bosch Foundation of Medical
Research, Stuttgart, Germany; Genome Spain Foundation; Chief Physician
Johan Boserup and Lise Boserup Fund; Danish Medical Research Council;
Copenhagen County; CR-UK; Dutch Cancer Society [NKI 2001-2423,
2007-3839]; Dutch National Genomics Initiative; National Health and
Medical Research Council (NHMRC) [145684, 288704, 454508, 199600];
Victorian Health Promotion Foundation; New South Wales Cancer Council;
National Cancer Institute (USA) [CA-95-003]; National Cancer Institute
(NCI) [CA63464, CA54281, CA2 R01, CA58860-14]; NCT [CA 0657245,
CA098233]; Dutch Cancer Society; Agency for Science, Technology and
Research of Singapore (A*STAR); Susan G. Komen Breast Cancer Foundation;
Yorkshire Cancer Research; Breast Cancer Campaign; Cancer Research-UK
(CR-UK); National Research and Development Program for Cancer Control,
Ministry of Health and Welfare, Republic of Korea [0620410-1];
Department of Health, Taiwan; Lon v smith Foundation (LVSF) [LVSF-41027,
3834, 42344]; American Registry of Radiologic Technologists; Susan G.
Komen Foundation [BCTR0706911]; Utah Cancer Registry [N01-PC-35141];
Utah State Department of Health; University of Utah; National Breast
Cancer Foundation; Queensland Cancer Fund; Cancer Councils of New South
Wales, Victoria, Tasmania and South Australia; Cancer Foundation of
Western Australia. ACS/AOCS; U.S. Army Medical Research and Materiel
Command [DAMD17-01-1-0729]
FX The authors are grateful to Study Coordinators, Laboratory Specialst Kim
Nguyen, and Computer Specialist Jathine Wong. We wish to thank Heather
Thorne, Eveline Niedermayr, all the kConFab research nurses and staff,
the heads and staff of the Family Cancer Clinics, and the Clinical
Follow Up Study (funded by NHMRC grants 145684, 288704 and 454508) for
their contributions to this resource, and the many families who
contribute to kConFab. kConFab is supported by grants from the National
Breast Cancer Foundation, the National Health and Medical Research
Council (NHMRC) and by the Queensland Cancer Fund, the Cancer Councils
of New South Wales, Victoria, Tasmania and South Australia, and the
Cancer Foundation of Western Australia. ACS/AOCS: The AOCS Management
Group (D Bowtell, G Chenevix-Trench, A deFazio, D Gertig, A Green, P
Webb) gratefully acknowledges the contribution of all the clinical and
scientific collaborators (see http://www.aocstudy.org/), AOCS and the
ACS Management Group (A Green, P Parsons, N Hayward, P Webb, D Whiteman)
thank all of the project staff, collaborating institutions and Study
participants. Financial support was provided by: U.S. Army Medical
Research and Materiel Command under DAMD17-01-1-0729, the Cancer Council
Tasmania and Cancer Foundation of Western Australia (AOCS study); The
National Health and Medical Research Council of Australia (199600) (ACS
study). The content of this manuscript does not necessarily reflect the
views or policies of the National Cancer Institute or any of the
collaborating centres in the CFRs, nor does mention of trade names,
commercial products, or organizations imply endorsement by the U.S.
Government or the CFRs Centers. The genotyping and analysis were
supported by grants from the National Health and Medical Research
Council (NHMRC). ABS was funded by an NHMRC Career Development Award,
and GC-T and JLH are NHMRC Senior Principal Research Fellows.
NR 20
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U2 12
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2009
VL 18
IS 5
BP 1610
EP 1616
DI 10.1158/1055-9965.EPI-08-0745
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 445WF
UT WOS:000266081500037
PM 19423537
ER
PT J
AU Koshiol, J
Hildesheim, A
Gonzalez, P
Bratti, MC
Porras, C
Schiffman, M
Herrero, R
Rodriguez, AC
Wacholder, S
Yeager, M
Chanock, SJ
Burk, RD
Wang, SS
AF Koshiol, Jill
Hildesheim, Allan
Gonzalez, Paula
Bratti, M. Concepcion
Porras, Carolina
Schiffman, Mark
Herrero, Rolando
Rodriguez, Ana C.
Wacholder, Sholom
Yeager, Meredith
Chanock, Stephen J.
Burk, Robert D.
Wang, Sophia S.
TI Common Genetic Variation in TP53 and Risk of Human Papillomavirus
Persistence and Progression to CIN3/Cancer Revisited
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID P53 CODON-72 POLYMORPHISM; INVASIVE CERVICAL-CANCER; COSTA-RICA;
METAANALYSIS; NEOPLASIA; INFECTION; POPULATION; HAPLOTYPE; WOMEN;
CARCINOGENESIS
AB Driven by findings that human papillomavirus (HPV)induced degradation of p53 differs by a TP53 polymorphism at codon 72 (Pro72Arg), past studies of TP53 genetic variants and cervical cancer have focused on this nonsynonymous polymorphism, with mixed results. We analyzed common single nucleotide polymorphisms (SNP) across the TP53 locus in a population-based nested case-control study in Guanacaste, Costa Rica. We evaluated 11 SNPs, including Pro72Arg (rs1042522), among 1,281 women: 465 with cervical intraepithelial neoplasia grade 3/cancer (CIN3+), 380 with HPV persistence (median, 25 months), and 436 random population controls. We combined HPV persistence and CIN3+ into one case group because they did not differ in TP53 genotypic frequencies and calculated odds ratios and 95% confidence intervals (CI) for individual SNPs and inferred haplotypes. We observed that proline at codon 72 was associated with increased risk of CIN3+/persistence compared with population controls. Relative to GG (Arg), the CG (Pro/Arg) and CC (Pro) genotypes had a 1.3-fold (95% CI, 0.99-1.6) and 1.8-fold (95% CI, 1.2-2.7) increased risk, respectively (P(trend) < 0.01). rs12951053 and rs1642785 were also associated with CIN3+/persistence (P(trend), 0.05 and 0.04, respectively), as was a haplotype containing the codon 72 variant (rs1042522), rs12951053, rs1642785, and rs12947788 (odds ratio, 1.6; 95% CI, 1.1-2.3 versus the most common haplotype, which comprised the major alleles for all 11 SNPs). Although genetic variation in TP53 might affect the natural history of HPV and cervical cancer, further work is needed to elucidate the possible mechanism. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1631-7)
C1 [Koshiol, Jill] NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, NIH, Bethesda, MD 20892 USA.
[Koshiol, Jill] NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
[Hildesheim, Allan] NCI, Infect & Immunoepidemiol Branch, NIH, Bethesda, MD 20892 USA.
[Schiffman, Mark; Rodriguez, Ana C.; Wang, Sophia S.] NCI, Hormonal & Reprod Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
[Wacholder, Sholom] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Yeager, Meredith; Chanock, Stephen J.] NCI, Core Genotyping Facil, NIH, Gaithersburg, MD USA.
[Chanock, Stephen J.] NCI, Lab Translat Gen, Div Canc Epidemiol & Genet, NIH, Gaithersburg, MD USA.
[Gonzalez, Paula; Bratti, M. Concepcion; Porras, Carolina; Herrero, Rolando] Fdn INCIENSA, San Jose, Costa Rica.
[Burk, Robert D.] Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10467 USA.
[Burk, Robert D.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Burk, Robert D.] Albert Einstein Coll Med, Dept Microbiol & Immunol, Bronx, NY 10467 USA.
[Burk, Robert D.] Albert Einstein Coll Med, Dept Obstet Gynecol, Bronx, NY 10467 USA.
[Burk, Robert D.] Albert Einstein Coll Med, Dept Womens Hlth, Bronx, NY 10467 USA.
RP Koshiol, J (reprint author), NIH, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 7059, Rockville, MD 20852 USA.
EM koshiolj@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU NIH; National Cancer Institute; Infections and Immunoepiderniology
Branch
FX Intramural Research Program of the NIH and the National Cancer
Institute. R. Welch contributed as an author on this article until the
time of his death in 2008. J. Koshiol is now a Research Fellow in the
Infections and Immunoepiderniology Branch.
NR 33
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U2 2
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2009
VL 18
IS 5
BP 1631
EP 1637
DI 10.1158/1055-9965.EPI-08-0830
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 445WF
UT WOS:000266081500040
PM 19423538
ER
PT J
AU Rajaraman, P
Brenner, AV
Butler, MA
Wang, SS
Pfeiffer, RM
Ruder, AM
Linet, MS
Yeager, M
Wang, ZM
Orr, N
Fine, HA
Kwon, D
Thomas, G
Rothman, N
Inskip, PD
Chanock, SJ
AF Rajaraman, Preetha
Brenner, Alina V.
Butler, Mary Ann
Wang, Sophia S.
Pfeiffer, Ruth M.
Ruder, Avima M.
Linet, Martha S.
Yeager, Meredith
Wang, Zhaoming
Orr, Nick
Fine, Howard A.
Kwon, Deukwoo
Thomas, Gilles
Rothman, Nathaniel
Inskip, Peter D.
Chanock, Stephen J.
TI Common Variation in Genes Related to Innate Immunity and Risk of Adult
Glioma
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; BRAIN-TUMORS; SERUM IGE; POLYMORPHISMS;
HISTORY; PRIVILEGE; ALLERGIES; SUSCEPTIBILITY; IDENTIFICATION;
POPULATION
AB Current evidence suggests that immune system alterations contribute to the etiology of adult glioma, the most common adult brain tumor. Although previous studies have focused on variation in candidate genes in the adaptive immune system, the innate immune system has emerged as a critical avenue for research given its known link with carcinogenesis. To identify genetic markers in pathways critical to innate immunity, we conducted an association study of 551 glioma cases and 865 matched controls of European ancestry to investigate "tag" single nucleotide polymorphisms (SNP) in 148 genetic regions. Two independent U.S. case-control studies included were as follows: a hospital-based study conducted by the National Cancer Institute (263 cases, 330 controls) and a community-based study conducted by the National Institute for Occupational Safety and Health (288 cases, 535 controls). Tag SNPs (1,397) chosen on the basis of an r(2) of >0.8 and minor allele frequency of >5% in Caucasians in HapMap1 were genotyped. Glioma risk was estimated by odds ratios. Nine SNPs distributed across eight genetic regions (ALOX5, IRAK3, ITGB2, NCF2, NFKB1, SELP, SOD1, and STAT1) were associated with risk of glioma with P value of <0.01. Although these associations were no longer statistically significant after controlling for multiple comparisons, the associations were notably consistent in both studies. Region-based tests were statistically significant (P < 0.05) for SELP, SOD, and ALOX5. Analyses restricted to glioblastoma (n = 254) yielded significant associations for the SELP, DEFB126/127, SERPINI1, and LY96 genetic regions. We have identified a promising set of innate immunity-related genetic regions for further investigation. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1651-8)
C1 [Rajaraman, Preetha; Brenner, Alina V.; Wang, Sophia S.; Pfeiffer, Ruth M.; Linet, Martha S.; Kwon, Deukwoo; Rothman, Nathaniel; Inskip, Peter D.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Fine, Howard A.] NCI, Neurooncol Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Butler, Mary Ann; Ruder, Avima M.] NIOSH, Ctr Dis Control & Prevent, Dept Hlth & Human Serv, Cincinnati, OH 45226 USA.
[Yeager, Meredith; Wang, Zhaoming; Orr, Nick; Thomas, Gilles; Chanock, Stephen J.] NCI, Core Genotyping Facil, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Rajaraman, P (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS Room 7058, Rockville, MD 20852 USA.
EM rajarama@mail.nih.gov
RI Pfeiffer, Ruth /F-4748-2011; Ruder, Avima/I-4155-2012
OI Ruder, Avima/0000-0003-0419-6664
FU NCI, NIH, Department of Health and Human Services [N01-CO-12400]
FX Intramural funds from the NCI, NIH, Department of Health and Human
Services, and has been funded in whole or in part with federal funds
from the NCI, NIH, under contract N01-CO-12400. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, or does mention of trade names,
commercial products, or organizations imply endorsement by the U.S.
Government.
NR 43
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U1 1
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2009
VL 18
IS 5
BP 1651
EP 1658
DI 10.1158/1055-9965.EPI-08-1041
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 445WF
UT WOS:000266081500043
PM 19423540
ER
PT J
AU Symes, JC
Siatskas, C
Fowler, DH
Medin, JA
AF Symes, J. C.
Siatskas, C.
Fowler, D. H.
Medin, J. A.
TI Retrovirally transduced murine T lymphocytes expressing FasL mediate
effective killing of prostate cancer cells
SO CANCER GENE THERAPY
LA English
DT Article
DE apoptosis; c-FLIP; docetaxel; Fas; gene transfer; mitoxantrone
ID MHC CLASS-I; GENE-TRANSFER; CD95-MEDIATED APOPTOSIS; ANTITUMOR-ACTIVITY;
CARCINOMA-CELLS; CD95 EXPRESSION; TUMOR-CELLS; LONG FORM; LIGAND;
ACTIVATION
AB Adoptively transferred T cells possess anticancer activities partially mediated by T-cell FasL engagement of Fas tumor targets. However, antigen-induced T-cell activation and clonal expansion, which stimulates FasL activity, is often inefficient in tumors. As a gene therapy approach to overcome this obstacle, we have created oncoretroviral vectors to overexpress FasL or non-cleavable FasL (ncFasL) on murine T cells of a diverse T-cell receptor repertoire. Expression of c-FLIP was also engineered to prevent apoptosis of transduced cells. Retroviral transduction of murine T lymphocytes has historically been problematic, and we describe optimized T-cell transduction protocols involving CD3/CD28 co-stimulation of T cells, transduction on ice using concentrated oncoretrovirus, and culture with IL-15. Genetically modified T cells home to established prostate cancer tumors in vivo. Co-stimulated T cells expressing FasL, ncFasL and ncFasL/c-FLIP each mediated cytotoxicity in vitro against RM-1 and LNCaP prostate cancer cells. To evaluate the compatibility of this approach with current prostate cancer therapies, we exposed RM-1, LNCaP, and TRAMP-C1 cells to radiation, mitoxantrone, or docetaxel. Fas and H-2(b) expression were upregulated by these methods. We have developed a novel FasL-based immuno-gene therapy for prostate cancer that warrants further investigation given the apparent constitutive and inducible Fas pathway expression in this malignancy.
C1 [Medin, J. A.] Univ Toronto, Univ Hlth Network, Dept Med Biophys, Div Stem Cell & Differentiat, Toronto, ON, Canada.
[Siatskas, C.; Medin, J. A.] Ontario Canc Inst, Div Stem Cell & Dev Biol, Toronto, ON M4X 1K9, Canada.
[Fowler, D. H.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Medin, J. A.] Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A1, Canada.
RP Medin, JA (reprint author), Univ Toronto, Univ Hlth Network, Dept Med Biophys, Div Stem Cell & Differentiat, 67 Coll St,CBS Bldg Room 406, Toronto, ON, Canada.
EM jmedin@uhnres.utoronto.ca
FU Prostate Cancer Research Foundation of Canada
FX We thank Anton Neschadim and Dr Richard Miller for helpful discussions
about transductions and T-cell biology. This work is supported by a
grant from the Prostate Cancer Research Foundation of Canada.
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U1 0
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0929-1903
J9 CANCER GENE THER
JI Cancer Gene Ther.
PD MAY
PY 2009
VL 16
IS 5
BP 439
EP 452
DI 10.1038/cgt.2008.96
PG 14
WC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity;
Medicine, Research & Experimental
SC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity;
Research & Experimental Medicine
GA 433ZR
UT WOS:000265245500007
PM 19096446
ER
PT J
AU Zimonjic, DB
Ullmannova-Benson, V
Factor, VM
Thorgeirsson, SS
Popescu, NC
AF Zimonjic, Drazen B.
Ullmannova-Benson, Veronika
Factor, Valentina M.
Thorgeirsson, Snorri S.
Popescu, Nicholas C.
TI Recurrent and nonrandom DNA copy number and chromosome alterations in
Myc transgenic mouse model for hepatocellular carcinogenesis:
implications for human disease
SO CANCER GENETICS AND CYTOGENETICS
LA English
DT Article
ID GROWTH-FACTOR-ALPHA; CARCINOMA CELL-LINES; EXPRESSING C-MYC; FRAGILE
SITES; II RECEPTOR; FHIT GENE; LIVER; CANCER; MICE; TUMORS
AB Mouse models for hepatocellular carcinoma (HCC) provide an experimental ground for dissecting the genetic and biological complexities of human liver cancer and contribute to our ability to gain insights into the relevance of candidate cancer genes. We examined, using spectral karyotyping (SKY) and array-based CGH (aCGH), seven cell lines derived from HCC spontaneously developed in transgenic Myc mice (Myc), and four cell lines established from tumors induced in nude mice by inoculation with the original Myc cells (nuMyc). All the cell lines exhibited gain of material from chromosomes 5, 6, 8, 10, 11, 15, and 19 and DNA copy-number loss from chromosomes 2, 4, 7, 9, 12, 14, and X. In addition, several recurrent chromosome reorganizations were found, including del(3), t(3;8), del(4), t(4;11), t(6;5), del(7), del(8), del(9), t(10;14), del(11), and del(16). Chromosome breakpoints underlying rearrangements clustered in the regions previously identified as important for the early stages of Myc-induced hepatocarcinogenesis. The results strongly suggest the importance of recurrent breakage and loss of chromosomes 4, 9, and 14 and gain of chromosomes 15 and 19 in mouse liver neoplasia. Genomic changes observed in Myc HCC cell lines are also recurrent in HCC developed in other transgenic mouse models, in mouse spontaneous HCC and derivative cell lines, and in preneoplastic liver lesions induced with chemical carcinogens. Overall, the present results document selective, nonrandom genomic changes involving chromosomal regions homologous to those implicated in human HCC. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Zimonjic, Drazen B.; Ullmannova-Benson, Veronika; Factor, Valentina M.; Thorgeirsson, Snorri S.; Popescu, Nicholas C.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Popescu, NC (reprint author), NCI, Expt Carcinogenesis Lab, Ctr Canc Res, 37 Convent Dr MSC 4262,Bldg 37,Room 4128B, Bethesda, MD 20892 USA.
EM popescun@mail.nih.gov
RI Benson, Veronika/D-9942-2014
OI Benson, Veronika/0000-0003-4770-9909
FU Intramural Research Program of the National Cancer Institute; National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health.
NR 48
TC 6
Z9 7
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0165-4608
J9 CANCER GENET CYTOGEN
JI Cancer Genet. Cytogenet.
PD MAY
PY 2009
VL 191
IS 1
BP 17
EP 26
DI 10.1016/j.cancergencyto.2008.12.014
PG 10
WC Oncology; Genetics & Heredity
SC Oncology; Genetics & Heredity
GA 445BD
UT WOS:000266023700003
PM 19389504
ER
PT J
AU Kelloff, GJ
Sigman, CC
Contag, CH
AF Kelloff, Gary J.
Sigman, Caroline C.
Contag, Christopher H.
TI Early Detection of Oral Neoplasia: Watching with New Eyes
SO CANCER PREVENTION RESEARCH
LA English
DT Editorial Material
ID NECK-CANCER; DRUG DEVELOPMENT; INTRAEPITHELIAL NEOPLASIA;
CHEMOPREVENTION; HEAD; AUTOFLUORESCENCE; PREVENTION; PROGRESS; FIELD;
RISK
C1 [Kelloff, Gary J.] NCI, Div Canc Treatment & Diag, Canc Imaging Program, Rockville, MD 20852 USA.
[Sigman, Caroline C.] CCS Associates, Mountain View, CA USA.
[Contag, Christopher H.] Stanford Univ, Dept Pediat, Sch Med, Stanford, CA 94305 USA.
[Contag, Christopher H.] Stanford Univ, Dept Microbiol & Immunol, Sch Med, Stanford, CA 94305 USA.
[Contag, Christopher H.] Stanford Univ, Dept Radiol, Sch Med, Stanford, CA 94305 USA.
[Contag, Christopher H.] Stanford Univ, Mol Imaging Program, Sch Med, Stanford, CA 94305 USA.
RP Kelloff, GJ (reprint author), NCI, Div Canc Treatment & Diag, Canc Imaging Program, 6130 Execut Blvd,Room 6058, Rockville, MD 20852 USA.
EM kelloffg@dcpcepn.nci.nih.gov
NR 40
TC 9
Z9 9
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2009
VL 2
IS 5
BP 405
EP 408
DI 10.1158/1940-6207.CAPR-09-0064
PG 4
WC Oncology
SC Oncology
GA 441IU
UT WOS:000265763300002
PM 19401527
ER
PT J
AU Vitale-Cross, L
Czerninski, R
Amornphimoltham, P
Patel, V
Molinolo, AA
Gutkind, JS
AF Vitale-Cross, Lynn
Czerninski, Rakefet
Amornphimoltham, Panomwat
Patel, Vyomesh
Molinolo, Alfredo A.
Gutkind, J. Silvio
TI Chemical Carcinogenesis Models for Evaluating Molecular-Targeted
Prevention and Treatment of Oral Cancer
SO CANCER PREVENTION RESEARCH
LA English
DT Review
ID SQUAMOUS-CELL CARCINOMAS; UPPER AERODIGESTIVE TISSUE; 4-NITROQUINOLINE
N-OXIDE; GROUP-A GENE; NECK-CANCER; ESOPHAGEAL CARCINOGENESIS; MUCOSAL
CARCINOGENESIS; MOUSE TONGUE; K-RAS; MICE
C1 [Vitale-Cross, Lynn; Czerninski, Rakefet; Amornphimoltham, Panomwat; Patel, Vyomesh; Molinolo, Alfredo A.; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Gutkind, JS (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, 30 Convent Dr,Bldg 30,Room 212, Bethesda, MD 20892 USA.
EM sg39v@nih.gov
RI Gutkind, J. Silvio/A-1053-2009
FU NIH; National Institute of Dental and Craniofacial Research
FX Intramural Research Program of NIH, National Institute of Dental and
Craniofacial Research.
NR 41
TC 37
Z9 38
U1 0
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2009
VL 2
IS 5
BP 419
EP 422
DI 10.1158/1940-6207.CAPR-09-0058
PG 4
WC Oncology
SC Oncology
GA 441IU
UT WOS:000265763300004
PM 19401522
ER
PT J
AU Cekanova, M
Lee, SH
Donnell, RL
Sukhthankar, M
Eling, TE
Fischer, SM
Baek, SJ
AF Cekanova, Maria
Lee, Seong-Ho
Donnell, Robert L.
Sukhthankar, Mugdha
Eling, Thomas E.
Fischer, Susan M.
Baek, Seung Joon
TI Nonsteroidal Anti-inflammatory Drug-Activated Gene-1 Expression Inhibits
Urethane-Induced Pulmonary Tumorigenesis in Transgenic Mice
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID COLORECTAL-CANCER CELLS; BETA SUPERFAMILY MEMBER; GROWTH-FACTOR-BETA;
LUNG CARCINOGENESIS; CARCINOMA-CELLS; GAMMA LIGAND; NAG-1; PROTEIN;
APOPTOSIS; MOUSE
AB The expression of nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) inhibits gastrointestinal tumorigenesis in NAG-1 transgenic mice (C57/BL6 background). In the present study, we investigated whether the NAG-1 protein would alter urethane-induced pulmonary lesions in NAG-1 transgenic mice on an FVB background (NAG-1(Tg+/FVB)). NAG-1Tg+/FVB mice had both decreased number and size of urethane-induced tumors, compared with control littermates (NAG-1(Tg+/FVB) = 16 +/- 4 per mouse versus control = 20 +/- 7 per mouse, P < 0.05). Urethane-induced pulmonary adenomas and adenocarcinomas were observed in control mice; however, only pulmonary adenomas were observed in NAG-1(Tg+/FVB) mice. Urethane-induced tumors from control littermates and NAG-1(Tg+/FVB) mice highly expressed proteins in the arachidonic acid pathway (cyclooxygenases 1/2, prostaglandin E synthase, and prostaglandin E(2) receptor) and highly activated several kinases (phospho-Raf-1 and phosphorylated extracellular signal-regulated kinase 1/2). However, only urethane-induced p38 mitogen-activated protein kinase (MAPK) phosphorylation was decreased in NAG-1(Tg+/FVB) mice. Furthermore, significantly increased apoptosis in tumors of NAG-1(Tg+/FVB) mice compared with control mice was observed as assessed by caspase-3/7 activity. In addition, fewer inflammatory cells were observed in the lung tissue isolated from urethane-treated NAG-1(Tg+/FVB) mice compared with control mice. These results paralleled in vitro assays using human A549 pulmonary carcinoma cells. Less phosphorylated p38 MAPK was observed in cells overexpressing NAG-1 compared with control cells. Overall, our study revealed for the first time that the NAG-1 protein inhibits urethane-induced tumor formation, probably mediated by the p38 MAPK pathway, and is a possible new target for lung cancer chemoprevention.
C1 [Cekanova, Maria; Lee, Seong-Ho; Donnell, Robert L.; Sukhthankar, Mugdha; Baek, Seung Joon] Univ Tennessee, Coll Vet Med, Dept Pathobiol, Knoxville, TN 37996 USA.
[Eling, Thomas E.] Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC USA.
[Fischer, Susan M.] Univ Texas MD Anderson Canc Ctr, Div Sci Pk Res, Dept Carcinogenesis, Smithville, TX USA.
RP Baek, SJ (reprint author), Univ Tennessee, Coll Vet Med, Dept Pathobiol, Knoxville, TN 37996 USA.
EM sbaek2@utk.edu
OI Cekanova, Maria/0000-0002-9651-1619; Donnell, Robert
L./0000-0002-6778-954X
FU American Cancer Society [CNE-111611]; NIH [RO1CA108975]; The University
of Tennessee Center of Excellence in Livestock Diseases and Human
Health; National Institute of Environmental Health Sciences/NIH
FX American Cancer Society grant CNE-111611, NIH grant RO1CA108975, The
University of Tennessee Center of Excellence in Livestock Diseases and
Human Health (S.J. Baek), and National Institute of Environmental Health
Sciences/NIH intramural research program (T. E. Eling).
NR 35
TC 26
Z9 29
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2009
VL 2
IS 5
BP 450
EP 458
DI 10.1158/1940-6207.CAPR-09-0057
PG 9
WC Oncology
SC Oncology
GA 441IU
UT WOS:000265763300008
PM 19401523
ER
PT J
AU Danforth, KN
Gierach, GL
Brinton, LA
Hollenbeck, AR
Katki, HA
Leitzmann, MF
Schatzkin, A
Lacey, JV
AF Danforth, Kim N.
Gierach, Gretchen L.
Brinton, Louise A.
Hollenbeck, Albert R.
Katki, Hormuzd A.
Leitzmann, Michael F.
Schatzkin, Arthur
Lacey, James V., Jr.
TI Nonsteroidal Anti-Inflammatory Drug Use and Endometrial Cancer Risk in
the NIH-AARP Diet and Health Study
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID ADIPOSE-TISSUE; CYCLOOXYGENASE-2; INFLAMMATION; EXPRESSION; OBESITY
AB Chronic inflammation may play an etiologic role in endometrial cancer. Nonsteroidal antiinflammatory drugs (NSAIDs) reduce inflammatory activity by inhibiting the proinflammatory cyclooxygenase enzymes and, therefore, may decrease cancer risk. However, few studies have examined the association between NSAID use and endometrial cancer. We conducted a prospective study among 72,524 women in the NIH-AARP Diet and Health Study. Women completed a questionnaire in 1996-1997 on lifestyle and health-related factors, including type and frequency of NSAID use within the past year, and were followed through 2003 by linkages to cancer registries and vital status databases. During 488,261 person-years of follow-up, there were 732 incident endometrial cancers. NSAID use, compared with non-use of NSAIDs, was not significantly associated with endometrial cancer risk [relative risk (RR), 0.90; 95% confidence interval (95% CI), 0.74-1.09]. Null associations were also observed by type of NSAID use [aspirin only: RR, 0.88; 95% CI, 0.70-1.11; nonaspirin NSAID (NA-NSAID) only: RR, 1.01; 95% CI, 0.79-1.29; both aspirin and NA-NSAIDs: RR, 0.85; 95% CI, 0.68-1.06]. Generally, results were not statistically significant by frequency of use for aspirin or NA-NSAIDs. Results did not change when women with a history of heart disease, hypertension, or diabetes were excluded to minimize the potential for confounding by indication. Overall, our data do not support an association between aspirin or NA-NSAID use and endometrial cancer risk.
C1 [Danforth, Kim N.; Gierach, Gretchen L.; Brinton, Louise A.; Katki, Hormuzd A.; Leitzmann, Michael F.; Schatzkin, Arthur; Lacey, James V., Jr.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Gierach, Gretchen L.] NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
[Leitzmann, Michael F.] Univ Hosp, Inst Epidemiol & Prevent Med, Regensburg, Germany.
RP Danforth, KN (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,Suite 550,MSC 7234, Rockville, MD 20852 USA.
EM danfortk@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015; Brinton, Louise/G-7486-2015; Gierach,
Gretchen/E-1817-2016
OI Brinton, Louise/0000-0003-3853-8562; Gierach,
Gretchen/0000-0002-0165-5522
FU National Cancer Institute; NIH; Sallie Rosen Kaplan
FX Intramural Research Program of the National Cancer Institute, NIH. K.
Danforth was supported in part by the Sallie Rosen Kaplan Fellowship for
Women Scientists in Cancer Research, National Cancer Institute, NIH.
NR 17
TC 17
Z9 17
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2009
VL 2
IS 5
BP 466
EP 472
DI 10.1158/1940-6207.CAPR-08-0239
PG 7
WC Oncology
SC Oncology
GA 441IU
UT WOS:000265763300010
PM 19401534
ER
PT J
AU Watters, JL
Gail, MH
Weinstein, SJ
Virtamo, J
Albanes, D
AF Watters, Joanne L.
Gail, Mitchell H.
Weinstein, Stephanie J.
Virtamo, Jarmo
Albanes, Demetrius
TI Associations between alpha-Tocopherol, beta-Carotene, and Retinol and
Prostate Cancer Survival
SO CANCER RESEARCH
LA English
DT Article
ID DIETARY VITAMIN-E; RANDOMIZED CONTROLLED-TRIAL; LIFE-STYLE; PHYSICIANS
HEALTH; UNITED-STATES; FOLLOW-UP; RISK; SUPPLEMENTATION; SERUM;
PREVENTION
AB Previous studies suggest that carotenoids and tocopherols (vitamin E compounds) may be inversely associated with prostate cancer risk, yet little is known about how they affect prostate cancer progression and survival. We investigated whether serum alpha-tocopherol, P-carotene, and retinol concentrations, or the alpha-tocopherol and beta-carotene trial supplementation, affected survival of men diagnosed with prostate cancer during the alpha-Tocopherol, beta-Carotene Cancer Prevention Study, a randomized, double-blind, placebo-controlled primary prevention trial testing the effects of beta-carotene and alpha-tocopherol supplements on cancer incidence in adult male smokers in southwestern Finland (n = 29,133). Prostate cancer survival was examined using the Kaplan-Meier method with deaths from other causes treated as censoring, and using Cox proportional hazards regression models with hazard ratios (HR) and 95% confidence intervals (CI) adjusted for family history of prostate cancer, age at randomization, benign prostatic hyperplasia, age and stage at diagnosis, height, body mass index, and serum cholesterol. As of April 2005, 1,891 men were diagnosed with prostate cancer and 395 died of their disease. Higher serum alpha-tocopherol at baseline was associated with improved prostate cancer survival (HR, 0.67; 95% CI, 0.45-1.00), especially among cases who had received the alpha-tocopherol intervention of the trial and who were in the highest quintile of alpha-tocopherol at baseline (HR, 0.51; 95% CI, 0.20-0.90) or at the 3-year follow-up measurement (HR, 0.26; 95% CI, 0.09-0.71). Serum beta-carotene, serum retinol, and supplemental beta-carotene had no apparent effects on survival. These findings suggest that higher alpha-tocopherol (and not beta-carotene or retinol) status increases overall prostate cancer survival. Further investigations, possibly including randomized studies, are needed to confirm this observation. [Cancer Res 2009;69(9):3833-41]
C1 [Watters, Joanne L.; Weinstein, Stephanie J.; Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Gail, Mitchell H.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Virtamo, Jarmo] Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, Helsinki, Finland.
RP Watters, JL (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd,EPS Suite 320, Bethesda, MD 20892 USA.
EM wattersj@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015
FU NIH; National Cancer Institute.; USPHS [N01-CN-45165, N01-RC-45035,
N01-RC-37004]; Department of Health and Human Services.
FX Intramural Research Program of the NIH and the National Cancer
Institute. Additionally, this research was supported by USPHS contracts
N01-CN-45165, N01-RC-45035, and N01-RC-37004 from the National Cancer
Institute, Department of Health and Human Services.
NR 46
TC 25
Z9 26
U1 1
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
IS 9
BP 3833
EP 3841
DI 10.1158/0008-5472.CAN-08-4640
PG 9
WC Oncology
SC Oncology
GA 441IG
UT WOS:000265761900016
PM 19383902
ER
PT J
AU Hodge, DL
Yang, J
Buschman, MD
Schaughency, PM
Dang, H
Bere, W
Yang, YL
Savan, R
Subleski, JJ
Yin, XM
Loughran, TP
Young, HA
AF Hodge, Deborah L.
Yang, Jun
Buschman, Matthew D.
Schaughency, Paul M.
Dang, Hong
Bere, William
Yang, Yili
Savan, Ram
Subleski, Jeff J.
Yin, Xiao-Ming
Loughran, Thomas P., Jr.
Young, Howard A.
TI Interleukin-15 Enhances Proteasomal Degradation of Bid in Normal
Lymphocytes: Implications for Large Granular Lymphocyte Leukemias
SO CANCER RESEARCH
LA English
DT Article
ID NATURAL-KILLER-CELLS; DNA-DAMAGE RESPONSE; LYMPHOPROLIFERATIVE DISEASE;
APOPTOSIS INDUCTION; SIGNALING PATHWAYS; IL-2 RECEPTOR; BETA-CHAIN;
MICE; SURVIVAL; PROLIFERATION
AB Large granular lymphocyte (LGL) leukemia is a clonal proliferative disease of T and natural killer (NK) cells. Interleukin (IL)-15 is important for the development and progression of LGL leukemia and is a survival factor for normal NK and T memory cells. IL-15 alters expression of Bcl-2 family members, Bcl-2, Bcl-XL, Bim, Noxa, and Mcl-1; however, effects on Bid have not been shown. Using an adoptive transfer model, we show that NK cells from Bid-deficient mice survive longer than cells from wild-type control mice when transferred into IL-15-null mice. In normal human NK cells, IL-15 significantly reduces Bid accumulation. Decreases in Bid are not due to alterations in RNA accumulation but result from increased proteasomal degradation. IL-15 up-regulates the E3 ligase HDM2 and we find that HDM2 directly interacts with Bid. HDM2 suppression by short hairpin RNA increases Bid accumulation lending further support for HDM2 involvement in Bid degradation. In primary leukemic LGLs, Bid levels are low but are reversed with bortezomib treatment with subsequent increases in LGL apoptosis. Overall, these data provide a novel molecular mechanism for IL-15 control of Bid that potentially links this cytokine to leukemogenesis through targeted proteasome degradation of Bid and offers the possibility that proteasome inhibitors may aid in the treatment of LGL leukemia. [Cancer Res 2009;69(9):3986-94]
C1 [Hodge, Deborah L.; Schaughency, Paul M.; Dang, Hong; Bere, William; Savan, Ram; Subleski, Jeff J.; Young, Howard A.] NCI, Expt Immunol Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Hodge, Deborah L.; Schaughency, Paul M.; Dang, Hong; Bere, William; Savan, Ram; Subleski, Jeff J.; Young, Howard A.] SAIC Frederick, Frederick, MD 21702 USA.
[Yang, Yili] NCI, Lab Prot Dynam & Signaling, Frederick, MD 21702 USA.
[Buschman, Matthew D.] Burnham Inst Med Res, La Jolla, CA USA.
[Yang, Jun; Loughran, Thomas P., Jr.] Penn State Univ, Penn State Canc Inst, Coll Med, Hershey, PA USA.
[Yin, Xiao-Ming] Univ Pittsburgh, Sch Med, Dept Pathol, Div Mol Diagnost, Pittsburgh, PA USA.
RP Young, HA (reprint author), NCI, Expt Immunol Lab, Canc & Inflammat Program, Ctr Canc Res, 1050 Boyles St,Bldg 560,Room 31-93, Frederick, MD 21702 USA.
EM younghow@mail.nih.gov
FU Intramural Research Program of die National Cancer Institute; NIH Center
for Cancer Research; National Cancer Institute/NIH [N01CO-12400]
FX Intramural Research Program of die National Cancer Institute/NIH Center
for Cancer Research and National Cancer Institutc/NIH contract
N01CO-12400.
NR 47
TC 27
Z9 31
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
IS 9
BP 3986
EP 3994
DI 10.1158/0008-5472.CAN-08-3735
PG 9
WC Oncology
SC Oncology
GA 441IG
UT WOS:000265761900034
PM 19366803
ER
PT J
AU Woo, HG
Park, ES
Lee, JS
Lee, YH
Ishikawa, T
Kim, YJ
Thorgeirsson, SS
AF Woo, Hyun Goo
Park, Eun Sung
Lee, Ju-Seog
Lee, Yun-Han
Ishikawa, Tsuyoshi
Kim, Yoon Jun
Thorgeirsson, Snorri S.
TI Identification of Potential Driver Genes in Human Liver Carcinoma by
Genomewide Screening
SO CANCER RESEARCH
LA English
DT Article
ID HUMAN HEPATOCELLULAR-CARCINOMA; MTOR PATHWAY; IN-VIVO; CANCER;
EXPRESSION; CLASSIFICATION; METFORMIN; TUMORS; GROWTH; TRANSCRIPTION
AB Genomic copy number aberrations and corresponding transcriptional deregulation in the cancer genome have been suggested to have regulatory roles in cancer development and progression. However, functional evaluation of individual genes from lengthy lists of candidate genes from genomic data sets presents a significant challenge. Here, we report effective gene selection strategies to identify potential driver genes based on systematic integration of genome scale data of DNA copy numbers and gene expression profiles. Using regional pattern recognition approaches, we discovered the most probable copy number-dependent regions and 50 potential driver genes. At each step of the gene selection process, the functional relevance of the selected genes was evaluated by estimating the prognostic significance of the selected genes. Further validation using small interference RNA-mediated knockdown experiments showed proof-of-principle evidence for the potential driver roles of the genes in hepatocellular carcinoma progression (i.e., NCSTN and SCRIB). In addition, systemic prediction of drug responses implicated the association of the 50 genes with specific signaling molecules (mTOR, AMPK, and EGFR). In conclusion, the application of an unbiased and integrative analysis of multidimensional genomic data sets can effectively screen for potential driver genes and provides novel mechanistic and clinical insights into the pathobiology of hepatocellular carcinoma. [Cancer Res 2009;69(9):4059-66]
C1 [Thorgeirsson, Snorri S.] NCI, Ctr Excellence Integrat Canc Biol & Genom, Expt Carcinogenesis Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Park, Eun Sung; Lee, Ju-Seog] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Div Canc Med, Houston, TX 77030 USA.
[Kim, Yoon Jun] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 151, South Korea.
[Kim, Yoon Jun] Seoul Natl Univ, Coll Med, Liver Res Inst, Seoul, South Korea.
RP Thorgeirsson, SS (reprint author), NCI, Ctr Excellence Integrat Canc Biol & Genom, Expt Carcinogenesis Lab, Ctr Canc Res,NIH, 37 Convent Dr,MSC 4262,Bldg 37,Room 4146A, Bethesda, MD 20892 USA.
EM snorri_thorgeirsson@nih.gov
RI Kim, Yoon Jun/J-2746-2012
FU Intramural NIH HHS [Z99 CA999999]
NR 39
TC 60
Z9 64
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
IS 9
BP 4059
EP 4066
DI 10.1158/0008-5472.CAN-09-0164
PG 8
WC Oncology
SC Oncology
GA 441IG
UT WOS:000265761900043
PM 19366792
ER
PT J
AU Abraham, I
Jain, S
Wu, CP
Kuang, YH
Lee, J
Chen, X
El Sayed, K
Ambudkar, S
Chen, ZS
AF Abraham, Ioana
Jain, Sandeep
Wu, Chung-Pu
Kuang, Yehong
Lee, Jefferson
Chen, Xiang
El Sayed, Khalid
Ambudkar, Suresh
Chen, Zhe-Sheng
TI Marine sponge-derived sipholane triterpenes reverse P-glycoprotein
(ABCB1)-mediated multidrug resistance in cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 St Johns Univ, Jamaica, NY 11439 USA.
Univ Louisiana, Monroe, LA USA.
NCI, Bethesda, MD 20892 USA.
Cent S Univ, Xiang Ya Hosp, Changsha, Hunan, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 896
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802005
ER
PT J
AU Adiseshaiah, P
Stern, S
Dobrovolskaia, M
Clogston, J
Zeng, JW
Hall, J
Patri, A
McNeil, S
AF Adiseshaiah, Pavan
Stern, Stephan
Dobrovolskaia, Marina
Clogston, Jeffrey
Zeng, Jiwen
Hall, Jennifer
Patri, Anil
McNeil, Scott
TI Preclinical characterization of nanomaterial intended for cancer
diagnosis and therapy
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 ATP NCL, Frederick, MD USA.
NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5362
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701085
ER
PT J
AU Adiseshaiah, P
Stern, S
Devalapally, H
Ganta, S
Dobrovolskaia, M
Potter, T
Mcleland, C
Clogston, J
Patri, A
Amiji, M
McNeil, S
AF Adiseshaiah, Pavan
Stern, Stephan
Devalapally, Harikrishna
Ganta, Srinivas
Dobrovolskaia, Marina
Potter, Timothy
Mcleland, Christopher
Clogston, Jeffrey
Patri, Anil
Amiji, Mansoor
McNeil, Scott
TI An evaluation of a novel nanoemulsion formulation of paclitaxel for
cytotoxicity and apoptotic activity in human colon cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 ATP NCL, Frederick, MD USA.
NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
Northeastern Univ, Dept Pharmaceut Sci, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5374
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701096
ER
PT J
AU Ahn, J
Schumacher, F
Berndt, S
Pfeiffer, R
Kaaks, R
Thun, M
Hunter, D
Hayes, R
AF Ahn, Jiyoung
Schumacher, Fredrick
Berndt, Sonja
Pfeiffer, Ruth
Kaaks, Rudolf
Thun, Michael
Hunter, David
Hayes, Richard
CA Breast Prostate Canc Cohort
TI Quantitative trait loci predicting circulating sex steroid hormones in
men from the NCI-Breast and Prostate Cancer Cohort Consortium (BPC3)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, DCEG, Rockville, MD USA.
Univ So Calif, Los Angeles, CA USA.
German Canc Res Ctr, Heidelberg, Germany.
Amer Canc Soc, Atlanta, GA 30329 USA.
Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-239
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702706016
ER
PT J
AU Alessandro, R
Fontana, S
Barranca, M
Corrado, C
Giordano, M
Zanella-Cleon, I
Becchi, M
Kohn, E
De Leo, G
AF Alessandro, Riccardo
Fontana, Simona
Barranca, Marilisa
Corrado, Chiara
Giordano, Margherita
Zanella-Cleon, Isabel
Becchi, Michel
Kohn, Elise
De Leo, Giacomo
TI Molecular profiling of chronic myelogenous leukemia cell lines:
identification of new molecular markers for the characterization of
leukemia phenotype
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Palermo, Palermo, Italy.
CNRS, Inst Biol & Chim Prot, Lyon, France.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4742
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701168
ER
PT J
AU Alley, M
Plater, K
Borgel, S
Anver, M
Hollingshead, M
AF Alley, Michael
Plater, Kevin
Borgel, Suzanne
Anver, Miriam
Hollingshead, Melinda
TI A method for obtaining improved growth of tumor xenografts from the
surgical implantation of limited numbers of colonies derived from human
colon cancer cell lines
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Dev Therapeut Program, Frederick, MD 21701 USA.
SAIC Frederick Inc, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3170
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803462
ER
PT J
AU Anderson, K
Mongin, S
Sinha, R
Gross, M
Church, T
AF Anderson, Kristin
Mongin, Steven
Sinha, Rashmi
Gross, Myron
Church, Timothy
TI Pancreatic cancer risk: associations with meat-derived carcinogen intake
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Minnesota SPH, Minneapolis, MN USA.
Univ Minnesota, Minneapolis, MN USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-224
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703453
ER
PT J
AU Andreotti, G
Hou, LF
Freeman, LB
Mahajan, R
Koutros, S
Coble, J
Blair, A
Hoppin, J
Alavanja, M
AF Andreotti, Gabriella
Hou, Lifang
Freeman, Laura Beane
Mahajan, Rajeev
Koutros, Stella
Coble, Joseph
Blair, Aaron
Hoppin, Jane
Alavanja, Michael
TI Obesity, agricultural pesticide use and cancer incidence in the
Agricultural Health Study Cohort
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Rockville, MD USA.
NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2136
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704078
ER
PT J
AU Aprelikova, O
Yu, X
Palla, J
John, S
Yi, M
Stephens, R
Han, H
Risinger, J
Jazaeri, A
Niederhuber, J
AF Aprelikova, Olga
Yu, Xiang
Palla, John
John, Simone
Yi, Ming
Stephens, Robert
Han, Hui
Risinger, John
Jazaeri, Amir
Niederhuber, John
TI Differential expression of microRNAs in endometrial cancer
microenvironment
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
SAIC, Frederick, MD USA.
Mem Hlth Univ Med Ctr, Savannah, GA 31404 USA.
Univ Virginia, Charlottesville, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 591
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803131
ER
PT J
AU Arun, P
Brown, M
Ehsanian, R
Chen, Z
Van Waes, C
AF Arun, Pattatheyil
Brown, Matthew
Ehsanian, Reza
Chen, Zhong
Van Waes, Carter
TI Nuclear localized NF-kB Rel A is phosphorylated at Serine 276 by protein
kinase A and contributes to the malignant phenotype of head and neck
cancer.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Arun, Pattatheyil; Brown, Matthew; Ehsanian, Reza; Chen, Zhong; Van Waes, Carter] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2758
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804131
ER
PT J
AU Bai, R
Hamel, E
AF Bai, Ruoli
Hamel, Ernest
TI Interaction of [H-3]halichondrin B with tubulin
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Bai, Ruoli; Hamel, Ernest] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5570
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604329
ER
PT J
AU Baird, B
Dickey, J
Sedelnikova, O
Redon, C
Nakamura, A
Bonner, W
AF Baird, Brandon
Dickey, Jennifer
Sedelnikova, Olga
Redon, Christophe
Nakamura, Asako
Bonner, William
TI The bystander effect: a general cellular mechanism in response to
various stresses including tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Baird, Brandon; Dickey, Jennifer; Sedelnikova, Olga; Redon, Christophe; Nakamura, Asako; Bonner, William] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1308
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801390
ER
PT J
AU Bandele, O
Wang, XT
Noureddine, M
Resnick, M
Bell, D
AF Bandele, Oman
Wang, Xuting
Noureddine, Maher
Resnick, Michael
Bell, Douglas
TI Single nucleotide polymorphisms alter sequence-specific p53-DNA binding
to gene regulatory elements
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Bandele, Oman; Wang, Xuting; Noureddine, Maher; Resnick, Michael; Bell, Douglas] NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4223
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802133
ER
PT J
AU Baranello, L
Bertozzi, D
Pommier, Y
Capranico, G
AF Baranello, Laura
Bertozzi, Davide
Pommier, Yves
Capranico, Giovanni
TI Induction of a novel long antisense RNA from the human HIF-1\#945; locus
may contribute to HIF-1\#945; regulation and inhibition by camptothecins
in cancer cells.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Bologna, Dept Biochem, I-40126 Bologna, Italy.
NCI, Mol Pharmacol Lab, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3753
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604162
ER
PT J
AU Beck, G
Camalier, C
Young, M
Yi, M
Hood, B
Perella, C
Bobe, G
Stephens, R
Conrads, T
Colburn, N
AF Beck, George
Camalier, Corinne
Young, Matthew
Yi, Ming
Hood, Brian
Perella, Christine
Bobe, Gerd
Stephens, Robert
Conrads, Thomas
Colburn, Nancy
TI Inorganic phosphate is a mitogen that alters cell growth, transformation
and tumorigenesis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Emory Univ, Sch Med, Atlanta, GA USA.
NCI, Frederick, MD 21701 USA.
SAIC NCI Frederick, Frederick, MD USA.
Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 970
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801304
ER
PT J
AU Beckstead, W
Wei, J
Song, Y
Chen, QR
Khan, J
AF Beckstead, Wesley
Wei, Jun
Song, Young
Chen, Qing-Rong
Khan, Javed
TI Massively parallel sequencing of microRNAs in neuroblastoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Beckstead, Wesley; Wei, Jun; Song, Young; Chen, Qing-Rong; Khan, Javed] NCI, Oncogen Sect, Pediat Oncol Branch, Adv Technol Ctr, Gaithersburg, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2595
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804115
ER
PT J
AU Behrsing, H
Furniss, M
Robillard, K
Mesa, D
Richards, R
Hamre, J
Tomaszewski, J
Parchment, R
AF Behrsing, Holger
Furniss, Michael
Robillard, Kristine
Mesa, Danielle
Richards, Ryan
Hamre, John
Tomaszewski, Joseph
Parchment, Ralph
TI In vitro detection of O4 benzylfolate modulated, BCNU toxicity in human
bone marrow using CFU-GM and tumor cell lines
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI Frederick, SAIC Frederick, Frederick, MD USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4582
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705107
ER
PT J
AU Bekaii-Saab, T
Phelps, M
Li, XB
Saji, M
Kosuri, K
Goff, L
Kauh, J
O'Neil, B
South, C
Thomas, J
Balsom, S
Chattah, N
Balint, C
Liersemann, R
Vasko, V
Marsh, W
Doyle, LA
Ellison, G
Ringel, M
Calero, MV
AF Bekaii-Saab, Tanios
Phelps, Mitch
Li, Xiaobai
Saji, Motoyasu
Kosuri, Kavitha
Goff, Laura
Kauh, John
O'Neil, Bert
South, Christopher
Thomas, James
Balsom, Stephanie
Chattah, Nicole
Balint, Catherine
Liersemann, Ryan
Vasko, Vasily
Marsh, William
Doyle, L. Austin
Ellison, Gilian
Ringel, Matthew
Calero, Miguel Villalona
TI A Multi-institutional Study of AZD6244 (ARRY-142886) in Patients with
Advanced Biliary Cancers.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Ohio State Univ, Comp Canc Ctr, Columbus, OH 43210 USA.
Vanderbilt Univ, Nashville, TN 37235 USA.
Emory Univ, Atlanta, GA 30322 USA.
Univ N Carolina, Raleigh, NC USA.
Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
NCI, CTEP, Bethesda, MD 20892 USA.
Astra Zeneca, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-129
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805307
ER
PT J
AU Bendiabdellah, Y
Zinzalla, G
Badarch, U
Nahar, K
Antonow, D
Rahman, K
Shoemaker, R
Melillo, G
Thurston, D
AF Bendiabdellah, Yassine
Zinzalla, Giovanna
Badarch, Uranchimeg
Nahar, Kazi
Antonow, Dyeison
Rahman, Khondaker
Shoemaker, Robert
Melillo, Giovanni
Thurston, David
TI Design, synthesis and biological evaluation of potential inhibitors of
the HIF-1 \#945;:HIF-1\#946; protein-protein interaction
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ London, CR UK Prot Prot Interact Drug Discovery Res Grp, London, England.
NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
NCI, Dev Therapeut Program, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4646
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604187
ER
PT J
AU Berndt, S
Huang, WY
Yeager, M
Schoen, R
Chanock, S
Hayes, R
AF Berndt, Sonja
Huang, Wen-Yi
Yeager, Meredith
Schoen, Robert
Chanock, Stephen
Hayes, Richard
TI Large-scale investigation of candidate genes and risk of advanced
colorectal adenoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 93
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704042
ER
PT J
AU Beumer, J
Parise, R
Eiseman, J
Covey, J
Egorin, M
AF Beumer, Jan
Parise, Robert
Eiseman, Julie
Covey, Joseph
Egorin, Merrill
TI Nonenzymatic formation of active products of benzaldehyde dimethane
sulfonate (NSC 281612) and benzoic acid dimethane sulfonate: relevance
for future trials
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4520
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704383
ER
PT J
AU Bi, K
Wang, J
Machleidt, T
Hermanson, S
Sakamuru, S
Huang, RL
Xia, MH
AF Bi, Kun
Wang, Jun
Machleidt, Thomas
Hermanson, Spencer
Sakamuru, Srilatha
Huang, Ruili
Xia, Menghang
TI Identification of small molecule inducers of endoplasmic reticulum
stress response
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Invitrogen, Madison, WI USA.
NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5246
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803322
ER
PT J
AU Black, A
Sherman, M
Duggan, M
Carreon, J
Berg, C
Kessel, B
Buys, S
Ragard, L
Johnson, K
Dunn, B
Lamerato, L
Kreimer, A
AF Black, Amanda
Sherman, Mark
Duggan, Maire
Carreon, J.
Berg, Christine
Kessel, Bruce
Buys, Saundra
Ragard, Lawrence
Johnson, Karen
Dunn, Barbara
Lamerato, Lois
Kreimer, Aimee
TI Pathologic findings following false positive CA-125 or transvaginal
ultrasound screens for ovarian cancer in the Prostate, Lung, Colorectal
and Ovarian (PLCO) Cancer Screening Trial
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Calgary, Calgary, AB, Canada.
Queens Med Ctr, Honolulu, HI USA.
Univ Utah, Salt Lake City, UT USA.
Westat Corp, Rockville, MD USA.
Henry Ford Hlth Syst, Detroit, MI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4824
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801154
ER
PT J
AU Bobe, G
Albert, P
Lanza, E
Schatzkin, A
Colburn, N
Cross, A
AF Bobe, Gerd
Albert, Paul
Lanza, Elaine
Schatzkin, Arthur
Colburn, Nancy
Cross, Amanda
TI Interleukin-6 as a potential biomarker for dietary prevention of
advanced colorectal adenoma recurrence in the polyp prevention trial
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, CCR, Frederick, MD 21701 USA.
NCI, DCTD, Rockville, MD USA.
NCI, CCR, Rockville, MD USA.
NCI, DCEG, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1915
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603174
ER
PT J
AU Boehm, A
Higgins, J
Franzusoff, A
Schlom, J
Hodge, J
AF Boehm, Amanda
Higgins, Jack
Franzusoff, Alex
Schlom, Jeffrey
Hodge, James
TI Vaccination with two distinct vaccine vector platforms targeting the
same antigen generates phenotypically and functionally distinct T-cell
populations
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
GlobeImmune Inc, Louisville, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 347
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805243
ER
PT J
AU Bosquet, JG
Yeager, M
Kraft, P
Jacobs, K
Wacholder, S
Hoover, R
Thomas, G
Hunter, D
Chanock, S
AF Bosquet, Jesus Gonzalez
Yeager, Meredith
Kraft, Peter
Jacobs, Kevin
Wacholder, Sholom
Hoover, Robert
Thomas, Gilles
Hunter, David
Chanock, Stephen
TI Fine mapping breast cancer risk with haplotype association analysis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, CGEMS Initiat, DCEG, NIH,DHHS, Gaithersburg, MD USA.
Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
NCI, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 101
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704051
ER
PT J
AU Bulut, G
Chen, K
Glasgow, E
Hong, SH
Lee, HS
Toretsky, J
Daar, I
Khanna, C
Uren, A
AF Bulut, Gulay
Chen, Kevin
Glasgow, Eric
Hong, Sung-Hyeok
Lee, Hyun-Shik
Toretsky, Jeffrey
Daar, Ira
Khanna, Chand
Uren, Aykut
TI Small molecule inhibitors of ezrin as anti-metastatic agents in
osteosarcoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Georgetown Univ, Lombardi Comp Canc Ctr, Washington, DC USA.
NCI, Bethesda, MD 20892 USA.
NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4961
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603371
ER
PT J
AU Burgess, D
Rodesch, M
Bainbridge, M
Nazareth, L
Boland, J
Munzy, D
Kitzman, J
D'Ascenzo, M
Matthews, C
Amundadottir, L
Dannenberg, L
Zhang, XM
Richmond, T
Jeddeloh, J
Albert, T
Channock, S
Gibbs, R
AF Burgess, Daniel
Rodesch, Matthew
Bainbridge, Matthew
Nazareth, Lynne
Boland, Joseph
Munzy, Donna
Kitzman, Jacob
D'Ascenzo, Mark
Matthews, Casey
Amundadottir, Laufrey
Dannenberg, Luke
Zhang, Xinmin
Richmond, Todd
Jeddeloh, Jeffrey
Albert, Thomas
Channock, Stephen
Gibbs, Richard
TI Sequence capture approaches coupled to next generation sequencing to
identify candidate somatic mutations in human tumors, and germ-line
mutations predisposing human cancers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Roche NimbleGen Inc, Madison, WI USA.
Human Genome Sequencing Ctr, Houston, TX USA.
NCI, Gaithersburg, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1399
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803465
ER
PT J
AU Burrell, A
Porter-Gill, P
Kohaar, I
Arhancet, J
Prokunina-Olsson, L
AF Burrell, Allison
Porter-Gill, Patricia
Kohaar, Indu
Arhancet, Juan
Prokunina-Olsson, Ludmila
TI Translational and genetic studies on JazF1 in prostate cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Burrell, Allison; Porter-Gill, Patricia; Kohaar, Indu; Arhancet, Juan; Prokunina-Olsson, Ludmila] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 91
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704040
ER
PT J
AU Calvert, R
Maciag, A
Gupta, M
Anderson, L
AF Calvert, Richard
Maciag, Anna
Gupta, Meghana
Anderson, Lucy
TI Mutant K-ras 4A protein expression shows a strong positive correlation
with superoxide production in human lung adenocarcinoma cell lines
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 US FDA, College Pk, MD USA.
SAIC Frederick Inc, Frederick, MD USA.
Case Western Reserve Univ, Cleveland, OH 44106 USA.
NCI Frederick, Comparat Carcinogenesis Lab, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 437
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801314
ER
PT J
AU Camphausen, K
AF Camphausen, Kevin
TI Histone deacetylase inhibitors combined with radiation in the treatment
of high grade gliomas
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Camphausen, Kevin] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY28-3
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702600112
ER
PT J
AU Camps, J
Hummon, A
Grade, M
Emons, G
Nguyen, Q
Ghadimi, BM
Difilippantonio, M
Caplen, N
Ried, T
AF Camps, Jordi
Hummon, Amanda
Grade, Marian
Emons, Georg
Quang Nguyen
Ghadimi, B. Michael
Difilippantonio, Michael
Caplen, Natasha
Ried, Thomas
TI Functional validation of deregulated genes on chromosome 13 identifies
novel candidate oncogenes in colon cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Med Gottingen, Gottingen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1444
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804016
ER
PT J
AU Carlson, M
Chen, YY
Annunziata, C
Kohn, E
Chiosis, G
Robles, A
Varticovski, L
AF Carlson, Marisa
Chen, Yun-Yun
Annunziata, Christina
Kohn, Elise
Chiosis, Gabriela
Robles, Ana
Varticovski, Lyuba
TI The novel HSP90 inhibitor, PU-H71, synergizes with cisplatin and blocks
invasion and migration of ovarian cell lines.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Denver, Denver, CO USA.
Univ Maryland, Bethesda, MD USA.
NCI, CCR, Bethesda, MD 20892 USA.
MSKCC, New York, NY USA.
RI Annunziata, Christina/L-3219-2016
OI Annunziata, Christina/0000-0003-2033-6532
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1857
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802179
ER
PT J
AU Carol, H
Lock, R
Houghton, P
Morton, C
Maris, J
Courtright, J
Kolb, E
Gorlick, R
Friedman, H
Keir, S
Kang, M
Reynolds, C
Smith, M
AF Carol, Hernan
Lock, Richard
Houghton, Peter
Morton, Christopher
Maris, John
Courtright, Joshua
Kolb, E.
Gorlick, Richard
Friedman, Henry
Keir, Stephen
Kang, Min
Reynolds, C.
Smith, Malcolm
TI Pediatric preclinical testing program (PPTP) evaluation of the Akt
inhibitor GSK690693
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Childrens Canc Inst, Sydney, NSW, Australia.
St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
Alfred I DuPont Hosp Children, Wilmington, DE USA.
Montefiore Med Ctr, Bronx, NY 10467 USA.
Duke Univ, Durham, NC USA.
Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
NCI, CTEP, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3193
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803487
ER
PT J
AU Cerchietti, L
Lopes, E
Yang, SN
Hatzi, K
Shaknovich, R
Robles, A
Walling, J
Bhalla, K
Chiosis, G
Melnick, A
AF Cerchietti, Leandro
Lopes, Eloisi
Yang, Shao Ning
Hatzi, Katerina
Shaknovich, Rita
Robles, Ana
Walling, Jennifer
Bhalla, Kapil
Chiosis, Gabriela
Melnick, Ari
TI A purine scaffold heat shock protein 90 (Hsp90) inhibitor destabilizes
BCL6 and has specific anti-tumor activity in BCL6 dependent lymphomas in
vitro and in vivo
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Cornell Univ, Weill Cornell Med Coll, New York, NY 10021 USA.
Sloan Kettering Inst, Dept Mol Pharmacol & Chem, New York, NY USA.
NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
NCI, Neurooncol Branch, NIH, Bethesda, MD 20892 USA.
Med Coll Georgia, Ctr Canc, Augusta, GA 30912 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2937
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802118
ER
PT J
AU Chapman, C
Perez-Galan, P
Wiestner, A
AF Chapman, Colby
Perez-Galan, Patricia
Wiestner, Adrian
TI ON 01910.Na, a novel clinical grade PLK-1 inhibitor, selectively induces
apoptosis in human B-cell chronic lymphocytic leukemia (B-CLL)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chapman, Colby; Perez-Galan, Patricia; Wiestner, Adrian] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3654
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705185
ER
PT J
AU Chen, G
Ghosh, P
Longo, D
AF Chen, Gang
Ghosh, Paritosh
Longo, Dan
TI MEK1 activation results in sustained TGF-beta signaling and growth
inhibition by stabilizing type II receptor expression in human B-cell
lymphoma cell lines
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chen, Gang; Ghosh, Paritosh; Longo, Dan] NIH NIA, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4382
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804028
ER
PT J
AU Chen, QR
Song, Y
Yu, LR
Wei, J
Veenstra, T
Khan, J
AF Chen, Qing-Rong
Song, Yong
Yu, Li-Rong
Wei, Jun
Veenstra, Timothy
Khan, Javed
TI Genomic and proteomic analysis identifies biological pathways related to
high-risk neuroblastoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Gaithersburg, MD USA.
SAIC Frederick Inc, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2768
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802263
ER
PT J
AU Cheuk, A
Taylor, J
Tsang, P
Chung, JY
Song, Y
Desai, K
Yu, YL
Chen, QR
Shah, K
Mendoza, A
Wei, J
Khanna, C
Catchpoole, D
Qualman, S
Hewitt, S
Merlino, G
Chanock, S
Khan, J
AF Cheuk, Adam
Taylor, James
Tsang, Patricia
Chung, Joon-Yong
Song, Young
Desai, Krupa
Yu, Yanlin
Chen, Qing-Rong
Shah, Kushal
Mendoza, Arnulfo
Wei, Jun
Khanna, Chand
Catchpoole, Daniel
Qualman, Stephen
Hewitt, Stephen
Merlino, Glenn
Chanock, Stephen
Khan, Javed
TI Identification and characterization of activating mutations in the
fibroblast growth factor receptor 4 in rhabdomyosarcoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
NHLBI, Bethesda, MD 20892 USA.
Childrens Hosp Westmead, Westmead, NSW, Australia.
Nationwide Childrens Hosp, Columbus, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1883
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805008
ER
PT J
AU Chuang, SC
Jenab, M
Heck, J
Olshan, A
Bencko, V
Schantz, S
Curado, MP
Mates, D
McClean, M
Daudt, A
Franceschi, S
Zaridze, D
Koifman, S
Lazarus, P
Herrero, R
Fabianova, E
Luigino, DM
Zhang, ZF
Muscat, J
Talamini, R
Rudnai, P
Fernandez, L
Lissowska, J
Menezes, A
Levi, F
Hayes, R
Benhamou, S
Eluf-Neto, J
Boccia, S
Matos, E
AF Chuang, Shu-Chun
Jenab, Mazda
Heck, Julia
Olshan, Andrew
Bencko, Vladimir
Schantz, Stimson
Paula Curado, Maria
Mates, Dana
McClean, Michael
Daudt, Alexander
Franceschi, Silvia
Zaridze, David
Koifman, Sergio
Lazarus, Philip
Herrero, Rolando
Fabianova, Eleonora
Maso Luigino, Dal
Zhang, Zuo-Feng
Muscat, Joshua
Talamini, Renato
Rudnai, Peter
Fernandez, Leticia
Lissowska, Jola
Menezes, Ana
Levi, Fabio
Hayes, Richard
Benhamou, Simone
Eluf-Neto, Jose
Boccia, Stefania
Matos, Elena
TI Diet and the risk of head and neck cancer: A pooled analysis in the
INHANCE consortium
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 IARC, Lyon, France.
UNC, Chapel Hill, NC USA.
Charles Univ Prague, Prague, Czech Republic.
MSKCC, New York, NY USA.
Inst Publ Hlth, Bucharest, Romania.
Boston Univ, Boston, MA 02215 USA.
Hosp Clin Porto Allegre, Porto Alegre, RS, Brazil.
Russian Acad Med Sci, Canc Res Ctr, Moscow, Russia.
Escola Nacl Saude Publica, Rio De Janeiro, Brazil.
Penn State Coll Med, Hershey, PA USA.
Inst Invest Epidemiol, San Jose, Costa Rica.
Specialized State Hlth Inst, Banska Bystrica, Slovakia.
Aviano Canc Ctr, I-33081 Aviano, Italy.
Univ Calif Los Angeles, Los Angeles, CA USA.
Natl Inst Environm Hlth, Budapest, Hungary.
Inst Oncol & Radiol, Havana, Cuba.
Canc Ctr & Maria Sklodowska Curie, Warsaw, Poland.
Univ Fed Pelotas, Pelotas, Brazil.
Inst Univ Med Sociale & Prevent, CH-1005 Lausanne, Switzerland.
NCI, Bethesda, MD 20892 USA.
INSERM, Paris, France.
Univ Sao Paulo, Sao Paulo, Brazil.
Univ Cattolica Sacro Cuore, Rome, Italy.
Univ Buenos Aires, Buenos Aires, DF, Argentina.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1978
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703105
ER
PT J
AU Costantino, C
Witkiewicz, A
Kuwano, Y
Cozzitorto, J
Yeo, C
Gorospe, M
Brody, J
AF Costantino, Christina
Witkiewicz, Agnieszka
Kuwano, Yuki
Cozzitorto, Joseph
Yeo, Charles
Gorospe, Myriam
Brody, Jonathan
TI Increased HuR expression in pancreatic cancer cells dramatically
optimizes gemcitabine efficacy
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5539
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803239
ER
PT J
AU Coulouarn, C
Factor, V
Durkin, M
Thorgeirsson, S
AF Coulouarn, Cedric
Factor, Valentina
Durkin, Marian
Thorgeirsson, Snorri
TI Functional and clinical implications of miR-122 expression levels in
human hepatocellular carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Coulouarn, Cedric; Factor, Valentina; Durkin, Marian; Thorgeirsson, Snorri] NIH, Bethesda, MD 20892 USA.
RI Coulouarn, Cedric/E-5472-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2546
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803173
ER
PT J
AU Crende, O
Sabatino, M
Valcarcel, M
Wang, E
Marincola, F
Vidal-Vanaclocha, F
AF Crende, Olatz
Sabatino, Marianna
Valcarcel, Maria
Wang, Ena
Marincola, Francesco
Vidal-Vanaclocha, Fernando
TI Interleukin-18-dependent genes in highly metastatic VLA-4
integrin-expressing human melanoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Basque Country, Sch Med, Leioa 48940, Bizkaia, Spain.
NCI, Dept Transfus Med, Infect Dis & Immunogenet Sect, Bethesda, MD 20892 USA.
Pharmakine SL, Derio, Spain.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4972
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603415
ER
PT J
AU Daffier, M
Ford, M
Jones, R
Kovatich, A
Hood, B
Zhang, J
Veenstra, T
Conrads, T
Krizman, D
AF Daffier, Marlene
Ford, Michael
Jones, Richard
Kovatich, Albert
Hood, Brian
Zhang, Jeff
Veenstra, Timothy
Conrads, Thomas
Krizman, David
TI Quantitation of Her2 protein expression in formalin fixed breast cancer
tissue using a mass spectrometry based MRM assay
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Express Pathol Inc, Gaithersburg, MD USA.
NextGen Sci, Ann Arbor, MI USA.
MDR Global Syst LLC, Windber, PA USA.
Univ Pittsburgh, Pittsburgh, PA USA.
Merck & Co Inc, Rahway, NJ 07065 USA.
NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2620
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805282
ER
PT J
AU Dai, CL
Wang, YS
Tiwari, A
Wu, CP
Su, XD
Wang, SR
Liu, DG
Ashby, C
Huang, Y
Robey, R
Liang, YJ
Chen, LM
Shi, CJ
Ambudkar, S
Chen, ZS
Fu, LW
AF Dai, Chun-ling
Wang, Yan-sheng
Tiwari, Amit
Wu, Chung-pu
Su, Xiao-dong
Wang, Si-rong
Liu, Dong-geng
Ashby, Charles, Jr.
Huang, Yan
Robey, Robert
Liang, Yong-ju
Chen, Li-ming
Shi, Cheng-jun
Ambudkar, Suresh
Chen, Zhe-sheng
Fu, Liwu
TI Lapatinib could reverse ABCB1 and ABCG2 mediated-multidrug resistance in
Vitro, ex-vivo and in Vivo but increase exposure of chemotherapeutic
agent
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Sun Yat Sen Univ, Ctr Canc, Guangzhou 510275, Guangdong, Peoples R China.
St Johns Univ, Coll Pharm & Allied Hlth Profess, Dept Pharmaceut Sci, New York, NY USA.
NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 894
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802002
ER
PT J
AU Danforth, K
Gierach, G
Brinton, L
Hollenbeck, A
Katki, H
Leitzmann, M
Schatzkin, A
Lacey, J
AF Danforth, Kim
Gierach, Gretchen
Brinton, Louise
Hollenbeck, Albert
Katki, Hormuzd
Leitzmann, Michael
Schatzkin, Arthur
Lacey, James, Jr.
TI Nonsteroidal anti-inflammatory drug use and endometrial cancer risk in
the NIH-AARP Diet and Health Study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
AARP, Washington, DC USA.
Univ Hosp, Inst Epidemiol & Prevent Med, Regensburg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4862
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704145
ER
PT J
AU Nguyen, D
Zajac-Kaye, M
Voeller, D
Rubinstein, L
Tomaszewski, J
Kummar, S
Pommier, Y
Doroshow, J
Yang, S
AF Dat Nguyen
Zajac-Kaye, Maria
Voeller, Donna
Rubinstein, Larry
Tomaszewski, Joseph
Kummar, Shivaani
Pommier, Yves
Doroshow, James
Yang, Sherry
TI UCN-01 significantly enhances anti-cancer activity of poly(ADP-ribose)
polymerase inhibition in combination with DNA damaging agent
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Dat Nguyen; Zajac-Kaye, Maria; Voeller, Donna; Rubinstein, Larry; Tomaszewski, Joseph; Kummar, Shivaani; Pommier, Yves; Doroshow, James; Yang, Sherry] NCI, Div Canc Treatment & Diag, Med Oncol Branch, Lab Mol Pharmacol,Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4701
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604311
ER
PT J
AU Daugherty, S
Pfeiffer, R
Hayes, R
Leitzmann, M
Sigurdson, A
Silverman, D
AF Daugherty, Sarah
Pfeiffer, Ruth
Hayes, Richard
Leitzmann, Michael
Sigurdson, Alice
Silverman, Debra
TI Non-steroidal anti-inflammatory drugs and bladder cancer: A pooled
multi-cohort study.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
NYU, New York, NY USA.
Univ Regensburg, D-93053 Regensburg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-223
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703452
ER
PT J
AU De Luca, P
Vazquez, E
Moiola, C
Gueron, G
Zalazar, F
Gardner, K
De Siervi, A
AF De Luca, Paola
Vazquez, Elba
Moiola, Cristian
Gueron, Geraldine
Zalazar, Florencia
Gardner, Kevin
De Siervi, Adriana
TI BRCA1 orchestrates a novel molecular interplay at the BRCA1 and GADD153
promoters to regulate transcriptional responses to DNA damage
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Buenos Aires, Dept Biol Chem, Buenos Aires, Argentina.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1514
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804313
ER
PT J
AU DeCicco-Skinner, K
Trovato, E
Simmons, J
Wiest, J
AF DeCicco-Skinner, Kathleen
Trovato, Erika
Simmons, John
Wiest, Jonathan
TI Tpl2 knockout mice have a heightened inflammatory response to TPA:
involvement of the NFkB signal transduction pathway
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Amer Univ, Washington, DC 20016 USA.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3454
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803380
ER
PT J
AU Devor, C
Hanson, J
Bandle, R
Emmert-Buck, M
Pinto, P
Levens, D
Meltzer, P
Killian, JK
Rodriguez-Canales, J
AF Devor, Christopher
Hanson, Jeffrey
Bandle, Russell
Emmert-Buck, Michael
Pinto, Peter
Levens, David
Meltzer, Paul
Killian, J. Keith
Rodriguez-Canales, Jaime
TI Global histone modification and genome-wide methylation profiling
reveals distinct epigenetic signatures in human prostate cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Devor, Christopher; Hanson, Jeffrey; Bandle, Russell; Emmert-Buck, Michael; Pinto, Peter; Levens, David; Meltzer, Paul; Killian, J. Keith; Rodriguez-Canales, Jaime] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4744
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801457
ER
PT J
AU Diskin, S
Cole, K
Mosse, Y
Sennett, R
Lynch, J
LaQuaglia, M
Hou, CP
Khan, J
Asgharzadeh, S
Seeger, R
London, W
Madhavan, S
Gerhard, D
Smith, M
Attiyeh, E
Maris, J
AF Diskin, Sharon
Cole, Kristina
Mosse, Yael
Sennett, Rachel
Lynch, Jill
LaQuaglia, Michael
Hou, Cuiping
Khan, Javed
Asgharzadeh, Shahab
Seeger, Robert
London, Wendy
Madhavan, Subha
Gerhard, Daniela
Smith, Malcolm
Attiyeh, Edward
Maris, John
TI Identification of RAN as a neuroblastoma oncogene
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
NCI, Bethesda, MD 20892 USA.
Childrens Hosp Los Angeles, Los Angeles, CA USA.
Univ Florida, Gainesville, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5679
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702702209
ER
PT J
AU Diskin, S
Cole, K
Mosse, Y
Sennett, R
Lynch, J
LaQuaglia, M
Hou, CP
Khan, J
Asgharzadeh, S
Seeger, R
London, W
Madhavan, S
Gerhard, D
Smith, M
Attiyeh, E
Maris, J
AF Diskin, Sharon
Cole, Kristina
Mosse, Yael
Sennett, Rachel
Lynch, Jill
LaQuaglia, Michael
Hou, Cuiping
Khan, Javed
Asgharzadeh, Shahab
Seeger, Robert
London, Wendy
Madhavan, Subha
Gerhard, Daniela
Smith, Malcolm
Attiyeh, Edward
Maris, John
TI Identification of RAN as a neuroblastoma oncogene
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
NCI, Bethesda, MD 20892 USA.
Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
Univ Florida, Gainesville, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5679
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804368
ER
PT J
AU Diwan, B
Waalkes, M
AF Diwan, Bhalchandra
Waalkes, Michael
TI Induction of premalignant and malignant uterine lesions in mice exposed
to "whole life" arsenic exposure: Overexpression of ER-alpha, COX-2,
NF-kB and Cyclin D1.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21701 USA.
NIEHS, NCI, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1219
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800080
ER
PT J
AU Dong, LD
Shu, XO
Gao, YT
Milne, G
Ji, BT
Yang, G
Lai, HL
Rothman, N
Zheng, W
Chow, WH
Abnet, C
AF Dong, Linda
Shu, Xiao-Ou
Gao, Yu-Tang
Milne, Ginger
Ji, Bu-Tian
Yang, Gong
Lai, Hong-Lan
Rothman, Nathaniel
Zheng, Wei
Chow, Wong-Ho
Abnet, Christian
TI Urinary Prostaglandin E2 metabolite and Gastric Cancer Risk in the
Shanghai Women\#8217;s Health Study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, DCEG, Bethesda, MD 20892 USA.
Vanderbilt Univ, Nashville, TN 37235 USA.
Shanghai Canc Inst, Shanghai, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1013
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801487
ER
PT J
AU Duell, E
Lucenteforte, E
La Vecchia, C
Bracci, P
Holly, E
Li, DH
Silverman, D
Talamini, R
Baghurst, P
Bueno-de-Mesquita, HB
Ghadirian, P
Miller, A
Zatonski, W
Vrieling, A
Fontham, E
Su, J
Gallinger, S
Cotterchio, M
Brennan, P
Holcatova, I
Ji, BT
Olson, S
Maisonneuve, P
Lowenfels, AI
Petersen, G
Boffetta, P
AF Duell, Eric
Lucenteforte, Ersilia
La Vecchia, Carlo
Bracci, Paige
Holly, Elizabeth
Li, Donghui
Silverman, Debra
Talamini, Renato
Baghurst, Peter
Bueno-de-Mesquita, H. Bas
Ghadirian, Parviz
Miller, Anthony
Zatonski, Witold
Vrieling, Alina
Fontham, Elizabeth
Su, Joseph
Gallinger, Steven
Cotterchio, Michelle
Brennan, Paul
Holcatova, Ivana
Ji, Bu-Tian
Olson, Sara
Maisonneuve, Patrick
Lowenfels, A. I.
Petersen, Gloria
Boffetta, Paolo
TI Pancreatitis and pancreatic cancer risk: A pooled analysis in the
international pancreatic pancer case-control consortium (PanC4)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 IARC, Lyon, France.
Ist Ric Farmacol Mario Negri, Milan, Italy.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NCI, Bethesda, MD 20892 USA.
Ctr Riferimento Oncol, I-33081 Aviano, Italy.
Womens & Childrens Hosp, Adelaide, SA, Australia.
Natl Inst Publ Hlth & Environm, NL-3720 BA Bilthoven, Netherlands.
Hop Hotel Dieu, Ctr Rech CHUM, Montreal, PQ, Canada.
Univ Toronto, Dept Publ Hlth Sci, Toronto, ON, Canada.
Maria Sklodowska Curie Mem Canc Ctr & Inst Oncol, Warsaw, Poland.
Louisiana State Univ, Hlth Sci Ctr, Sch Publ Hlth, New Orleans, LA USA.
Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Program Mol Biol & Canc, 600 Univ Ave, Toronto, ON M5G 1X5, Canada.
Canc Care Ontario, Div Prevent Oncol, Toronto, ON, Canada.
Inst Hyg & Epidemiol, CR-10042 Prague, Czech Republic.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
European Inst Oncol, Milan, Italy.
New York Med Coll, Valhalla, NY 10595 USA.
Mayo Clin, Coll Med, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2140
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704083
ER
PT J
AU Eiseman, J
Bai, LH
Liggett, D
Egorin, M
Covey, J
Beumer, J
AF Eiseman, Julie
Bai, Lihua
Liggett, Dana
Egorin, Merrill
Covey, Joseph
Beumer, Jan
TI In vivo evaluation of combination treatment with gemcitabine (dFdC) and
tetrahydrouridine (THU) in xenograft models of pancreatic cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4524
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704387
ER
PT J
AU Eliassen, AH
Ziegler, R
Xu, X
Veenstra, T
Hankinson, S
AF Eliassen, A. Heather
Ziegler, Regina
Xu, Xia
Veenstra, Timothy
Hankinson, Susan
TI Reproducibility of fifteen urinary estrogens and estrogen metabolites
(EM) in premenopausal women over 2 to 3 years
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Harvard Univ, Boston, MA 02115 USA.
NCI, Bethesda, MD 20892 USA.
SAIC Frederick Inc, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3025
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703158
ER
PT J
AU ElMasri, W
Kimm, D
Devoogdt, N
Virador, V
Kohn, E
AF ElMasri, Wafic
Kimm, Daniel
Devoogdt, Nick
Virador, Victoria
Kohn, Elise
TI SLPI promotes EMT in HeyA8 and HaCaT cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [ElMasri, Wafic; Kimm, Daniel; Devoogdt, Nick; Virador, Victoria; Kohn, Elise] NCI, Bethesda, MD 20892 USA.
RI Devoogdt, Nick/H-5156-2013
OI Devoogdt, Nick/0000-0001-9220-4833
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2211
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604082
ER
PT J
AU Elmore, E
Jain, A
Steele, V
Redpath, J
AF Elmore, Eugene
Jain, Aarti
Steele, Vernon
Redpath, John
TI Time dependent gene expression changes induced by NO-aspirin in a human
colon polyp cell line
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 UC Irvine, Irvine, CA USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 956
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801289
ER
PT J
AU Engel, L
Satagopan, J
Orlow, I
Sandler, D
Sima, C
Alavanja, M
AF Engel, Lawrence
Satagopan, Jaya
Orlow, Irene
Sandler, Dale
Sima, Camelia
Alavanja, Michael
TI Sun exposure, vitamin D receptor polymorphisms, and breast cancer risk
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-225
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703454
ER
PT J
AU Erickson, H
Rodriguez-Canales, J
Albert, P
Yan, WS
Mukherjee, S
Hu, N
Goldstein, A
Chuaqui, R
Taylor, P
Emmert-Buck, M
AF Erickson, Heidi
Rodriguez-Canales, Jaime
Albert, Paul
Yan, Wusheng
Mukherjee, Sumana
Hu, Nan
Goldstein, Alisa
Chuaqui, Rodrigo
Taylor, Philip
Emmert-Buck, Michael
TI Expression Analysis of Transcripts on Chromosome Band 13q12 in
Esophageal Squamous Cell Carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 UT MD Anderson, Houston, TX USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4329
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803252
ER
PT J
AU Feigelson, H
Setiawan, V
Ziegler, R
Dossus, L
Henderson, B
AF Feigelson, Heather
Setiawan, Veronica
Ziegler, Regina
Dossus, Laure
Henderson, Brian
TI Comprehensive analysis of genetic variation in 37 genes related to
steroid hormone metabolism and risk of breast cancer in the Breast and
Prostate Cancer Cohort Consortium (BPC3)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Kaiser Permanente, Denver, CO USA.
Univ So Calif, Los Angeles, CA USA.
NCI, Bethesda, MD 20892 USA.
German Canc Res Ctr, Heidelberg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-240
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702706027
ER
PT J
AU Ferrucci, L
Sinha, R
Huang, WY
Berndt, S
Pinsky, P
Schoen, R
Hayes, R
Cross, A
AF Ferrucci, Leah
Sinha, Rashmi
Huang, Wen-Yi
Berndt, Sonja
Pinsky, Paul
Schoen, Robert
Hayes, Richard
Cross, Amanda
TI Meat and heme iron and risk of incident colorectal adenoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
NCI, Canc Prevent Div, Rockville, MD USA.
Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 61
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704390
ER
PT J
AU Finkelstein, D
Edwards, C
Kaplan-Singer, B
Hozumi, K
Koblinski, J
AF Finkelstein, David
Edwards, Chevaunne
Kaplan-Singer, Benjamin
Hozumi, Kenta
Koblinski, Jennifer
TI The laminin-\#945;1 chain peptide, AG73, binds to syndecan-1 and-4 on
breast cancer cells, promotes up-regulation of oncogenes JUN and
tenascin C, and increases bone and brain metastasis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Northwestern Univ, Chicago, IL 60611 USA.
Natl Inst Dent & Craniofacial Res, Bethesda, MD USA.
Tokyo Univ Pharm & Life Sci, Tokyo, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2072
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804098
ER
PT J
AU Fiscus, R
Johlfs, M
Wong, J
Bathina, M
Goodman, O
Vogelzang, N
AF Fiscus, Ronald
Johlfs, Mary
Wong, Janica
Bathina, Madhavi
Goodman, Oscar
Vogelzang, Nicholas
TI Knockdown of the protein kinase G isoform PKG-I\#945; using siRNA and
shRNA significantly decreases cell proliferation and increases apoptosis
in mesothelioma and prostate cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Fiscus, Ronald; Johlfs, Mary; Wong, Janica; Bathina, Madhavi; Goodman, Oscar; Vogelzang, Nicholas] NCI, Las Vegas, NV USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2501
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802494
ER
PT J
AU Fiskus, W
Wang, YC
Rao, R
Yang, YH
Chen, JG
Joshi, A
Koul, S
Upadhyay, S
Balusu, R
Fernandez, P
Joshi, R
Buckley, K
Jillella, A
Ustun, C
Atadja, P
Marquez, V
Bhalla, K
AF Fiskus, Warren
Wang, Yongchao
Rao, Rekha
Yang, Yonghua
Chen, Jianguang
Joshi, Atul
Koul, Sanjay
Upadhyay, Sunil
Balusu, Ramesh
Fernandez, Pravina
Joshi, Rajeshree
Buckley, Kate
Jillella, Anand
Ustun, Celalettin
Atadja, Peter
Marquez, Victor
Bhalla, Kapil
TI Synergistic pre-clinical activity of combined epigenetic therapy with
the EZH2 antagonist 3-Deazaneplanocinand HDAC inhibitor panobinostat
against human AML and Mantle Cell Lymphoma cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Med Coll Georgia, Augusta, GA 30912 USA.
Novartis Inst Biomed Res Inc, Cambridge, MA USA.
NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4544
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704439
ER
PT J
AU Franco, A
Malguarnera, R
Kimura, S
Pritchard, C
Marais, R
Ghossein, R
Fagin, J
AF Franco, Aime
Malguarnera, Roberta
Kimura, Shioko
Pritchard, Catrin
Marais, Richard
Ghossein, Ronald
Fagin, James
TI Endogenous expression of oncogenic Braf cooperates with Pten loss to
induce poorly differentiated thyroid cancers with complete penetrance
and early lethality
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NIH, Bethesda, MD 20892 USA.
Univ Leicester, Leicester, Leics, England.
Inst Canc Res, London SW3 6JB, England.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2086
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804387
ER
PT J
AU Fukuda, T
Sone, H
Akanuma, H
Toyoshiba, H
Yamanaka, T
Portier, C
AF Fukuda, Tomokazu
Sone, Hideko
Akanuma, Hiromi
Toyoshiba, Hiroyoshi
Yamanaka, Takeharu
Portier, Christopher
TI Computational identification of oncogenic and tumor suppressor gene
networks that related to the cell cycle regulation
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Tohoku Univ, Sendai, Miyagi 980, Japan.
Natl Inst Environm Studies Jpn, Hlth Effect Team, Tokyo, Japan.
NIEHS, NIH, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-302
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800385
ER
PT J
AU Fung, KL
Effiong, U
Gottesman, M
AF Fung, King Leung
Effiong, Uduak
Gottesman, Michael
TI Effect of human MDR1 (ABCB1) haplotype in resistance to chemotherapeutic
drugs is substrate-dependent
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
Georgetown Univ, Washington, DC USA.
Cell Biol Lab, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 901
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802010
ER
PT J
AU Gadalla, S
Mueller, C
Pfeiffer, R
Moxley, R
Kristinsson, S
Bjorkolm, M
Landgren, O
Greene, M
AF Gadalla, Shahinaz
Mueller, Christine
Pfeiffer, Ruth
Moxley, Richard
Kristinsson, Sigurdur
Bjorkolm, Magnus
Landgren, Ola
Greene, Mark
TI Cancer risk in patients with myotonic dystrophy (DM): A population-based
study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
Karolinska Univ Hosp Solna, Stockholm, Sweden.
Karolinska Inst, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2141
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704084
ER
PT J
AU Gaedcke, J
Grade, M
Sokilde, R
Kaczkowski, B
Difilippantonio, M
Ghadimi, M
Ried, T
Litman, T
AF Gaedcke, Jochen
Grade, Marian
Sokilde, Rolf
Kaczkowski, Bogumil
Difilippantonio, Michael
Ghadimi, Michael
Ried, Thomas
Litman, Thomas
TI miRNA profiles predictive for response to chemoradiotherapy in rectal
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Med Ctr, Gottingen, Germany.
Exiqon, Vedbaek, Denmark.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 584
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803123
ER
PT J
AU Gail, M
AF Gail, Mitchell
TI The value for clinical and public health decisions of adding SNPs to a
model to project breast cancer risk
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Gail, Mitchell] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY26-3
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800014
ER
PT J
AU Gail, M
AF Gail, Mitchell
TI The value for clinical and public health decisions of adding SNPs to a
model to project breast cancer risk d
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Gail, Mitchell] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY26-3
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702602376
ER
PT J
AU Gao, Y
Bjorkholm, M
Krinstinsson, S
Goldin, L
Landgren, O
AF Gao, Ying
Bjorkholm, Magnus
Krinstinsson, Sigurdur
Goldin, Lynn
Landgren, Ola
TI Broad categories of infectious diseases in combination with genetic
factors might play a role in the etiology of hodgkin lymphoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Rockville, MD USA.
Karolinska Univ Hosp Solna, Stockholm, Sweden.
Karolinska Inst, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2147
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704091
ER
PT J
AU Garcia-Diaz, M
Kunkel, T
Chou, KM
AF Garcia-Diaz, Miguel
Kunkel, Thomas
Chou, Kai-ming
TI DNA polymerase lambda and therapeutic nucleoside analogs
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 SUNY Stony Brook, Stony Brook, NY 11794 USA.
NIEHS, Res Triangle Pk, NC 27709 USA.
IUPUI, Indianapolis, IN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-53
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705065
ER
PT J
AU Garimella, S
Murrow, L
Caplen, N
Lipkowitz, S
AF Garimella, Sireesha
Murrow, Lyndsay
Caplen, Natasha
Lipkowitz, Stan
TI Identification of Weel as a molecular target in basal-type breast cancer
by an siRNA screen of the human kinome
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, LCMB, CCR, NIH, Bethesda, MD 20892 USA.
NCI, Genet Branch, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2842
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802026
ER
PT J
AU Gaston, S
Kishawi, I
Guerra, A
Cheng, YL
Nadadur, R
Kearney, M
Meltzer, S
Pinsky, P
Sorbara, L
Srivastava, S
Gary, K
AF Gaston, Sandra
Kishawi, Iman
Guerra, Andrew
Cheng Yulan
Nadadur, Rangarajan
Kearney, Michael
Meltzer, Stephen
Pinsky, Paul
Sorbara, Lynn
Srivastava, Sudhir
Gary, Kearney
TI Expression of the metastatic prostate cancer biomarker miR-141 in
prostate biopsy tissues
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
Agilent Technol, Santa Clara, CA USA.
Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
NCI, Rockville, MD USA.
New England Baptist Hosp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3840
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805135
ER
PT J
AU Gaur, A
Colburn, N
Israel, M
AF Gaur, Arti
Colburn, Nancy
Israel, Mark
TI MicroRNA-21 is highly expressed in glioblastoma multiforme and may
contribute to its malignant behavior through inhibition of Programmed
Cell Death4 (Pdcd4)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Dartmouth Med Sch, Norris Cotton Canc Ctr, Lebanon, NH USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2543
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803169
ER
PT J
AU Gillet, JP
Rutledge, R
Wu, CP
Eliseeva, T
Chen, K
Fitzgerald, P
Fales, H
Xia, D
Ambudkar, S
Gottesman, M
AF Gillet, Jean-Pierre
Rutledge, Robert
Wu, Chung-pu
Eliseeva, Tatiana
Chen, Kevin
Fitzgerald, Peter
Fales, Henry
Xia, Di
Ambudkar, Suresh
Gottesman, Michael
TI Characterization of ABCB5, a poorly studied ABC transporter highly
expressed in melanomas ocr issue v22
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Gillet, Jean-Pierre; Rutledge, Robert; Wu, Chung-pu; Eliseeva, Tatiana; Chen, Kevin; Fitzgerald, Peter; Fales, Henry; Xia, Di; Ambudkar, Suresh; Gottesman, Michael] NCI CCR, Bethesda, MD USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3881
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604369
ER
PT J
AU Giubellino, A
Lee, MJ
Shi, ZD
Jenkins, L
Appella, E
Burke, T
Trepel, J
Bottaro, D
AF Giubellino, Alessio
Lee, Min-Jung
Shi, Zhen-Dan
Jenkins, Lisa
Appella, Ettore
Burke, Terrence
Trepel, Jane
Bottaro, Donald
TI Extracellular localization of the adaptor protein Grb2
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Giubellino, Alessio; Lee, Min-Jung; Shi, Zhen-Dan; Jenkins, Lisa; Appella, Ettore; Burke, Terrence; Trepel, Jane; Bottaro, Donald] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3513
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804279
ER
PT J
AU Glaze, E
Harder, JB
McCormick, D
Johnson, W
Detrisac, C
Pommier, Y
Tomaszewski, J
AF Glaze, Elizabeth
Harder, J. Brooks
McCormick, David
Johnson, William
Detrisac, Carol
Pommier, Yves
Tomaszewski, Joseph
TI Five-day intravenous toxicity study of indenoisoquinoline analogues in
dogs
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
IIT Res Inst, Chicago, IL USA.
Pathol Associates Inc, Chicago, IL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2933
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802115
ER
PT J
AU Glick, A
Perez-Lorenzo, R
Mordasky-Markell, L
Hogan, K
Yuspa, S
AF Glick, Adam
Perez-Lorenzo, Rolando
Mordasky-Markell, Laren
Hogan, Kelly
Yuspa, Stuart
TI TGF\#946;1 dependent activation of PKC enhances tumor promotion in skin
carcinogenesis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Penn State Univ, University Pk, PA 16802 USA.
NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2374
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800177
ER
PT J
AU Glogowska, A
Kehlen, A
Hoang-Vu, C
Cheng, SY
Klonisch, T
AF Glogowska, Aleksandra
Kehlen, Astrid
Cuong Hoang-Vu
Cheng, Sheue-yann
Klonisch, Thomas
TI Expression and regulation of helix-loop-helix (HLH) inhibitory
transcription factor Id2 in thyroid cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Manitoba, Winnipeg, MB, Canada.
Probiodrug AG, Halle, Germany.
Univ Halle Wittenberg, D-06108 Halle, Germany.
NIH, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 539
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802187
ER
PT J
AU Godiska, R
Mead, D
Usdin, K
Perrault, J
AF Godiska, Ronald
Mead, David
Usdin, Karen
Perrault, Jacques
TI Linear and circular vectors for cloning and mammalian expression of
difficult DNAs.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Lucigen Corp, Middleton, WI USA.
NIH, Bethesda, MD 20892 USA.
San Diego State Univ, San Diego, CA 92182 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5219
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802276
ER
PT J
AU Grade, M
Hummon, A
Camps, J
Emons, G
Spitzner, M
Gaedcke, J
Difilippantonio, M
Becker, H
Beissbarth, T
Ghadimi, M
Caplen, N
Ried, T
AF Grade, Marian
Hummon, Amanda
Camps, Jordi
Emons, Georg
Spitzner, Melanie
Gaedcke, Jochen
Difilippantonio, Michael
Becker, Heinz
Beissbarth, Tim
Ghadimi, Michael
Caplen, Natasha
Ried, Thomas
TI Validation of novel colorectal cancer genes as potential therapeutic
targets using functional genomics approaches
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Med Goettingen, Dept Gen & Visceral Surg, Gottingen, Germany.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1991
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604378
ER
PT J
AU Green, L
Gillet, JP
Calcagno, AM
Samuel, M
Hall, M
Varma, S
Shih, J
Ambudkar, S
Gottesman, M
AF Green, Lisa
Gillet, Jean Pierre
Calcagno, Anna Maria
Samuel, Michelle
Hall, Matthew
Varma, Sudhir
Shih, Joannah
Ambudkar, Suresh
Gottesman, Michael
TI Identification of a 3D model which best emulates clinical epithelial
ovarian cancer multi-drug resistance profiles
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Cell Biol Lab, Bethesda, MD 20892 USA.
NIH, Bioinformat & Computat Biosci Branch, Bethesda, MD 20892 USA.
NCI, Biometr Res Branch, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3214
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804324
ER
PT J
AU Griffin, L
Grohar, P
Pommier, Y
Khanna, C
Khan, J
Heiman, L
AF Griffin, Laurie
Grohar, Patrick
Pommier, Yves
Khanna, Chand
Khan, Javed
Heiman, Lee
TI ET-743 modulates EWS-FLi1 activity in Ewing\#8217;s sarcoma cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Griffin, Laurie; Grohar, Patrick; Pommier, Yves; Khanna, Chand; Khan, Javed; Heiman, Lee] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1501
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804303
ER
PT J
AU Gril, B
Lockman, P
Bohn, K
Adkins, C
Mittapali, R
Taskar, K
Radaruju, V
Palmieri, D
Smith, Q
Steeg, P
AF Gril, Brunilde
Lockman, Paul
Bohn, Kaci
Adkins, Chris
Mittapali, Rajendar
Taskar, Kunal
Radaruju, Vinay
Palmieri, Diane
Smith, Quentin
Steeg, Patricia
TI Vascular density in a brain metastasis of breast cancer mice model
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Texas Tech Univ, Hlth Sci Ctr, Sch Pharm, Dept Pharmaceut Sci, Amarillo, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3171
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803463
ER
PT J
AU Grohar, P
Woldemichael, G
Griffin, L
Yeung, C
Chen, QR
Khanna, C
Khan, J
McMahon, J
Heiman, L
AF Grohar, Patrick
Woldemichael, Girma
Griffin, Laurie
Yeung, Choh
Chen, Qingrong
Khanna, Chand
Khan, Javed
McMahon, James
Heiman, Lee
TI Identification of transcription factor inhibitors: A method used to
identify small molecules that block EWS-Fli1 transcription factor
activity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
Ctr Canc Res, Mol Targets Dev Program, Frederick, MD USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3805
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800362
ER
PT J
AU Grubbs, C
Kopelovich, L
Boring, D
Steele, V
Juliana, MM
Lubet, R
AF Grubbs, Clinton
Kopelovich, Levy
Boring, Daniel
Steele, Vernon
Juliana, M. Margaret
Lubet, Ronald
TI Preventive effects of naproxen and NO-Naproxen in chemically induced
models of urinary bladder and mammary cancers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Alabama Birmingham, Birmingham, AL USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2095
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801129
ER
PT J
AU Guenther, L
Wan, XL
Khanna, C
Helman, L
Kim, SY
AF Guenther, Lillian
Wan, Xiaolin
Khanna, Chand
Helman, Lee
Kim, Su Young
TI Investigation of MET modulation in osteosarcoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Guenther, Lillian; Wan, Xiaolin; Khanna, Chand; Helman, Lee; Kim, Su Young] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3398
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802472
ER
PT J
AU Guo, X
Song, Y
Chen, QR
Khan, J
AF Guo, Xiang
Song, Young
Chen, Qingrong
Khan, Javed
TI Alternative splicing profile for the prognosis of neuroblastoma patients
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI Frederick, Adv Biomed Comp Ctr, SAIC Frederick Inc, Frederick, MD USA.
NCI, Oncogen Sect, Pediat Oncol Branch, Gaithersburg, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2599
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804160
ER
PT J
AU Hagelstrom, R
Arora, S
Gonzales, I
Choudhary, A
Khan, J
Mousses, S
Azorsa, D
AF Hagelstrom, R.
Arora, Shilpi
Gonzales, Irma
Choudhary, Ashish
Khan, Javed
Mousses, Spyro
Azorsa, David
TI Application of high-T\throughput RNAi for the identification of genes
involved in proliferation and survival of Ewing\#8217;s sarcoma cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Translat Genom Res Inst, Scottsdale, AZ USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2188
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603038
ER
PT J
AU Han, S
Lee, KM
Park, SK
Lee, JE
Ahn, HS
Shin, HY
Kang, HJ
Koo, HH
Seo, JJ
Choi, JE
Ahn, YO
Kang, D
AF Han, Sohee
Lee, Kyoung-Mu
Park, Sue K.
Lee, Jong Eun
Ahn, Hyo Seop
Shin, Hee Young
Kang, Hyoung Jin
Koo, Hong Hoe
Seo, Jong Jin
Choi, Ji Eun
Ahn, Yoon-Ok
Kang, Daehee
TI A genome-wide association study for childhood acute lymphoblastic
leukemia
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Seoul Natl Univ, Coll Med, Dept Prevent Med, Seoul, South Korea.
NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
DNA Link Inc, Seoul, South Korea.
Seoul Natl Univ, Coll Med, Dept Pediat, Canc Res Inst, Seoul, South Korea.
Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pediat, Seoul, South Korea.
Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pediat, Seoul, South Korea.
Seoul Metropolitan Boramae Hosp, Dept Pediat, Seoul, South Korea.
Seoul Natl Univ, Coll Med, Dept Prevent Med, Canc Res Inst, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 97
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704047
ER
PT J
AU Han, YY
Davis, D
Weissfeld, J
Dinse, G
AF Han, Yueh-Ying
Davis, Devra
Weissfeld, Joel
Dinse, Gregg
TI Generational risks for cancers not related to tobacco, screening, or
treatment in the United States
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Pittsburgh, Pittsburgh, PA USA.
Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 973
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703388
ER
PT J
AU Hance, K
Rogers, C
Zaharoff, D
Schlom, J
Greiner, J
AF Hance, Kenneth
Rogers, Connie
Zaharoff, David
Schlom, Jeffrey
Greiner, John
TI Gemcitabine preconditioning improves antigen-specific immune and
antitumor responses to poxvirus vaccines
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Hance, Kenneth; Rogers, Connie; Zaharoff, David; Schlom, Jeffrey; Greiner, John] NCI, CCR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-161
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805379
ER
PT J
AU Hance, K
Rogers, C
Zaharoff, D
Schlom, J
Greiner, J
AF Hance, Kenneth
Rogers, Connie
Zaharoff, David
Schlom, Jeffrey
Greiner, John
TI Gemcitabine preconditioning improves antigen-specific immune and
antitumor responses to poxvirus vaccines.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Hance, Kenneth; Rogers, Connie; Zaharoff, David; Schlom, Jeffrey; Greiner, John] NCI, CCR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LE3-161
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702605341
ER
PT J
AU Harris, C
Yanaihara, N
Seike, M
Wang, X
Yokota, J
Croce, C
AF Harris, Curtis
Yanaihara, Nozomu
Seike, Masahiro
Wang, Xin
Yokota, Jun
Croce, Carlo
TI Inflammation and cancer: Microenvironment, cytokines, microRNA, and p53
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Natl Canc Ctr, Tokyo, Japan.
Ohio State Univ, Columbus, OH 43210 USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY04-2
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800269
ER
PT J
AU Heiskanen, M
Klemm, J
Messersmith, D
Derr, L
AF Heiskanen, Mervi
Klemm, Juli
Messersmith, Donna
Derr, Leslie
TI The cancer Biomedical Informatics Grid (R) (caBIG (R)): Resources to
support translational research
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Rockville, MD USA.
SAIC Frederick, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2446
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801041
ER
PT J
AU Henning, R
Yu, MS
Virador, V
Kimm, D
Perroy, A
Kohn, E
AF Henning, Ryan
Yu, Minshu
Virador, Victoria
Kimm, Daniel
Perroy, Alyssa
Kohn, Elise
TI A novel mechanism for L-asparaginase in solid tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Henning, Ryan; Yu, Minshu; Virador, Victoria; Kimm, Daniel; Perroy, Alyssa; Kohn, Elise] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4620
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705305
ER
PT J
AU Henson, B
Bhattacharjee, S
O'Dee, D
Feingold, E
Gollin, S
AF Henson, Brian
Bhattacharjee, Samsiddhi
O'Dee, Dawn
Feingold, Eleanor
Gollin, Susanne
TI The expression of miR-125b and miR-100 in OSCC and their contribution to
malignancy
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Pittsburgh, Pittsburgh, PA USA.
NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2548
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803175
ER
PT J
AU Hollingshead, B
Baker, A
Hegamyer, G
Colburn, N
AF Hollingshead, Brett
Baker, Alyson
Hegamyer, Glenn
Colburn, Nancy
TI The identification of genes regulated by the AP-1 protein FRA-1 and
required for its tumorigenic activity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Hollingshead, Brett; Baker, Alyson; Hegamyer, Glenn; Colburn, Nancy] NCI CCR, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4237
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802150
ER
PT J
AU Hosgood, HD
Liu, CS
Rothman, N
Weinstein, S
Bonner, M
Shen, M
Lim, U
Virtamo, J
Albanes, D
Lan, Q
AF Hosgood, H. Dean
Liu, Chin-San
Rothman, Nathaniel
Weinstein, Stephanie
Bonner, Matthew
Shen, Min
Lim, Unhee
Virtamo, Jarmo
Albanes, Demetrius
Lan, Qing
TI Mitochondrial DNA copy number and lung cancer risk in a prospective
cohort study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Changhua Christian Hosp, Changhua, Taiwan.
Univ Buffalo State Univ New York, Buffalo, NY USA.
Canc Res Ctr Hawaii, Honolulu, HI USA.
Inst Publ Hlth, Helsinki, Finland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 998
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801471
ER
PT J
AU Hsieh, SM
Look, M
Smith, R
Lintell, N
Sieuwerts, A
Foekens, J
Lyn, G
Hunter, K
AF Hsieh, Szu-Min
Look, Maxine
Smith, Robert
Lintell, Nicholas
Sieuwerts, Anieta
Foekens, John
Lyn, Griffiths
Hunter, Kent
TI Polymorphisms in the SIPA1 gene are associated with sporadic breast
cancer susceptibility and hallmarks of poor prognosis in two independent
studies
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, CCR, Bethesda, MD 20892 USA.
Erasmus MC, Rotterdam, Netherlands.
Griffith Inst Hlth & Med Res, Gold Coast, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1911
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603169
ER
PT J
AU Hsing, A
Yeboah, E
Biritwum, R
Tettey, Y
DeMarzo, A
Adjei, A
Netto, G
Yu, K
Li, Y
Chokkalingam, A
Chia, D
Jadallah, S
Partin, A
Thompson, I
Quraishi, S
Addo-Ayensu, G
Niwa, S
Tarone, R
Hoover, R
AF Hsing, Ann
Yeboah, Edward
Biritwum, Richard
Tettey, Yao
DeMarzo, Angelo
Adjei, Andrew
Netto, George
Yu, Kai
Li, Yan
Chokkalingam, Anand
Chia, David
Jadallah, Sana
Partin, Alan
Thompson, Ian
Quraishi, Sabah
Addo-Ayensu, Gloria
Niwa, Shelley
Tarone, Robert
Hoover, Robert
TI High prevalence of screen detected prostate cancer in West Africans:
Implications for racial disparity of prostate cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, DCEG, Rockville, MD USA.
Univ Ghana, Accra, Ghana.
Johns Hopkins Univ, Baltimore, MD USA.
NCI, Bethesda, MD 20892 USA.
Univ Calif Berkeley, Berkeley, CA 94720 USA.
Univ Calif Los Angeles, Los Angeles, CA USA.
Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
Fairfax Dept Hlth, Fairfax, VA USA.
Westat Corp, Rockville, MD USA.
Int Inst Epidemiol, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1973
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703099
ER
PT J
AU Hudson, R
Yi, M
Volfovsky, N
Tietcheu, S
Liu, CG
Stephens, R
Calin, G
Croce, C
Ambs, S
AF Hudson, Robert
Yi, Ming
Volfovsky, Natalia
Tietcheu, Steves
Liu, Chang-Gong
Stephens, Robert
Calin, George
Croce, Carlo
Ambs, Stefan
TI Transcripts encoded by ultraconserved regions are altered in prostate
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Human Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
NCI, Adv Biomed Comp Ctr, SAIC Frederick Inc, Frederick, MD 21701 USA.
Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA.
Univ Texas MD Anderson Canc Ctr, Dept Canc Genet, Houston, TX 77030 USA.
Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1968
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803143
ER
PT J
AU Huff, L
Sackett, D
Poruchynsky, M
Fojo, T
AF Huff, Lyn
Sackett, Dan
Poruchynsky, Marianne
Fojo, Tito
TI Tubulin homeostasis in neural cells but not in cancer cells leads to
rapid proteasome-mediated tubulin degradation following drug-induced
microtubule depolymerization
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3870
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604078
ER
PT J
AU Huh, JI
Sato, M
Calvo, A
Green, J
Tchou, J
Herlyn, M
AF Huh, Jung-Im
Sato, Misako
Calvo, Alfonso
Green, Jeffrey
Tchou, Julia
Herlyn, Meenhard
TI Amphiregulin regulates mammary epithelial cell motility and interaction
between mammary epithelial cells and fibroblasts
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Korea Inst Toxicol, Daejeon, South Korea.
NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
Univ Navarra, Div Oncol, CIMA, E-31080 Pamplona, Spain.
Univ Navarra, Dept Histol & Pathol, E-31080 Pamplona, Spain.
Univ Penn Hlth Syst, Dept Surg, Philadelphia, PA USA.
Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4301
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802302
ER
PT J
AU Hwang, C
Fields, J
Anderson, L
Shiao, YH
AF Hwang, Christopher
Fields, Janet
Anderson, Lucy
Shiao, Yih-Horng
TI Human lung adenocarcinoma cells have increases in precursor and mature
rRNA and an antisense non-coding RNA species
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Hwang, Christopher; Fields, Janet; Anderson, Lucy; Shiao, Yih-Horng] NCI, Comparat Carcinogenesis Lab, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 589
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803129
ER
PT J
AU Janakiram, N
Mohammed, A
Qian, L
Choi, CI
Steele, V
Rao, C
AF Janakiram, Naveena
Mohammed, Altaf
Qian, Li
Choi, Chang-In
Steele, Vernon
Rao, Chinthalapally
TI Bexarotene, a selective RXR agonist, suppresses intestinal polyp
formation and hyperlipidemia in Min mice
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Oklahoma, Inst Canc, OUHSC, Oklahoma City, OK USA.
NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 933
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801263
ER
PT J
AU Jeon, S
Han, S
Park, AK
Lee, KM
Park, SK
Ahn, HS
Shin, HY
Kang, HJ
Koo, HH
Seo, JJ
Ahn, JE
Ahn, YO
Kim, H
Kang, D
AF Jeon, Sujee
Han, Sohee
Park, Ae Kyung
Lee, Kyoung-Mu
Park, Sue K.
Ahn, Hyo Seop
Shin, Hee Young
Kang, Hyoung Jin
Koo, Hong Hoe
Seo, Jong Jin
Ahn, Ji Eun
Ahn, Yoon-Ok
Kim, Ho
Kang, Daehee
TI Association of SNPs in hematological malignancies and Leukemia in Korean
children
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Seoul Natl Univ, Coll Med, Dept Canc Biol, Seoul, South Korea.
Seoul Natl Univ, Coll Med, Dept Prevent Med, Seoul, South Korea.
Sch Publ Hlth, Div Epidemiol & Biostat, Seoul, South Korea.
NIH, Div Canc Epidemiol & Genet, DHHS, Baltimore, MD USA.
Dept Prevent Med, Seoul, South Korea.
Seoul Natl Univ, Coll Med, Canc Res Inst, Seoul, South Korea.
Seoul Natl Univ, Dept Pediat, Seoul, South Korea.
Seoul Natl Univ, Canc Res Inst, Seoul, South Korea.
Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pediat, Seoul, South Korea.
Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pediat, Seoul, South Korea.
Seoul Metropolitan Boramae Hosp, Dept Pediat, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3044
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703252
ER
PT J
AU Jiao, L
Mitrou, P
Reedy, J
Graubard, B
Hollenbeck, A
Schatzkin, A
Stoizenberg-Solomon, R
AF Jiao, Li
Mitrou, Panagiota
Reedy, Jill
Graubard, Barry
Hollenbeck, Albert
Schatzkin, Arthur
Stoizenberg-Solomon, Rachael
TI Is a combined healthy lifestyle score associated with pancreatic cancer
risk? - a large cohort study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, DCEG, Rockville, MD USA.
World Canc Res Fund Int, London, England.
NCI, DCCPS, Rockville, MD USA.
AARP, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4882
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704168
ER
PT J
AU Jin, CY
Yang, YA
Anver, M
Morris, N
Wang, XC
Zhang, Y
AF Jin, Chaoyang
Yang, Yu-an
Anver, Miriam
Morris, Nicole
Wang, Xiangchun
Zhang, Ying
TI Smurf2 promotes metastasis of breast cancer cells by enhancing migration
and invasivenes
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, CCR, Bethesda, MD 20892 USA.
NCI Frederick, SAIC Frederick Inc, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2212
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604084
ER
PT J
AU Johannessen, L
Remsberg, J
Tarasov, S
Jiang, S
Tarasova, N
AF Johannessen, Liv
Remsberg, Jarrett
Tarasov, Sergey
Jiang, Sheng
Tarasova, Nadya
TI Peptide structure stabilization by lipidation for development of potent
inhibitors of protein-protein interactions: Application for generation
of selective IGF1R antagonists
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21701 USA.
NCI Frederick, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-79
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701031
ER
PT J
AU Johnson, W
Glaze, E
McCormick, D
Detrisac, C
Pommier, Y
Tomaszewski, J
AF Johnson, William
Glaze, Elizabeth
McCormick, David
Detrisac, Carol
Pommier, Yves
Tomaszewski, Joseph
TI Five-day intravenous toxicity study of indenoisoquinoline analogues in
F344 rats
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 IIT Res Inst, Chicago, IL USA.
NCI, Bethesda, MD 20892 USA.
Pathol Associates Inc, Chicago, IL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2934
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802116
ER
PT J
AU Joo, KM
Lee, J
Kang, YJ
Jin, J
Kang, BG
Kim, MH
Lee, SJ
Jo, MY
Kim, H
Nam, DH
AF Joo, Kyeung Min
Lee, Jeongwu
Kang, Yun Jung
Jin, Juyoun
Kang, Bong Gu
Kim, Mi Hyun
Lee, Se Jeong
Jo, Mi-Young
Kim, Hyunggee
Nam, Do-Hyun
TI An essential role of c-Met/HGF signaling in glioblastoma initiating
cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
NCI, Bethesda, MD 20892 USA.
Korea Univ, Sch Life Sci & Biotechnol, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4895
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603240
ER
PT J
AU Juhasz, A
Ge, Y
Holbeck, S
Shoemaker, R
Roy, K
Doroshow, J
AF Juhasz, Agnes
Ge, Yun
Holbeck, Susan
Shoemaker, Robert
Roy, Krishnendu
Doroshow, James
TI Distinct pharmacologic mechanisms of action of the flavin dehydrogenase
inhibitors diphenylene iodonium (DPI) and di-2-thienyliodonium (DTI)
based on NCI60 tumor cell line panel profiling
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Juhasz, Agnes; Ge, Yun; Holbeck, Susan; Shoemaker, Robert; Roy, Krishnendu; Doroshow, James] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1549
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702700378
ER
PT J
AU Katayama, K
Ambudkar, S
AF Katayama, Kazuhiro
Ambudkar, Suresh
TI The mechanism of degradation of multidrug resistance-linked
P-glycoprotein (ABCB1)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Katayama, Kazuhiro; Ambudkar, Suresh] NCI, LCB, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 899
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802008
ER
PT J
AU Kauer, M
Ban, J
Jug, G
Schwentner, R
Walker, B
Meltzer, P
Kovar, H
AF Kauer, Maximilian
Ban, Jozef
Jug, Gunhild
Schwentner, Raphaela
Walker, Bob
Meltzer, Paul
Kovar, Heinrich
TI Motif analysis reveals a potential new link between EWS-FLI1 and cell
cycle in Ewing Sarcoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 St Anna Children 92s Canc Res Inst, Vienna, Austria.
NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2463
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801060
ER
PT J
AU Kaur, G
Frary, S
Holbeck, S
Monks, A
Hollingshead, M
AF Kaur, Gurmeet
Frary, Sadie
Holbeck, Susan
Monks, Anne
Hollingshead, Melinda
TI Evaluation of NSC83265: Histone H3, BubR1 and monoastral formation are
potential pharmacodynamic biomarkers.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21701 USA.
SAIC Frederick, Frederick, MD USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4616
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705300
ER
PT J
AU Kedei, N
Czifra, G
Telek, A
Kraft, M
Truong, A
Li, W
Sanchez, C
Keck, G
Blumberg, P
AF Kedei, Noemi
Czifra, Gabriella
Telek, Andrea
Kraft, Matthew
Anh Truong
Li, Wei
Sanchez, Carina
Keck, Gary
Blumberg, Peter
TI What distinguishes a PKC activator like phorbol ester from a PKC
functional antagonist like bryostatin 1? Bryologues permit dissection of
intermediate patterns of activity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
Univ Utah, Dept Chem, Salt Lake City, UT 84112 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2667
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702700419
ER
PT J
AU Kenney, S
Vistica, D
Stockwin, L
Burkett, S
Hollingshead, M
Borgel, S
Schrump, D
Shoemaker, R
AF Kenney, Susan
Vistica, David
Stockwin, Luke
Burkett, Sandra
Hollingshead, Melinda
Borgel, Suzanne
Schrump, David
Shoemaker, Robert
TI Establishment and characterization of ASPS-1, a novel cell line derived
from metastatic alveolar soft part sarcoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21701 USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4044
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804081
ER
PT J
AU Killian, K
Bilke, S
Davis, S
Walker, R
Giaccone, G
Smith, W
Meltzer, P
AF Killian, Keith
Bilke, Sven
Davis, Sean
Walker, Robert
Giaccone, Guiseppe
Smith, William
Meltzer, Paul
TI Archival fine needle aspiration (FNA) smears: a novel resource for
clinical molecular profiling
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Suburban Hosp, Dept Pathol, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1649
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702702009
ER
PT J
AU Kim, G
Henning, R
Yu, MS
Davidson, B
Kohn, E
AF Kim, Geoffrey
Henning, Ryan
Yu, Minshu
Davidson, Ben
Kohn, Elise
TI Proteomic array analysis of cell adhesion molecules of malignant ovarian
cancer effusions
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Norwegian Radium Hosp, Oslo, Norway.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2265
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803174
ER
PT J
AU Kim, JM
Kim, JK
Shim, M
Anna, C
Chrysovergis, K
Bradbury, J
Kissling, GE
Germolec, D
Zeldin, DC
Eling, TE
AF Kim, Jeong-Min
Kim, Jin Kook
Shim, Minsub
Anna, Colleen
Chrysovergis, Kaliopi
Bradbury, J.
Kissling, Grace E.
Germolec, Dori
Zeldin, Darryl C.
Eling, Thomas E.
TI NAG-1 suppresses LPS-induced inflammation
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kim, Jeong-Min; Kim, Jin Kook; Shim, Minsub; Anna, Colleen; Chrysovergis, Kaliopi; Bradbury, J.; Kissling, Grace E.; Germolec, Dori; Zeldin, Darryl C.; Eling, Thomas E.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5337
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804489
ER
PT J
AU Kinsinger, C
Mesri, M
Hiltke, T
Rodriguez, H
AF Kinsinger, Chris
Mesri, Mehdi
Hiltke, Tara
Rodriguez, Henry
TI Building a robust and reliable proteomics biomarker pipeline:
NCI\#8217;s CPTAC network
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kinsinger, Chris; Mesri, Mehdi; Hiltke, Tara; Rodriguez, Henry] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3556
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701125
ER
PT J
AU Klonisch, T
Wark, L
Hombach-Klonisch, S
Cuong, HV
Cheng, SY
Mai, S
AF Klonisch, Thomas
Wark, Landon
Hombach-Klonisch, Sabine
Cuong Hoang-Vu
Cheng, Sheue-yann
Mai, Sabine
TI Nuclear architecture in human thyroid carcinoma revealed by
three-dimensional (3D) telomere imaging: New insight into genomic
instability and potential diagnostic application
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Manitoba, Winnipeg, MB, Canada.
Manitoba Inst Cell Biol, CancerCare Manitoba, Winnipeg, MB, Canada.
Univ Halle Wittenberg, D-06108 Halle, Germany.
NIH, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 469
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801349
ER
PT J
AU Kobayashi, H
Ogawa, M
Kosaka, N
Choyke, P
Urano, Y
AF Kobayashi, Hisataka
Ogawa, Mikako
Kosaka, Nobuyuki
Choyke, Peter
Urano, Yasuteru
TI Simultaneous imaging of quantum dot-labeled cancer cell migration and
lymphatic drainage using dendrimer-based optical agents
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, CCR, Bethesda, MD 20892 USA.
NCI, NIH, Bethesda, MD 20892 USA.
Univ Tokyo, Tokyo, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3991
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803201
ER
PT J
AU Koch, K
Zhang, CO
Guo, L
Shahjee, H
Kaczmarek, P
Michejda, C
Barchi, J
Keay, S
AF Koch, Kristopher
Zhang, Chen-Ou
Guo, Li
Shahjee, Hanief
Kaczmarek, Piotr
Michejda, Christopher
Barchi, Joseph
Keay, Susan
TI Inhibition of carcinoma and melanoma cell proliferation in vitro by a
novel frizzled 8 protein-related anti proliferative factor (APF)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Maryland, Sch Med, VAMC, Baltimore, MD 21201 USA.
NCI, Med Chem Lab, CCR, Frederick, MD 21701 USA.
NCI, Mol Aspects Drug Design Sect, Struct Biophys Lab, CCR, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 851
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604404
ER
PT J
AU Kolb, E
Gorlick, R
Houghton, P
Morton, C
Maris, J
Courtright, J
Carol, H
Lock, R
Friedman, H
Keir, S
Kang, M
Reynolds, C
Smith, M
AF Kolb, E.
Gorlick, Richard
Houghton, Peter
Morton, Christopher
Maris, John
Courtright, Joshua
Carol, Hernan
Lock, Richard
Friedman, Henry
Keir, Stephen
Kang, Min
Reynolds, C.
Smith, Malcolm
TI Pediatric Preclinical Testing Program (PPTP) evaluation of the
multi-targeted kinase inhibitor Sorafenib
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Alfred I DuPont Hosp Children, Wilmington, DE USA.
Montefiore Med Ctr, Bronx, NY 10467 USA.
St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
Childrens Canc Inst, Sydney, NSW, Australia.
Duke Univ, Durham, NC USA.
Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
NCI, CTEP, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3196
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803490
ER
PT J
AU Komlodi-Pasztor, E
Trostel, S
Sackett, D
Poruchynsky, M
Fojo, T
AF Komlodi-Pasztor, Edina
Trostel, Shana
Sackett, Dan
Poruchynsky, Marianne
Fojo, Tito
TI Impaired p53 binding to importin: A novel mechanism of cytoplasmic
sequestration identified in oxaliplatin-resistant cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 599
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804396
ER
PT J
AU Kong, HS
Lee, S
Jung, YJ
Bchiri, J
Trepel, J
Neckers, L
AF Kong, Hye-Sik
Lee, Sunmin
Jung, Yun-Jin
Bchiri, Jamila
Trepel, Jane
Neckers, Leonard
TI Nonsense-mediated mRNA decay regulates HIF-1\#945; expression in 786-O
renal cell carcinoma cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Pusan Natl Univ, Busan, South Korea.
INSERM, UMR S893, Team Microsatellite Instabil & Canc 13, Paris, France.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1530
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804330
ER
PT J
AU Kosak, K
Saavedra, J
Keefer, L
Shami, P
AF Kosak, Ken
Saavedra, Joseph
Keefer, Larry
Shami, Paul
TI A Pluronic (R) micelle formulation increases the stability of the novel
anti-cancer nitric oxide prodrug JS-K.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA.
SAIC Frederick, Frederick, MD USA.
NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 643
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701020
ER
PT J
AU Koshiol, J
Rotunno, M
Consonni, D
Pesatori, A
Goldstein, A
Chaturvedi, A
Wacholder, S
Landi, MT
Lubin, J
Caporaso, N
AF Koshiol, Jill
Rotunno, Melissa
Consonni, Dario
Pesatori, Angela
Goldstein, Alisa
Chaturvedi, Anil
Wacholder, Sholom
Landi, Maria Teresa
Lubin, Jay
Caporaso, Neil
TI Previous lung diseases and altered risk of lung cancer in
population-based case-control study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
Univ Milan, EPOCA Epidemiol Occupaz Clin & Ambientale, Milan, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2148
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704092
ER
PT J
AU Koutros, S
Schumacher, F
Ma, J
Crawford, ED
Huang, WY
Hayes, R
Berndt, S
AF Koutros, Stella
Schumacher, Fredrick
Ma, Jing
Crawford, E. David
Huang, Wen-Yi
Hayes, Richard
Berndt, Sonja
TI Pooled analysis of variants in the phosphatidylinositol 3-kinase (PI3K)
pathway and risk of prostate cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Rockville, MD USA.
Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
Univ Colorado Hlth Sci, Denver, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 92
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704041
ER
PT J
AU Kummar, S
Rubinstein, L
Kinders, R
Ji, JP
Parchment, R
Gutierrez, M
Murgo, A
Chen, A
Khin, S
Zhang, YP
Simmons, D
Yancey, MA
Allen, D
Horneffer, Y
Juwara, L
Chang, R
Gordon, G
Tomaszewski, J
Doroshow, J
AF Kummar, Shivaani
Rubinstein, Larry
Kinders, Robert
Ji, Jiuping
Parchment, Ralph
Gutierrez, Martin
Murgo, Anthony
Chen, Alice
Khin, Sonny
Zhang, Yiping
Simmons, Dwight
Yancey, Mary Ann
Allen, Deborah
Horneffer, Yvonne
Juwara, Lamin
Chang, Richard
Gordon, Gary
Tomaszewski, Joseph
Doroshow, James
TI Correlation between inhibition of the activity of poly(ADP-ribose)
polymerase (PARP) in human peripheral blood mononuclear cells (PBMCs)
and tumor biopsies following treatment with ABT-888, an inhibitor of
PARP
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
NCI Frederick, SAIC Frederick Inc, Frederick, MD USA.
Abbott Labs, Abbott Pk, IL 60064 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5456
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701484
ER
PT J
AU Kwon, HC
Oh, S
Kil, W
Burgan, W
Carter, D
Beam, K
Tofilon, P
Gardner, K
Camphausen, K
AF Kwon, Hyuk-Chan
Oh, Sung
Kil, Whoon
Burgan, William
Carter, Donna
Beam, Katie
Tofilon, Philip
Gardner, Kevin
Camphausen, Kevin
TI Enhancement of radiosensitivity in DU145 human prostate carcinoma cells
by a novel functional class of thalidomide analogs
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Dong A Univ, Med Ctr, Busan, South Korea.
NCI, NIH, Bethesda, MD 20892 USA.
Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5594
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802128
ER
PT J
AU Kwon, MJ
Kim, SS
Choi, YL
Marquez, V
Shin, YK
AF Kwon, Mi Jeong
Kim, Sung-Su
Choi, Yoon-La
Marquez, Victor
Shin, Young Kee
TI Loss of repressive histone methylation is associated with CLDN3
overexpression and multiple histone modifications regulate CLDN3
expression in ovarian cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Seoul Natl Univ, Coll Pharm, Seoul, South Korea.
Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 488
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802049
ER
PT J
AU Lai, E
Horak, K
Machida, EO
Havekes, B
Huynh, TT
Ohta, S
Adams, K
Albanese, C
Baylin, S
Pacak, K
AF Lai, Edwin
Horak, Kyle
Machida, Emi Ota
Havekes, Bas
Thanh-Truc Huynh
Ohta, Shoichiro
Adams, Karen
Albanese, Chris
Baylin, Stephen
Pacak, Karel
TI High frequency of ASC/TMS1, Rassf1A, and p16INK4A promoter methylation
in succinate dehydrogenase complex B pheochromocytomas
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NICHD, NIH, Bethesda, MD USA.
Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Georgetown Univ, Med Ctr, Dept Oncol, Lombardi Canc Comprehens Ctr, Washington, DC 20007 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5151
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801403
ER
PT J
AU Lai, JP
Han, T
Moser, C
Aderca, I
Lee, JS
Thorgeirsson, S
Roberts, L
AF Lai, Jinping
Han, Tao
Moser, Catherine
Aderca, Ileana
Lee, Ju-Seog
Thorgeirsson, Snorri
Roberts, Lewis
TI Sulfatase 2 (SULF2) functions as a novel oncogenic protein in
hepatocellular carcinoma (HCC)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mayo Clin, Rochester, MN USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5612
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802116
ER
PT J
AU Lam, E
Ringel, M
Kloos, R
Collamore, M
Arbogast, D
Liang, J
Hall, N
Knopp, M
Wright, J
Shah, M
AF Lam, Elaine
Ringel, Matthew
Kloos, Richard
Collamore, Minden
Arbogast, Dada
Liang, Jiachao
Hall, Nathan
Knopp, Michael
Wright, John
Shah, Manisha
TI A phase II study of sorafenib in patients with metastatic medullary
thyroid carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
NCI, IDB, CTEP, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4513
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805363
ER
PT J
AU Landi, M
Chatterjee, N
Yu, K
Jacobs, K
Bergen, A
Goldin, L
Goldstein, A
Wang, ZM
Burdette, L
Albanes, D
Oken, M
Thun, M
Consonni, D
Pesatori, A
Amos, C
Houlston, R
Brennan, P
Hung, R
Gaborieau, V
Spitz, M
Wang, YF
Krokan, H
Vatten, L
Benhamou, S
Metsapalu, A
Field, J
Chen, C
Goodman, G
Bickeboller, H
Risch, A
Wichmann, HE
Rafnar, T
Stefansson, K
Lathrop, M
Bertazzi, PA
Tucker, M
Chanock, S
Caporaso, N
AF Landi, Maria
Chatterjee, Nilanjan
Yu, Kai
Jacobs, Kevin
Bergen, Andrew
Goldin, Lynn
Goldstein, Alisa
Wang, Zhaoming
Burdette, Laurie
Albanes, Demetrius
Oken, Martyn
Thun, Michael
Consonni, Dario
Pesatori, Angela
Amos, Christopher
Houlston, Richard
Brennan, Paul
Hung, Rayjean
Gaborieau, Valerie
Spitz, Margaret
Wang, Yufei
Krokan, Hans
Vatten, Lars
Benhamou, Simone
Metsapalu, Andres
Field, John
Chen, Chu
Goodman, Gary
Bickeboller, Heike
Risch, Angela
Wichmann, H-Erich
Rafnar, Thorunn
Stefansson, Kari
Lathrop, Mark
Bertazzi, Pier Alberto
Tucker, Margaret
Chanock, Stephen
Caporaso, Neil
CA Geneva STUDY
TI A comprehensive genome-wide association study of lung cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Washington, Seattle, WA 98195 USA.
Univ Minnesota, Minneapolis, MN USA.
Amer Canc Soc, Atlanta, GA 30329 USA.
OMPMaRE, Milan, Italy.
Univ Milan, Milan, Italy.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Inst Canc Res, Sutton, Surrey, England.
Int Agcy Res Canc, F-69372 Lyon, France.
Univ Toronto, Toronto, ON, Canada.
Norwegian Univ Sci & Technol, N-7034 Trondheim, Norway.
INSERM, Paris, France.
Univ Tartu, EE-50090 Tartu, Estonia.
Univ Liverpool, Liverpool L69 3BX, Merseyside, England.
Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
Univ Gottingen, D-37073 Gottingen, Germany.
German Canc Res Ctr, Heidelberg, Germany.
Helmholtz Ctr, Munich, Germany.
DeCODE Genet, Reykjavik, Iceland.
CNG, Paris, France.
Fdn Jean Dausset, CEPH, Paris, France.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-139
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805317
ER
PT J
AU Landi, MT
Zhao, YD
Rotunnno, M
Koshiol, J
Pesatori, A
Burdette, L
Linnoila, I
Marincola, F
Bertazzi, PA
Caporaso, N
McShane, L
Wang, E
AF Landi, Maria Teresa
Zhao, Yingdong
Rotunnno, Melissa
Koshiol, Jill
Pesatori, Angela
Burdette, Laurie
Linnoila, Ilona
Marincola, Francesco
Bertazzi, Pier Alberto
Caporaso, Neil
McShane, Lisa
Wang, Ena
TI MicroRNA expression, tobacco smoking, and genetic polymorphisms in lung
cancer histology and survival
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Milan, Milan, Italy.
NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 585
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803124
ER
PT J
AU Lee, KM
Baris, D
Zhang, YW
Hosgood, D
Menashe, I
Yeager, M
Zahm, S
Wang, S
Purdue, M
Chanock, S
Zheng, TZ
Rothman, N
Lan, Q
AF Lee, Kyoung-Mu
Baris, Dalsu
Zhang, Yawei
Hosgood, Dean
Menashe, Idan
Yeager, Meredith
Zahm, Shelia
Wang, Sophia
Purdue, Mark
Chanock, Stephen
Zheng, Tongzhang
Rothman, Nathaniel
Lan, Qing
TI Common single nucleotide polymorphisms in immunoregulatory genes and
multiple myeloma risk among women in Connecticut
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Yale Univ, Sch Med, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3049
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703257
ER
PT J
AU Lee, YH
Song, HT
Judge, A
Andersen, J
Ishikawa, T
Avital, I
Durkin, M
Raggi, C
Ton, A
Conner, E
MacLachlan, I
Factor, V
Thorgeirsson, S
AF Lee, Yun-Han
Song, Ho-Taek
Judge, Adam
Andersen, Jesper
Ishikawa, Tsuyoshi
Avital, Itzhak
Durkin, Marian
Raggi, Chiara
Ton, Anita
Conner, Elizabeth
MacLachlan, Ian
Factor, Valentina
Thorgeirsson, Snorri
TI Suppression of tumor growth in human hepatocellular carcinoma by
systemic delivery of SNALP-formulated siRNA for downregulation of HDAC2
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Yonsei Univ, Seoul 120749, South Korea.
Protiva Biotherapeut Inc, Burnaby, BC, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2857
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802180
ER
PT J
AU Li, GL
Cai, QY
Gao, YT
Wen, WQ
Shu, XO
Yang, G
Rothman, N
Li, HL
Chow, WH
Zheng, W
AF Li, Guoliang
Cai, Qiuyin
Gao, Yu-Tang
Wen, Wanqing
Shu, Xiao Ou
Yang, Gong
Rothman, Nathaniel
Li, Hong-Lan
Chow, Wong-Ho
Zheng, Wei
TI Copy number variation in the GSTM1 and GSTT1 genes and risk of breast,
colorectal, and lung cancers: Results from the Shanghai Women\#8217;s
Health Study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Vanderbilt Univ, Nashville, TN 37235 USA.
Shanghai Canc Inst, Shanghai, Peoples R China.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3933
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703216
ER
PT J
AU Li, M
Rayburn, E
Wang, W
Wang, F
Covey, J
Lee, M
Zhang, RW
AF Li, Mao
Rayburn, Elizabeth
Wang, Wei
Wang, Feng
Covey, Joseph
Lee, Moses
Zhang, Ruiwen
TI Preclinical pharmacological evaluations of indolecarboxamine ML-970 (NSC
716970)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 UAB, Ctr Comprehens Canc, Birmingham, AL USA.
NCI, Dev Therapeut Program, DCTD, Rockville, MD USA.
Hope Coll, Dept Chem, Holland, MI 49423 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2930
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802112
ER
PT J
AU Li, SW
Wang, JA
Rajesh, S
Moss, J
Darling, T
AF Li, Shaowei
Wang, Ji-an
Rajesh, Sangeetha
Moss, Joel
Darling, Thomas
TI Rapamycin inhibits hyperactivation of mTORC1 signaling in a novel
xenograft model of tuberous sclerosis complex skin tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1735
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705026
ER
PT J
AU Li, SL
Park, H
Trempus, C
Gordon, D
Cotsarelis, G
Morris, R
AF Li, Shulan
Park, Heuijoon
Trempus, Carol
Gordon, Derek
Cotsarelis, George
Morris, Rebecca
TI Evidence for polyfocal development of papillomas in the murine cutaneous
epithelium
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Columbia Univ, New York, NY USA.
NIEHS, Res Triangle Pk, NC 27709 USA.
Rutgers State Univ, Piscataway, NJ USA.
Univ Penn, Philadelphia, PA 19104 USA.
Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3144
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803434
ER
PT J
AU Li, Y
Li, WP
Jiao, ZX
Yao, ZX
Jessup, J
Mishra, L
AF Li, Ying
Li, Wenping
Jiao, Zhongxian
Yao, Zhixing
Jessup, John
Mishra, Lopa
TI CEA regulates CRC cells metastasis through multiple pathways
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Georgetown Univ, Washington, DC USA.
NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3515
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804281
ER
PT J
AU Li, ZJ
Tan, F
Tong, JN
McKee, A
Thiele, C
AF Li, Zhijie
Tan, Fei
Tong, Jenna
McKee, Amy
Thiele, Carol
TI Perifosine, as a single agent, inhibits neuroblastoma tumor cell growth
in in vitro and in vivo preclinical models.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Li, Zhijie; Tan, Fei; Tong, Jenna; McKee, Amy; Thiele, Carol] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3205
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804002
ER
PT J
AU Lim, M
Moore, H
Compton, C
AF Lim, Mark
Moore, Helen
Compton, Carolyn
TI The "biospecimen research network": a resource from NCI'S office of
biorepositories and biospecimen research
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Lim, Mark; Moore, Helen; Compton, Carolyn] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1654
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702702014
ER
PT J
AU Limgala, R
Yee, C
Terunuma, A
Martin, P
Kelly, K
Vogel, J
AF Limgala, Renuka
Yee, Carole
Terunuma, Atsushi
Martin, Philip
Kelly, Kathy
Vogel, Jonathan
TI Isolation of Prostate Cancer Stem Cells using Developmental Signaling
Pathway Activities
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Limgala, Renuka; Yee, Carole; Terunuma, Atsushi; Martin, Philip; Kelly, Kathy; Vogel, Jonathan] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-71
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603190
ER
PT J
AU Lintel, N
Walker, R
Hunter, K
AF Lintel, Nicholas
Walker, Renard
Hunter, Kent
TI Ttc9c abrogates the metastasis promoter Sipa1, ablates lung metastasis
and switches the Estrogen Receptor back on in a highly-metastatic, ER
negative mouse mammary carcinoma cell-line
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Lintel, Nicholas; Walker, Renard; Hunter, Kent] NCI, CCR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1181
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803152
ER
PT J
AU Liu, HF
Fulmer-Smentek, S
D'Andrade, P
Lorenzi, P
Weinstein, J
Kohn, K
Pommier, Y
Reinhold, W
AF Liu, Hongfang
Fulmer-Smentek, Stephanie
D'Andrade, Petula
Lorenzi, Philip
Weinstein, John
Kohn, Kurt
Pommier, Yves
Reinhold, William
TI Profiling and characterization of microRNA expression in the NCI-60
human cancer cell lines
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Georgetown Univ, Med Ctr, Washington, DC 20007 USA.
Agilent Technol, Santa Clara, CA USA.
NCI, Mol Pharmacol Lab, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 545
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803080
ER
PT J
AU Liu, W
Zabirnyk, O
Wang, HH
Liu, YM
Shiao, YH
Anderson, LM
Perantoni, AO
Phang, JM
AF Liu, Wei
Zabirnyk, Olga
Wang, Honghe
Liu, Yongmin
Shiao, Yih-Horng
Anderson, Lucy M.
Perantoni, Alan O.
Phang, James M.
TI Proline oxidase, a p53-induced cancer suppressor protein, is regulated
by miR-23b*in renal cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Comparat Carcinogenesis Lab, Ctr Canc Res, Basic Res Program,SAIC Frederick Inc, Frederick, MD 21701 USA.
NCI, Lab Canc & Dev Biol, Ctr Canc Res, Basic Res Program,SAIC Frederick Inc, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2528
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803154
ER
PT J
AU Liu, W
Zabirnyk, O
Liu, YM
Phang, JM
AF Liu, Wei
Zabirnyk, Olga
Liu, Yongmin
Phang, James M.
TI Hypoxia induction of Proline oxidase is independent of HIF but dependent
on the LKB1/AMPK signaling pathway
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Liu, Wei; Zabirnyk, Olga; Liu, Yongmin; Phang, James M.] NCI, Comparat Carcinogenesis Lab, Ctr Canc Res, Basic Res Program,SAIC Frederick Inc, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 271
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804079
ER
PT J
AU Liu, XF
Bera, T
Pastan, I
AF Liu, Xiu Fen
Bera, Tapan
Pastan, Ira
TI A primate-specific POTE-actin fusion protein has a role in
genotoxic-agent induced apoptosis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Liu, Xiu Fen; Bera, Tapan; Pastan, Ira] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5107
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801221
ER
PT J
AU Liu, YM
Borchert, G
Donald, S
Diwan, B
Phang, J
AF Liu, Yongmin
Borchert, Gregory
Donald, Steve
Diwan, Bhalchandra
Phang, James
TI Proline oxidase, a novel mitochondrial tumor suppressor in human
cancers, reduces HIF signaling
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 SAIC Frederick Inc, Basic Res Program, Frederick, MD USA.
NCI, Comparat Carcinogenesis Lab, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4448
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802289
ER
PT J
AU Liu, YM
Borchert, G
Donald, S
Diwan, B
Phang, J
AF Liu, Yongmin
Borchert, Gregory
Donald, Steve
Diwan, Bhalchandra
Phang, James
TI Proline oxidase, a novel mitochondrial tumor suppressor in human
cancers, reduces HIF signaling
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 SAIC Frederick Inc, Basic Res Program, Frederick, MD USA.
NCI, Comparat Carcinogenesis Lab, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4448
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804452
ER
PT J
AU Liu, ZF
Xie, ZL
Aimiuwu, J
Ling, YH
Covey, J
Chan, K
AF Liu, Zhongfa
Xie, Zhiliang
Aimiuwu, Josephine
Ling, Yonghua
Covey, Joseph
Chan, Kenneth
TI Cytotoxicity and hypomethylation activity of
5-Fluoro-2\#8217;-deoxycytidine and decitabine on human cancer cell
lines
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Ohio State Univ, Coll Pharm, Columbus, OH 43210 USA.
Ohio State Univ, Coll Med, Columbus, OH 43210 USA.
Ohio State Univ, Coll Publ Hlth, Columbus, OH 43210 USA.
NCI, Dev Therapeut Program, DCTD, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3377
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802039
ER
PT J
AU Longmire, M
Kosaka, N
Ogawa, M
Choyke, P
Kobayashi, H
AF Longmire, Michelle
Kosaka, Nobuyuki
Ogawa, Mikako
Choyke, Peter
Kobayashi, Hisataka
TI Multi-color in vivo targeted imaging to guide real-time surgery of
HER2-positive micro-metastases in a two-tumor coincident model of
ovarian cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NCI CCR, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-290
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604017
ER
PT J
AU Lopes, E
Cerchietti, L
Ahn, J
Robles, A
Varticovski, L
Melnick, A
Chiosis, G
AF Lopes, Eloisi
Cerchietti, Leandro
Ahn, James
Robles, Ana
Varticovski, Lyuba
Melnick, Ari
Chiosis, Gabriela
TI Targeting triple-negative breast cancer via PU-H71, a purine-scaffold
heat shock protein 90 (Hsp90) inhibitor
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Weill Cornell Med Oncol, New York, NY USA.
NCI, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-7
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801232
ER
PT J
AU Lou, H
Yeager, M
Li, HC
Bosquet, JG
Hayes, R
Orr, N
Hutchinson, A
Yu, K
Jacobs, K
Kraft, P
Wacholder, S
Chatterjee, N
Feigelson, H
Thun, M
Diver, WR
Albanes, D
Willett, W
Virtamo, J
Weinstein, S
Ma, J
Gaziano, JM
Stampfer, M
Schumacher, F
Giovannucci, E
Cancel-Tassin, G
Cussenot, O
Valeri, A
Andriole, G
Crawford, ED
Anderson, S
Tucker, M
Hoover, R
Fraumeni, J
Thomas, G
Hunter, D
Chanock, S
Dean, M
AF Lou, Hong
Yeager, Meredith
Li, Hongchuan
Bosquet, Jesus Gonzalez
Hayes, Richard
Orr, Nick
Hutchinson, Amy
Yu, Kai
Jacobs, Kevin
Kraft, Peter
Wacholder, Sholom
Chatterjee, Nilanjan
Feigelson, Heather
Thun, Michael
Diver, W. Ryan
Albanes, Demetrius
Willett, Walter
Virtamo, Jarmo
Weinstein, Stephanie
Ma, Jing
Gaziano, J. Michael
Stampfer, Meir
Schumacher, Fredrick
Giovannucci, Edward
Cancel-Tassin, Geraldine
Cussenot, Olivier
Valeri, Antoine
Andriole, Gerald
Crawford, E. David
Anderson, Stephen
Tucker, Margaret
Hoover, Robert
Fraumeni, Joseph
Thomas, Gilles
Hunter, David
Chanock, Stephen
Dean, Michael
TI Functional analysis of the promoter of the beta-microseminoprotein gene
MSMB demonstrates the importance of a single nucleotide polymorphism in
prostate cancer susceptibility
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21701 USA.
NCI, Bethesda, MD 20892 USA.
Bioinformed Consulting Serv, Gaithersburg, MD USA.
Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
Amer Canc Soc, Atlanta, GA 30329 USA.
Natl Publ Hlth Inst, Helsinki, Finland.
Harvard Univ, Brigham & Womens Hosp, Channing Lab, Sch Med, Boston, MA 02115 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
Hop Tenon, Assistance Publ Hop Paris, Ctr Rech Pathol Prostat CeRePP, F-75970 Paris, France.
Univ Colorado, Denver, CO 80202 USA.
Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5613
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802117
ER
PT J
AU Lowy, D
Day, P
Kines, R
Roberts, J
Thompson, C
Pang, S
Buck, C
Roden, R
Schille, J
AF Lowy, Douglas
Day, Patricia
Kines, Rhonda
Roberts, Jeffrey
Thompson, Cynthia
Pang, Susana
Buck, Christopher
Roden, Richard
Schille, John
TI HPV vaccination: Current realities and future prospects
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Johns Hopkins Univ, Baltimore, MD USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY35-1
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702600016
ER
PT J
AU Lu, H
Jaeschke, H
Sterneck, E
Klaassen, C
AF Lu, Hong
Jaeschke, Hartmut
Sterneck, Esta
Klaassen, Curtis
TI C/EBP\#946; in hepatocytes promotes inflammation and disrupts whole-body
metabolic homeostasis during endotoxemia
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Kansas, Med Ctr, Kansas City, KS 66103 USA.
NCI, Ctr Canc Res, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3804
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800361
ER
PT J
AU Lubet, R
Juliana, MM
Bode, A
Steele, V
Grubbs, C
AF Lubet, Ronald
Juliana, M. Margaret
Bode, Ann
Steele, Vernon
Grubbs, Clinton
TI Preventive effects of Lapatinib, a combined EGFR1 and EGFR2 inhibitor on
chemically-induced urinary bladder and estrogen receptor positive
mammary cancers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Alabama Birmingham, Birmingham, AL USA.
Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 940
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801271
ER
PT J
AU Lung, M
Chan, KC
Yau, WL
Lung, HL
Sedlacek, R
Miller, L
Liu, E
Lerman, M
Zabarovsky, E
Tsao, SW
Chua, D
AF Lung, Maria
Chan, King Chi
Yau, Wing Lau
Lung, Hong Lok
Sedlacek, Radek
Miller, Lance
Liu, Edison
Lerman, Michael
Zabarovsky, Eugene
Tsao, Sai Wah
Chua, Daniel
TI Matrix metalloproteinase-19 involvement in nasopharyngeal carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Hong Kong Univ Sci & Technol, Kowloon, Hong Kong, Peoples R China.
Inst Biotechnol, Prague, Czech Republic.
Genome Inst Singapore, Singapore, Singapore.
NCI, Bethesda, MD 20892 USA.
Karolinska Inst, Stockholm, Sweden.
Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3332
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801255
ER
PT J
AU Luo, JF
Gao, YT
Chow, WH
Shu, XO
Li, HL
Yang, G
Cai, QY
Rothman, N
Cai, H
Shrubsole, M
Franke, A
Zheng, W
Dai, Q
AF Luo, Jianfeng
Gao, Yu-Tang
Chow, Wong-Ho
Shu, Xiao-ou
Li, Honglan
Yang, Gong
Cai, Qiuyin
Rothman, Nathaniel
Cai, Hui
Shrubsole, Martha
Franke, Adrian
Zheng, Wei
Dai, Qi
TI Urinary polyphenols and breast cancer risk: results from the Shanghai
Women Health Study (SWHS)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Dept Med,Vanderbilt Epidemiol Ctr, Nashville, TN 37212 USA.
Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
US Dept HHS, Bethesda, MD USA.
Univ Hawaii, Canc Res Ctr Hawaii, Honolulu, HI 96813 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2056
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801370
ER
PT J
AU Luo, JF
Gao, YT
Chow, WH
Shu, XO
Li, HL
Yang, G
Cai, QY
Li, GL
Rothman, N
Cai, H
Shrubsole, M
Franke, A
Zheng, W
Dai, Q
AF Luo, Jianfeng
Gao, Yu-Tang
Chow, Wong-Ho
Shu, Xiao Ou
Li, Honglan
Yang, Gong
Cai, Qiuyin
Li, Guoliang
Rothman, Nathaniel
Cai, Hui
Shrubsole, Martha
Franke, Adrian
Zheng, Wei
Dai, Qi
TI Interaction between urinary tea polyphenols and Glutathione
S-transferase gene polymorphisms in relation to breast cancer risk:
Results from the Shanghai Women's Health Study (SWHS)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med, Nashville, TN 37212 USA.
Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
Univ Hawaii, Canc Res Ctr Hawaii, Honolulu, HI 96822 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-237
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704036
ER
PT J
AU Ly, D
Savage, J
Sowers, A
Soule, B
Saleh, A
Mitchell, J
Simone, N
AF Ly, David
Savage, Jason
Sowers, Anastasia
Soule, Benjamin
Saleh, Anthony
Mitchell, James
Simone, Nicole
TI Altered microRNA expression after irradiation may regulate the radiation
induced toxicity of fibrosis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Radiat Oncol Branch, Bethesda, MD 20892 USA.
NCI, NIH, Radiat Biol Branch, Bethesda, MD 20892 USA.
NIAID, NIH, Lab Host Def, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3967
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804029
ER
PT J
AU Maciag, A
Cheng, YSR
Romanowska, M
Anderson, L
AF Maciag, Anna
Cheng, Y. S. Robert
Romanowska, Malgorzata
Anderson, Lucy
TI Mutant K-rasV12 may upregulate COX-2 through Hmga1 and epiregulin,
leading to reactive oxygen species generation.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 SAIC Frederick, Frederick, MD USA.
NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4354
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803439
ER
PT J
AU Maris, J
Courtright, J
Houghton, P
Morton, C
Kolb, E
Gorlick, R
Carol, H
Lock, R
Friedman, H
Keir, S
Kang, M
Reynolds, C
Smith, M
AF Maris, John
Courtright, Joshua
Houghton, Peter
Morton, Christopher
Kolb, E.
Gorlick, Richard
Carol, Hernan
Lock, Richard
Friedman, Henry
Keir, Stephen
Kang, Min
Reynolds, C.
Smith, Malcolm
TI Pediatric Preclinical Testing Program (PPTP) evaluation of the novel
polyamine analogue PG11047
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
Alfred I DuPont Hosp Children, Wilmington, DE USA.
Montefiore Med Ctr, Bronx, NY 10467 USA.
Childrens Canc Inst, Sydney, NSW, Australia.
Duke Univ, Durham, NC USA.
Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
NCI, CTEP, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3194
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803488
ER
PT J
AU Marron, M
Boffetta, P
Benhamou, S
Boccia, S
Castellsague, X
Chen, C
Curado, MP
Dal Maso, L
Daudt, A
Eluf-Neto, J
Fabianova, E
Fernandez, L
Franceschi, S
Hayes, R
Herrero, R
Kelsey, K
Koifman, S
La Vecchia, C
Lazarus, P
Levi, F
Lissowska, J
Mates, IN
Purdue, M
Rudnai, P
Schwartz, S
AF Marron, Manuela
Boffetta, Paolo
Benhamou, Simone
Boccia, Stefania
Castellsague, Xavier
Chen, Chu
Curado, Maria Paula
Dal Maso, Luigino
Daudt, Alexander
Eluf-Neto, Jose
Fabianova, Eleonora
Fernandez, Leticia
Franceschi, Silvia
Hayes, Richard
Herrero, Rolando
Kelsey, Karl
Koifman, Sergio
La Vecchia, Carlo
Lazarus, Philip
Levi, Fabio
Lissowska, Jolanta
Mates, Ioan Nicolae
Purdue, Mark
Rudnai, Peter
Schwartz, Stephen
TI Alcohol drinking and the risk of head and neck cancer among younger,
middle age and older populations
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Int Agcy Res Canc, F-69372 Lyon, France.
INSERM, U794, Paris, France.
Inst Gustave Roussy, Villejuif, France.
Univ Cattolica Sacro Cuore, Rome, Italy.
CIBER ESP, IDIBELL, ICO, Barcelona, Spain.
Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
Hosp Araujo Jorge, Goiania, Go, Brazil.
Aviano Canc Ctr, I-33081 Aviano, Italy.
Hosp Clin Porto Alegre, Porto Alegre, RS, Brazil.
Univ Sao Paulo, Sao Paulo, Brazil.
Specialized State Hlth Inst, Bansk El Bystrica, Slovakia.
Inst Oncol & Radiobiol, Havana, Cuba.
NCI, Bethesda, MD 20892 USA.
Inst Invest Epidemiol, San Jose, Costa Rica.
Brown Univ, Boston, MA USA.
Escola Nacl Saude Publica, Rio De Janeiro, Brazil.
Ist Ric Farmacol Mario Negri, Milan, Italy.
Univ Milan, Milan, Italy.
Penn State Coll Med, Hershey, PA USA.
Inst Univ Med Sociale & Prevent, Lausanne, Switzerland.
M Sklodowska Curie Mem Canc Ctr, Warsaw, Poland.
Inst Oncol, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
Univ Med & Pharm, Bucharest, Romania.
Univ Buenos Aires, Inst Oncol Angel H Roffo, Buenos Aires, DF, Argentina.
Boston Univ, Boston, MA 02215 USA.
Univ Fed Pelotas, Pelotas, Brazil.
UNC Sch Publ Hlth, Chapel Hill, NC USA.
Natl Inst Environm Hlth, Budapest, Hungary.
RI Mates, Ioan Nicolae/E-9255-2017
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2132
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704074
ER
PT J
AU Marshall, JC
Collins, J
Ming, Z
Veenstra, T
Khanna, C
Vidal-Vanaclocha, F
Steeg, P
AF Marshall, Jean-Claude
Collins, Joshua
Ming, Zhou
Veenstra, Timothy
Khanna, Chand
Vidal-Vanaclocha, Fernando
Steeg, Patricia
TI An unbiased screen for Nm23-H1 interacting proteins identifies the
cytoskeletal regulator Ezrin.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
Univ Basque Country, Sch Med, Bizkaia, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4809
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803234
ER
PT J
AU Mckay, M
Ritt, D
Morrison, D
AF Mckay, Melissa
Ritt, Daniel
Morrison, Deborah
TI Signaling dynamics of the KSR1 scaffold complex
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Mckay, Melissa; Ritt, Daniel; Morrison, Deborah] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5233
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802409
ER
PT J
AU McNeely, S
Conti, C
Sheikh, T
Pommier, Y
Schwartz, G
Tse, A
AF McNeely, Samuel
Conti, Chiara
Sheikh, Tahir
Pommier, Yves
Schwartz, Gary
Tse, Archie
TI Chk1 inhibition after replicative stress causes a double strand break
response mediated primarily by DNA-dependent protein kinase
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2488
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801163
ER
PT J
AU Menashe, I
Anderson, W
Jatoi, I
Philip, R
AF Menashe, Idan
Anderson, William
Jatoi, Ismail
Philip, Rosenberg
TI Underlying causes of the Black-White racial disparity in breast cancer
mortality: A population-based analysis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Rockville, MD USA.
Natl Naval Med Ctr, Breast Care Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 972
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703387
ER
PT J
AU Menendez, D
Yan, J
Yang, XP
Jetten, AM
Resnick, M
AF Menendez, Daniel
Yan, Jun
Yang, Xiao-Ping
Jetten, Anton M.
Resnick, Michael
CA Ction
LRB Chromosome Stability Grp LMG
Cell BiologySe
TI A regulatory loop composed of RAP80-HDM2-p53 provides RAP80 enhanced p53
degradation by HDM2 in response to DNA damage
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Menendez, Daniel; Yan, Jun; Yang, Xiao-Ping; Jetten, Anton M.; Resnick, Michael; Ction; LRB Chromosome Stability Grp LMG; Cell BiologySe] NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 459
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801338
ER
PT J
AU Mirabello, L
Garcia-Closas, M
Cawthon, R
Lissowska, J
Peplonska, B
Brinton, L
Sherman, M
Savage, S
AF Mirabello, Lisa
Garcia-Closas, Montserrat
Cawthon, Richard
Lissowska, Jolanta
Peplonska, Beata
Brinton, Louise
Sherman, Mark
Savage, Sharon
TI Shorter germline telomere length is associated with increased ovarian
cancer risk in the population-based Polish Ovarian Cancer Study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, DCEG, NIH, Bethesda, MD 20892 USA.
Univ Utah, Dept Human Genet, Salt Lake City, UT USA.
M Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
Inst Oncol, Warsaw, Poland.
Nofer Inst Occupat Med, Dept Occupat & Environm Epidemiol, Lodz, Poland.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3489
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804108
ER
PT J
AU Mishra, P
Ha, LA
Rieker, J
Henrich, C
Bennett, D
Sviderskaya, E
Merlino, G
AF Mishra, Prasun
Ha, Linan
Rieker, Jennifer
Henrich, Curtis
Bennett, Dorothy
Sviderskaya, Elena
Merlino, Glenn
TI The p53 and Ink4A independent tumor suppressor activity of ARF in
melanoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
US FDA, Div Monoclonal Antibody, Ctr Drug Evaluat & Res, Bethesda, MD 20014 USA.
NCI, Mol Targets Dev Program, Frederick, MD 21701 USA.
SAIC Fredrick Inc, Frederick, MD USA.
Univ London, Div Basic Med Sci, St Georges, London, England.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5515
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803212
ER
PT J
AU Mohammed, A
Qian, L
Janakiram, N
Choi, CI
Zhang, YT
Steele, V
Rao, C
AF Mohammed, Altaf
Qian, Li
Janakiram, Naveena
Choi, Chang-In
Zhang, Yuting
Steele, Vernon
Rao, Chinthalapally
TI Chemoprevention of colon and small intestinal tumorigenesis in
Apc(Min/+) mice by licofelone, a novel dual 5-LOX/COX inhibitor
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Oklahoma, Inst Canc, OUHSC, Oklahoma City, OK USA.
NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4781
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801170
ER
PT J
AU Mohebtash, M
Madan, R
Tsang, K
Arlen, P
Pazdur, M
Jones, J
Schlom, J
Gulley, J
AF Mohebtash, Mahsa
Madan, Ravi
Tsang, Kwong
Arlen, Philip
Pazdur, Mary
Jones, Jacquin
Schlom, Jeffrey
Gulley, James
TI Clinical outcomes following immunotherapy with a MUC1/CEA vaccine in
patients with metastatic breast and ovarian cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Mohebtash, Mahsa; Madan, Ravi; Tsang, Kwong; Arlen, Philip; Pazdur, Mary; Jones, Jacquin; Schlom, Jeffrey; Gulley, James] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 718
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805217
ER
PT J
AU Monks, A
Hose, C
Zhang, JH
Wu, XL
Greenblum, S
Hu, Y
Clifford, R
Collins, J
Buetow, K
Doroshow, J
AF Monks, Anne
Hose, Curtis
Zhang, Jinghui
Wu, Xiaolin
Greenblum, Sharon
Hu, Ying
Clifford, Robert
Collins, Jerry
Buetow, Kenneth
Doroshow, James
TI Genomic taxonomy of anti-cancer drug activity: Profiling of
doxorubicin-induced gene expression changes in the NCI-60 cancer cell
line panel.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI Frederick, Frederick, MD USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2426
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801020
ER
PT J
AU Moody, T
Mantey, S
Sancho, V
Gonzalez, N
Jensen, R
AF Moody, Terry
Mantey, Samuel
Sancho, Veronica
Gonzalez, Nieves
Jensen, Robert
TI Bobmesin Receptor Subtype-3 regulates EGF receptor transactivation in
lung cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, CCR, Bethesda, MD 20892 USA.
NIDDK, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 800
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702702483
ER
PT J
AU Moore, L
Brennan, P
Nickerson, M
Jaeger, E
Rinsky, J
Zaridze, D
Janout, V
Kollarova, H
Bencko, V
Holcatova, I
Navratilova, M
Szesznenia-Dabrowska, N
Mates, D
Schmidt, L
Toro, J
Linehan, M
Merino, M
Zbar, B
Boffetta, P
Chow, WH
Waldman, F
Rothman, N
AF Moore, Lee
Brennan, Paul
Nickerson, Michael
Jaeger, Erich
Rinsky, Jessica
Zaridze, David
Janout, Vladimir
Kollarova, Hellen
Bencko, Vladimir
Holcatova, Ivana
Navratilova, Marie
Szesznenia-Dabrowska, Neonilia
Mates, Dana
Schmidt, Laura
Toro, Jorge
Linehan, Marston
Merino, Maria
Zbar, Berton
Boffetta, Paolo
Chow, Wong-Ho
Waldman, Frederick
Rothman, Nathaniel
TI VHL gene alteration and histopathologic risk factors in a large RCC
case-control study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
IARC, Lyon Frace, Finland.
NCI, Frederick, MD 21701 USA.
UCSF, San Francisco, CA USA.
CRC, Moscow, Russia.
Placky Univ, Sch Med, Olomouc, Czech Republic.
Charles Univ Prague, Sch Med, Prague, Czech Republic.
Masaryk Mem Canc Inst, Brno, Czech Republic.
Inst Occupat Med, Dept Epidemiol, Lodz, Poland.
Inst Publ Hlth, Bucharest, Romania.
SAIC Basic Res Program, Frederick, MD USA.
UCSF Canc Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1018
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801493
ER
PT J
AU Mor, G
Symanowski, J
Visintin, I
Birrer, M
Ward, D
AF Mor, Gil
Symanowski, James
Visintin, Irene
Birrer, Michael
Ward, David
TI Six biomarker panel detects early stage ovarian cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Yale Univ, Sch Med, New Haven, CT USA.
Nevada Canc Inst, Las Vegas, NV USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-244
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801214
ER
PT J
AU Morton, C
Houghton, P
Maris, J
Courtright, J
Kolb, E
Gorlick, R
Carol, H
Lock, R
Friedman, H
Keir, S
Kang, M
Reynolds, C
Smith, M
AF Morton, Christopher
Houghton, Peter
Maris, John
Courtright, Joshua
Kolb, E.
Gorlick, Richard
Carol, Hernan
Lock, Richard
Friedman, Henry
Keir, Stephen
Kang, Min
Reynolds, C.
Smith, Malcolm
TI Pediatric Preclinical Testing Program (PPTP) evaluation of PR-104
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
Alfred I DuPont Hosp Children, Wilmington, DE USA.
Montefiore Med Ctr, Bronx, NY 10467 USA.
Childrens Canc Inst, Sydney, NSW, Australia.
Duke Univ, Durham, NC USA.
Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79409 USA.
NCI, CTEP, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3195
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803489
ER
PT J
AU Moulick, K
Ahn, J
Beebe, K
Ma, YL
Zartoska, D
Taldone, T
Caldas-Lopez, E
Gross, S
Neckers, L
Chiosis, G
AF Moulick, Kamalika
Ahn, James
Beebe, Kristin
Ma, Yuliang
Zartoska, Danuta
Taldone, Tony
Caldas-Lopez, Eloise
Gross, Steven
Neckers, Len
Chiosis, Gabriela
TI Probing cancer-specific activating signaling pathways through a
tumor-specific Hsp90 inhibitor
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 MSKCC, New York, NY USA.
NCI, NIH, Bethesda, MD 20892 USA.
Cornell Univ, Weill Med Coll, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-86
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701170
ER
PT J
AU Mullighan, C
Zhang, J
Harvey, R
Collins-Underwood, JR
Tasian, S
Schulman, B
Phillips, L
Loh, M
Su, X
Liu, W
Devidas, M
Atlas, S
Chen, IM
Clifford, R
Gerhard, D
Carroll, W
Reaman, G
Smith, M
Downing, J
Hunger, S
Willman, C
AF Mullighan, Charles
Zhang, Jinghui
Harvey, Richard
Collins-Underwood, J. Racquel
Tasian, Sarah
Schulman, Brenda
Phillips, Letha
Loh, Mignon
Su, Xiaoping
Liu, Wei
Devidas, Meenakshi
Atlas, Susan
Chen, I-Ming
Clifford, Robert
Gerhard, Daniela
Carroll, William
Reaman, Gergory
Smith, Malcolm
Downing, James
Hunger, Stephen
Willman, Cheryl
CA Children's Oncology Grp
TI Frequent JAK mutations in pediatric acute lymphoblastic leukemia with
poor outcome: A new therapeutic target in resistant disease.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
NCI, Ctr Bioinformed Informat & Informat Technol, NIH, Rockville, MD USA.
Univ New Mexico, Canc Res & Treatment Ctr, Albuquerque, NM 87131 USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
Univ Florida, Coll Med, Gainesville, FL USA.
Univ New Mexico, Phys & Astron, Albuquerque, NM 87131 USA.
NCI, Lab Populat Genet, NIH, Bethesda, MD 20892 USA.
NCI, Off Canc Gen, NIH, Bethesda, MD 20892 USA.
NYU, Inst Canc, New York, NY USA.
George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
NCI, Canc Therapy Evaluat Program, NIH, Bethesda, MD 20892 USA.
Univ Colorado Denver, Sch Med, Aurora, CO USA.
Childrens Hosp, Aurora, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-92
PG 2
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803304
ER
PT J
AU Murff, H
Shu, XO
Li, HL
Chow, WH
Dai, Q
Kallianpur, A
Yang, G
Cai, H
Wen, WG
Gao, YT
Zheng, W
AF Murff, Harvey
Shu, Xiao-ou
Li, Honglan
Chow, Wong-Ho
Dai, Qi
Kallianpur, Asha
Yang, Gong
Cai, Hui
Wen, Wanging
Gao, Yu-Tang
Zheng, Wei
TI Dietary polyunsaturated fatty acids, prostaglandin E-2 production and
colorectal cancer risk in Chinese women
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA.
Shanghai Canc Inst, Shanghai, Peoples R China.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1006
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703364
ER
PT J
AU Murff, H
Shu, XO
Li, HL
Chow, WH
Dai, Q
Kallianpur, A
Yang, G
Cai, H
Wen, WG
Gao, YT
Zheng, W
AF Murff, Harvey
Shu, Xiao-ou
Li, Honglan
Chow, Wong-Ho
Dai, Qi
Kallianpur, Asha
Yang, Gong
Cai, Hui
Wen, Wanging
Gao, Yu-Tang
Zheng, Wei
TI Dietary polyunsaturated fatty acids, prostaglandin E-2 production and
colorectal cancer risk in Chinese women
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA.
Shanghai Canc Inst, Shanghai, Peoples R China.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1006
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801480
ER
PT J
AU Murphy, G
Pfeiffer, R
Camargo, M
Rabkin, C
AF Murphy, Gwen
Pfeiffer, Ruth
Camargo, Maria
Rabkin, Charles
TI Sex difference in Epstein-Barr virus-positive gastric cancer: Results of
a meta-analysis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Murphy, Gwen; Pfeiffer, Ruth; Camargo, Maria; Rabkin, Charles] NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2155
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704098
ER
PT J
AU Nagata, S
Ise, T
Egland, K
Onda, M
Ho, M
Pastan, I
AF Nagata, Satoshi
Ise, Tomoko
Egland, Kristi
Onda, Masanori
Ho, Mitchell
Pastan, Ira
TI Monoclonal antibodies to non-ligand-binding sites on CD30 induce
agonistic effects and growth inhibition of human lymphoma cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Sanford Res USD, Sioux Falls, SD USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 860
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604413
ER
PT J
AU Nam, JS
Kim, RJ
Kim, SR
Park, SB
Roh, KJ
Cho, EM
Kang, KS
Tang, BW
Yang, YA
Kohn, E
Wakefield, L
AF Nam, Jeong-Seok
Kim, Ran-Ju
Kim, Soo-Rim
Park, Sang-Bum
Roh, Kyung-Jin
Cho, Eun-Mi
Kang, Kyung-Sun
Tang, Binwu
Yang, Yu-An
Kohn, Ethan
Wakefield, Lalage
TI Ras activation contributes the maintenance and expansion of putative
cancer stem cells in breast cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Gachon Univ Med & Sci, Lee Gil Ya Canc & Diabet Res Inst, Lab Tumor Suppressor, Inchon, South Korea.
Seoul Natl Univ, Coll Vet Med, Dept Vet Publ Hlth, Lab Stem Cell & Tumor Biol, Seoul, South Korea.
NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3072
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603144
ER
PT J
AU Newman, D
AF Newman, David
TI Microbial natural products, derivatives, and mimics as antitumor agents
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Newman, David] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY30-1
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800024
ER
PT J
AU Newman, D
AF Newman, David
TI Microbial natural products, derivatives, and mimics as antitumor agents
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Newman, David] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY30-1
PG 2
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702806015
ER
PT J
AU Nick, A
Spannuth, W
Landen, C
Kim, HS
Kamat, A
Lin, Y
Merritt, W
Stone, R
Mangala, L
Armaiz-Pena, G
Deavers, M
Lopez-Berestein, G
Birrer, M
Coleman, R
Sood, A
AF Nick, Alpa
Spannuth, Whitney
Landen, Charles
Kim, Hye Sun
Kamat, Aparna
Lin, Yvonne
Merritt, William
Stone, Rebecca
Mangala, Lingegowda
Armaiz-Pena, Guillermo
Deavers, Michael
Lopez-Berestein, Gabriel
Birrer, Michael
Coleman, Robert
Sood, Anil
TI Targeting p130cas in ovarian carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 UT MD Anderson Canc Ctr, Houston, TX USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4657
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604200
ER
PT J
AU Ogawa, M
Kosaka, N
Choyke, P
Kobayashi, H
AF Ogawa, Mikako
Kosaka, Nobuyuki
Choyke, Peter
Kobayashi, Hisataka
TI Target-specific activatable molecular imaging probes using conjugates of
clinically approved monoclonal antibodies and indocyanine green, a near
infrared dye
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NCI, CCR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4468
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701079
ER
PT J
AU Ohnuma, S
Sauna, Z
Nandigama, K
Ambudkar, S
AF Ohnuma, Shinobu
Sauna, Zuben
Nandigama, Krishnamachary
Ambudkar, Suresh
TI The development of an ATP analog, 5-fluorosulfonylbenzonyl 5-adenosine
(FSBA) as a potent modulator of the multidrug resistance-linked
P-glycoprotein (ABCB1)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ohnuma, Shinobu; Sauna, Zuben; Nandigama, Krishnamachary; Ambudkar, Suresh] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 898
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802007
ER
PT J
AU Olivero, O
Gorgifard, S
Yu, M
Poirier, M
AF Olivero, Ofelia
Gorgifard, Sayeh
Yu, Mia
Poirier, Miriam
TI A novel mechanism of genotoxicity induced by antiretroviral nucleoside
reverse transcriptase inhibitors (NRTIs) in erythrocebus patas bone
marrow
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Olivero, Ofelia; Gorgifard, Sayeh; Yu, Mia; Poirier, Miriam] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1869
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800146
ER
PT J
AU Olivo-Marston, S
Yang, P
Mechanic, L
Bowman, E
Pine, S
Loffredo, C
Alberg, A
Caporaso, N
Shields, P
Chanock, S
Wu, YH
Jiang, RX
Cunningham, J
Jen, J
Harris, C
AF Olivo-Marston, Susan
Yang, Ping
Mechanic, Leah
Bowman, Elise
Pine, Sharon
Loffredo, Christopher
Alberg, Anthony
Caporaso, Neil
Shields, Peter
Chanock, Stephen
Wu, Yanhong
Jiang, Ruoxiang
Cunningham, Julie
Jen, Jin
Harris, Curtis
TI Childhood exposure to secondhand smoke and alterations in innate
immunity increase adult lung cancer risk among never smokers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Mayo Clin, Rochester, MN USA.
Westat Corp, Rockville, MD USA.
Georgetown Univ, Washington, DC USA.
Med Univ S Carolina, Charleston, SC 29425 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1976
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703103
ER
PT J
AU Onnis, B
Uranchimeg, B
Rapisarda, A
Shoemaker, R
Melillo, G
AF Onnis, Barbara
Uranchimeg, Badarch
Rapisarda, Annamaria
Shoemaker, Robert
Melillo, Giovanni
TI Response of colon cancer cells to the hypoxic microenvironment:
characterization of pathways involved in survival and tumorigenicity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Onnis, Barbara; Uranchimeg, Badarch; Rapisarda, Annamaria; Shoemaker, Robert; Melillo, Giovanni] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 250
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604009
ER
PT J
AU Ota, T
Bell, D
Gonzalez-Bosquet, J
Shridhar, V
Hartmann, L
Fan, JB
Chien, J
AF Ota, Takayo
Bell, Debra
Gonzalez-Bosquet, Jesus
Shridhar, Vijayalakshmi
Hartmann, Lynn
Fan, Jian-Bing
Chien, Jeremy
TI Molecular features and therapeutic targets in stage 1 epithelial ovarian
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mayo Clin, Rochester, MN USA.
NCI, Gaithersburg, MD USA.
Illumina Inc, San Diego, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5206
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802262
ER
PT J
AU Palmieri, D
Hua, E
Qian, YZ
Herring, J
Liewehr, D
Steinberg, S
Laquerre, S
Dar, M
Steeg, P
AF Palmieri, Diane
Hua, Emily
Qian, Yongzhen
Herring, Jeanne
Liewehr, David
Steinberg, Seth
Laquerre, Sylvie
Dar, Mohammed
Steeg, Patricia
TI Preclinical studies investigating the efficacy of GSK461364A, an
inhibitor of Polo-like kinase-1, for the prevention of breast cancer
brain metastases
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
NCI, SAIC Frederick, Frederick, MD USA.
GlaxoSmithKline, Collegeville, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4767
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604230
ER
PT J
AU Paoloni, M
Mazcko, C
Currier, D
Yu, YK
Cao, L
Khanna, C
AF Paoloni, Melissa
Mazcko, Christina
Currier, Duane
Yu, Yunkai
Cao, Liang
Khanna, Chand
TI Comparative oncology modeling of rapalog development
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Paoloni, Melissa; Mazcko, Christina; Currier, Duane; Yu, Yunkai; Cao, Liang; Khanna, Chand] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2345
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804283
ER
PT J
AU Pastorino, F
Loi, M
Marchio, S
Di Paolo, D
Becherini, P
Curnis, F
Longhi, R
Nico, B
Bussollno, F
Ribatti, D
Cilli, M
Arap, W
Pasqualini, R
Corti, A
Allen, T
Ponzoni, M
AF Pastorino, Fabio
Loi, Monica
Marchio, Serena
Di Paolo, Daniela
Becherini, Pamela
Curnis, Fiavio
Longhi, Renato
Nico, Beatrice
Bussollno, Fedrico
Ribatti, Domenico
Cilli, Michele
Arap, Wadih
Pasqualini, Renata
Corti, Angelo
Allen, Theresa
Ponzoni, Mirco
TI Combination of peptides-targeted liposomal chemotherapy against
neuroblastoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 G Gaslini Childrens Hosp, Genoa, Italy.
Univ Turin, Dept Oncol Sci, Candiolo, TO, Italy.
San Raffaele, Dept Mol Oncol, Milan, Italy.
CNR, Ist Chim Riconoscimento Mol, I-20133 Milan, Italy.
Univ Bari, Dept Human Anat & Histol, Bari, Italy.
Natl Canc Inst, Anim Res Facil, Genoa, Italy.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Univ Alberta, Dept Pharmacol, Edmonton, AB, Canada.
RI Di Paolo, Daniela/J-7681-2016
OI Di Paolo, Daniela/0000-0001-7264-6888
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3677
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705269
ER
PT J
AU Pastorino, F
Loi, M
Cilli, M
Zhao, H
Sapra, P
Greenberger, L
Ribatti, D
Ponzoni, M
AF Pastorino, Fabio
Loi, Monica
Cilli, Michele
Zhao, Hong
Sapra, Puja
Greenberger, Lee
Ribatti, Domenico
Ponzoni, Mirco
TI EZN-2208, a novel pegylated SN-38 drug conjugate, markedly inhibits
tumor growth and metastatic spreading of human neuroblastoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 G Gaslini Childrens Hosp, Lab Oncol, Genoa, Italy.
Natl Canc Inst, Anim Res Facil, Genoa, Italy.
Enzon Pharmaceut, Piscataway, NJ USA.
Univ Bari, Dept Human Anat, Bari, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1699
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704427
ER
PT J
AU Perez-Galan, P
Mora-Jensen, H
Weniger, M
Chapman, C
Wiestner, A
AF Perez-Galan, Patricia
Mora-Jensen, Helena
Weniger, Marc
Chapman, Colby
Wiestner, Adrian
TI Resistance to bortezomib in mantle cell lymphoma is associated with
differentiation towards a plasma cell phenotype
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Perez-Galan, Patricia; Mora-Jensen, Helena; Weniger, Marc; Chapman, Colby; Wiestner, Adrian] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4540
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704405
ER
PT J
AU Pichiorri, F
Sung-Suk, S
Taccioli, C
Hofmeister, C
Benson, D
Kuehl, M
Munker, R
Huebner, K
Ageilan, RI
Croce, CM
AF Pichiorri, Flavia
Sung-Suk, Suh
Taccioli, Cristian
Hofmeister, Craig
Benson, Don
Kuehl, Michael
Munker, Reinhold
Huebner, Kay
Ageilan, Rami I.
Croce, Carlo M.
TI Regulation of expression of multiple miRNAs defines the cellular
response to non genotoxic p53 activation in multiple myeloma cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Ohio State Univ, Columbus, OH 43210 USA.
NCI, Bethesda, MD 20892 USA.
Louisiana State Univ, Shreveport, LA 71105 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2637
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804063
ER
PT J
AU Pittman, G
Perera, F
Herbstman, J
Edwards, S
Tang, DL
Wang, XT
Jedrychowski, W
Bell, D
AF Pittman, Gary
Perera, Frederica
Herbstman, Julie
Edwards, Susan
Tang, Deliang
Wang, Xuting
Jedrychowski, Wieslaw
Bell, Douglas
TI In utero PAH exposure alters CpG methylation status in neonates
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
Jagiellonian Univ, Krakow, Poland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3015
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702703148
ER
PT J
AU Ptaszynska, M
Pendrak, M
Roberts, D
AF Ptaszynska, Malgorzata
Pendrak, Michael
Roberts, David
TI VEGF and ATX cross-talk presents a new aspect of tumor-endothelial cell
interaction in the tumor microenviorment
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3502
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804267
ER
PT J
AU Quinlan, S
Anderson, L
Pfieffer, R
Morton, L
Landgren, O
Berndt, S
Warren, J
Engels, E
AF Quinlan, Scott
Anderson, Lesley
Pfieffer, Ruth
Morton, Lindsay
Landgren, Ola
Berndt, Sonja
Warren, Joan
Engels, Eric
TI Spectrum of hematologic malignancies associated with solid organ
transplantation: results of a US population-based case-control study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI DCEG, Rockville, MD USA.
NCI DCCPS, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2145
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704088
ER
PT J
AU Raggi, C
Marquardt, J
Andersen, J
Avital, I
Factor, V
Thorgeirsson, S
AF Raggi, Chiara
Marquardt, Jens
Andersen, Jesper
Avital, Itzhak
Factor, Valentina
Thorgeirsson, Snorri
TI Epigenetic modulation of liver cancer cell lines reduces heterogeneity
of cancer stem cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Raggi, Chiara; Marquardt, Jens; Andersen, Jesper; Avital, Itzhak; Factor, Valentina; Thorgeirsson, Snorri] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3138
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803427
ER
PT J
AU Ramaswamy, B
Bhalla, K
Cohen, B
Pellegrino, C
Hershman, D
Chuang, E
Somlo, G
Goetz, M
Swaby, R
Stearns, V
Nonemaker, J
Hopkins, U
Christos, P
Espinoza-Delgado, I
Sparano, J
AF Ramaswamy, B.
Bhalla, K.
Cohen, B.
Pellegrino, C.
Hershman, D.
Chuang, E.
Somlo, G.
Goetz, M.
Swaby, R.
Stearns, V.
Nonemaker, J.
Hopkins, U.
Christos, P.
Espinoza-Delgado, I.
Sparano, J.
TI Phase I-II study of the histone deacetylase inhibitor vorinostat plus
paclitaxel and bevacizumab in patients with metastatic breast cancer:
New York Cancer Consortium trial P7703
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Ohio State Univ, Columbus, OH 43210 USA.
Med Coll Georgia, Augusta, GA 30912 USA.
Montefiore Einstein Canc Ctr, Bronx, NY USA.
New York Presbyterian Hosp, New York, NY USA.
Weill Cornell Univ, New York, NY USA.
City Hope Natl Med Ctr, Duarte, CA 91010 USA.
Mayo Clin, Rochester, MN USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Kimmel Canc Ctr, Baltimore, MD USA.
NCI, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3571
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805324
ER
PT J
AU Rao, C
Mohammed, A
Qian, L
Janakiram, N
Choi, CI
Zhang, YT
Lightfoot, S
Steele, V
AF Rao, Chinthalapally
Mohammed, Altaf
Qian, Li
Janakiram, Naveena
Choi, Chang-In
Zhang, Yuting
Lightfoot, Stan
Steele, Vernon
TI Delayed progression of pancreatic carcinoma in a conditional K-ras(G12D)
mice by nitric oxide (NO)-releasing aspirin
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Oklahoma, Inst Canc, OUHSC, Oklahoma City, OK USA.
Univ Oklahoma, Coll Med, Dept Pathol, Oklahoma City, OK 73190 USA.
NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2062
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801377
ER
PT J
AU Rapisarda, A
Uranchimeg, B
Scudiero, D
Ngo, A
Bee, NS
Everett, M
Cardellina, J
Shoemaker, R
Melillo, G
AF Rapisarda, Annamaria
Uranchimeg, Badarch
Scudiero, Dominic
Ngo, Anna
Bee, Ng Siew
Everett, Martin
Cardellina, John
Shoemaker, Robert
Melillo, Giovanni
TI Identification and characterization of a novel HIF-1 inhibitor that
selectively induces DNA damage under hypoxic conditions
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21701 USA.
MerLion Pharmaceut, Singapore, Singapore.
NCI, DTP, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 256
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804065
ER
PT J
AU Reid, J
McGovern, R
Buhrow, S
Jia, L
Ames, M
AF Reid, Joel
McGovern, Renee
Buhrow, Sarah
Jia, Lee
Ames, Matthew
TI LC/MS/MS assay and mouse pharmacokinetics of the eukaryotic elongation
factor-2 kinase inhibitor NSC 745343
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mayo Clin, Rochester, MN USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2932
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802114
ER
PT J
AU Reinhold, W
Pfister, T
Liu, HF
Gingeras, T
Kaldjian, E
Selzer, R
Ryan, M
Parchment, R
Tomaszewski, J
Kinders, R
Weinstein, J
Pommier, Y
AF Reinhold, William
Pfister, Thomas
Liu, Hongfang
Gingeras, Thomas
Kaldjian, Eric
Selzer, Rebecca
Ryan, Michael
Parchment, Ralph
Tomaszewski, Joseph
Kinders, Robert
Weinstein, John
Pommier, Yves
TI Transcript expression analysis of TOP1 at the exon level reveals
potential intragenic regulation, association with DNA copy number, and
is associated with genomic stability, and response to the
indenoisoquinolines in the NCI-60
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
SIAC, Frederick, MD USA.
Affymetrix Inc, Santa Clara, CA USA.
Transgenomic Inc, Omaha, NE USA.
Roche NimbleGen Inc, Madison, WI USA.
TigerTeam Consulting, Fairfax, VA USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1705
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704433
ER
PT J
AU Rime, BJ
Arur, S
Thaker, P
Golden, A
Schedl, T
Goodfellow, P
AF Rime, B. J.
Arur, Swathi
Thaker, Premal
Golden, Andy
Schedl, Tim
Goodfellow, Paul
TI DICER1 is a target of ERK1/2 in mammalian cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Washington Univ, Siteman Canc Ctr, St Louis, MO USA.
NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4381
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805476
ER
PT J
AU Roccaro, A
Sacco, A
Chen, CZ
Leleu, X
Runnels, J
Azab, AK
Azab, F
Jia, XY
Ngo, H
Melhem, M
Varticovski, L
Novina, C
Rollins, B
Anderson, K
Ghobrial, I
AF Roccaro, Aldo
Sacco, Antonio
Chen, Changzhong
Leleu, Xavier
Runnels, Judith
Azab, Abdel Kareem
Azab, Feda
Jia, Xiaoying
Ngo, Hai
Melhem, Molly
Varticovski, Lyuba
Novina, Carl
Rollins, Barrett
Anderson, Kenneth
Ghobrial, Irene
TI MicroRNA in the biology, prognosis and therapy of Waldenstrom
macroglobulinemia
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1393
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803205
ER
PT J
AU Rodriguez, V
Carlson, B
Noma, A
Elkahloun, A
Green, J
Suzuki, T
Chandrasekharappa, S
AF Rodriguez, Virginia
Carlson, Bradley
Noma, Akiko
Elkahloun, Abdel
Green, Jeffrey
Suzuki, Tsutomu
Chandrasekharappa, Settara
TI TRMT12 overexpression in cancer cells affects the cell cycle and the
nonsense mediated decay pathways by regulating the SMG-1 kinase, a
member of the PIKK family of kinases
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NHGRI, Bethesda, MD 20892 USA.
NCI, Bethesda, MD 20892 USA.
Univ Tokyo, Tokyo, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2486
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801161
ER
PT J
AU Rosenberg, S
AF Rosenberg, Steven
TI Effective cell transfer therapy for patients with metastatic melanoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Rosenberg, Steven] NCI, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA SY35-3
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800044
ER
PT J
AU Rotunno, M
Yu, K
Lubin, J
Consonni, D
Pesatori, A
Goldstein, A
Goldin, L
Wacholder, S
Welch, R
Burdette, L
Chanock, S
Caporaso, N
Bertazzi, PA
Tucker, M
Chatterjee, N
Bergen, A
Landi, MT
AF Rotunno, Melissa
Yu, Kai
Lubin, Jay
Consonni, Dario
Pesatori, Angela
Goldstein, Alisa
Goldin, Lynn
Wacholder, Sholom
Welch, Robert
Burdette, Laurie
Chanock, Stephen
Caporaso, Neil
Bertazzi, Pier Alberto
Tucker, Margaret
Chatterjee, Nilanjan
Bergen, Andrew
Landi, Maria Teresa
TI Phase I metalbolic genes and risk of lung cancer: multiple polymorphisms
and mRNA expression
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NIH, Rockville, MD USA.
Dept Occupat & Environm Hlth, Milan, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 106
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704056
ER
PT J
AU Ryscavage, A
Suh, K
Shukla, A
Malik, M
Crutchley, J
Nolan, L
Dumont, R
Cheng, C
Fernandez-Salas, E
Yuspa, S
AF Ryscavage, Andrew
Suh, Kwang
Shukla, Anjali
Malik, Mariam
Crutchley, John
Nolan, Lisa
Dumont, Rebecca
Cheng, Christina
Fernandez-Salas, Ester
Yuspa, Stuart
TI CLIC4 is a tumor suppressor for cutaneous squamous cell cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ryscavage, Andrew; Suh, Kwang; Shukla, Anjali; Malik, Mariam; Crutchley, John; Nolan, Lisa; Dumont, Rebecca; Cheng, Christina; Fernandez-Salas, Ester; Yuspa, Stuart] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5346
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804499
ER
PT J
AU Saleh, A
Ly, D
Soule, B
DeGraff, W
Savage, J
Mitchell, J
Gius, D
Simone, N
AF Saleh, Anthony
Ly, David
Soule, Benjamin
DeGraff, William
Savage, Jason
Mitchell, James
Gius, David
Simone, Nicole
TI The response of the microRNA let-7b to ionizing radiation may involve
p53
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
NIAID, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3976
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804036
ER
PT J
AU Samimi, G
Mok, S
Birrer, M
AF Samimi, Goli
Mok, Sam
Birrer, Michael
TI Expression of CTGF in ovarian tumor stroma and its role ovarian tumor
progression
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 270
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804078
ER
PT J
AU Samuels, Y
Palavalli, L
Prickett, T
Wunderlich, J
Wei, XM
Burrell, A
Porter-Gill, P
Lin, J
Molinolo, A
Weeraratna, A
Brody, L
Rosenberg, S
Davis, S
Wang, CW
Cronin, J
Agrawal, N
Westbroek, W
Hoogstraten-Miller, S
Fetsch, P
Filie, A
O'Connell, M
Buckhaults, P
Banister, C
Howard, J
AF Samuels, Yardena
Palavalli, Lavanya
Prickett, Todd
Wunderlich, John
Wei, Xiaomu
Burrell, Allison
Porter-gill, Patricia
Lin, Jimmy
Molinolo, Alfredo
Weeraratna, Ashani
Brody, Lawrrence
Rosenberg, Steven
Davis, Sean
Wang, Chenwei
Cronin, Julie
Agrawal, Neena
Westbroek, Wendy
Hoogstraten-Miller, Shelly
Fetsch, Patricia
Filie, Armando
O'Connell, Michael
Buckhaults, Phillip
Banister, Carolyn
Howard, Jason
TI Analysis of the Matrix Metalloproteinase Family Reveals MMP-8 is often
mutated in Melanoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
JHU, Baltimore, MD USA.
Univ S Carolina, Sch Med, Columbia, SC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-100
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802122
ER
PT J
AU Samuni, Y
Ishii, H
Krishna, M
Mitchell, J
AF Samuni, Yuval
Ishii, Hisanari
Krishna, Murali
Mitchell, James
TI Superoxide-dependent hepatotoxicity of the Hsp90 inhibiting anticancer
drugs geldanamycin and its two derivatives
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Samuni, Yuval; Ishii, Hisanari; Krishna, Murali; Mitchell, James] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1854
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802177
ER
PT J
AU Santhanam, A
Baker, A
Hegamyer, G
Kirschmann, D
Colburn, N
AF Santhanam, Arti
Baker, Alyson
Hegamyer, Glenn
Kirschmann, Dawn
Colburn, Nancy
TI Pdcd4 inhibition of lysyl oxidase contributes to hypoxia-induced breast
cancer invasion
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21701 USA.
Northwestern Univ, Childrens Mem Res Ctr, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3099
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803154
ER
PT J
AU Sato, M
Kadota, M
Robert, C
Zhang, HE
Lee, M
Wakefield, L
AF Sato, Misako
Kadota, Mitsutaka
Robert, Clifford
Zhang, Hongen
Lee, Maxwell
Wakefield, Lalage
TI Identification of direct Smad3 target genes mediating the
TGF-beta-dependent \#8220;metastatic switch\#8221;
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Sato, Misako; Kadota, Mitsutaka; Robert, Clifford; Zhang, Hongen; Lee, Maxwell; Wakefield, Lalage] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2589
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804049
ER
PT J
AU Schetter, A
Nguyen, G
Bowman, E
Matte, E
Yuen, S
Croce, C
Leung, S
Harris, C
AF Schetter, Aaron
Giang Nguyen
Bowman, Elise
Matte, Ewy
Yuen, Siu
Croce, Carlo
Leung, Suet
Harris, Curtis
TI Prediction of survival in early stage colon adenocarcinoma using the
expression of inflammatory genes and a microRNA
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1612
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805150
ER
PT J
AU Schmid, T
Blees, J
Baker, A
Henrich, C
Young, M
Brune, B
McMahon, J
Colburn, N
AF Schmid, Tobias
Blees, Johanna
Baker, Alyson
Henrich, Curtis
Young, Matthew
Bruene, Bernhard
McMahon, James
Colburn, Nancy
TI Targeting translation to inhibit tumorigenesis - development of a
high-throughput screen to discover compounds stabilizing tumor
suppressor Pdcd4
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Goethe Univ Frankfurt, D-60054 Frankfurt, Germany.
NCI, Frederick, MD 21701 USA.
NCI, MTDP, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1558
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702700387
ER
PT J
AU Shan, ZH
Simmons, J
Shakoori, A
Jen, J
Wiest, J
AF Shan, Zhihong
Simmons, John
Shakoori, Abbas
Jen, Jin
Wiest, Jonathan
TI TUSC1, a putative tumor suppressor gene in human lung cancer potentially
functions in autophagy
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
CCR, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 386
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800400
ER
PT J
AU Sharma, S
Wang, XJ
Gao, P
Steele, V
AF Sharma, Sheela
Wang, Xiaojuan
Gao, Pu
Steele, Vernon
TI Alternative approach to aerosolized chemopreventive agent delivery to
respiratory tract epithelium
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Hamner Inst Hlth Sci, Res Triangle Pk, NC USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2093
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702801127
ER
PT J
AU Shatz, M
Menendez, D
Resnick, M
AF Shatz, Maria
Menendez, Daniel
Resnick, Michael
TI The p53 tumor suppressor as a regulator of innate immunity genes
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Shatz, Maria; Menendez, Daniel; Resnick, Michael] NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4253
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802222
ER
PT J
AU Shebl, F
Engels, E
Goedert, J
Chaturvedi, A
AF Shebl, Fatma
Engels, Eric
Goedert, James
Chaturvedi, Anil
TI Pulmonary infactions and risk of lung cancer among people with AIDS
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Shebl, Fatma; Engels, Eric; Goedert, James; Chaturvedi, Anil] NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2149
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704093
ER
PT J
AU Simmons, J
DeCicco-Skinner, K
Pandey, J
Shan, ZH
Reddi, T
Wiest, J
AF Simmons, John
DeCicco-Skinner, Kathleen
Pandey, Jyotsna
Shan, Zhihong
Reddi, Tejaswini
Wiest, Jonathan
TI Loss of Tpl2 enhances tumorigenesis and affects tumor phenotype during
promotion
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Amer Univ, Washington, DC 20016 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 450
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801328
ER
PT J
AU Slager, S
Goldin, L
Strom, S
Lanasa, M
Spector, L
Rassenti, L
Leis, J
Camp, N
Kay, N
Vachon, C
Weinberg, J
Rabe, K
Achenbach, S
Hanson, C
Marti, G
Call, T
Caporaso, N
Cerhan, J
AF Slager, Susan
Goldin, Lynn
Strom, Sara
Lanasa, Mark
Spector, Logan
Rassenti, Laura
Leis, Jose
Camp, Nicola
Kay, Neil
Vachon, Celine
Weinberg, J.
Rabe, Kari
Achenbach, Sara
Hanson, Curtis
Marti, Gerald
Call, Timothy
Caporaso, Neil
Cerhan, James
TI Confirmation of a set of genetic susceptibility variants for chronic
lymphocytic leukemia (CLL)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Mayo Clin, Rochester, MN USA.
NCI, DCEG, Bethesda, MD 20892 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Duke Univ, Med Ctr, Durham, NC USA.
Univ Minnesota, Minneapolis, MN USA.
UCSD, Moores Canc Ctr, La Jolla, CA USA.
Mayo Clin, Scottsdale, AZ USA.
Univ Utah, Sch Med, Salt Lake City, UT USA.
US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 96
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704045
ER
PT J
AU Smith, S
Salcido, C
Carlson, M
Hursting, S
Varticovski, L
AF Smith, Sarah
Salcido, Crystal
Carlson, Marisa
Hursting, Stephen
Varticovski, Lyuba
TI Wnt-1 mammary tumors are enriched in CD44+/CD24-cells with cancer stem
cell characteristics.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Texas Austin, Austin, TX 78712 USA.
NCI, CCR, Bethesda, MD 20892 USA.
Univ Denver, Denver, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3087
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603161
ER
PT J
AU Smits, M
Mir, S
Niers, J
Marquez, V
Tannous, B
Cloos, J
Noske, D
Wurdinger, T
AF Smits, Michiel
Mir, Shahryar
Niers, Johanna
Marquez, Victor
Tannous, Bakhos
Cloos, Jacqueline
Noske, David
Wurdinger, Tom
TI MicroRNA-101 targets EZH2 and controls angiogenesis in glioblastoma
multiforme
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4761
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804254
ER
PT J
AU Sohn, J
Yfantis, H
Khan, M
Bowman, E
Trivers, G
Hussain, S
Zanetti, K
Harris, C
AF Sohn, Jane
Yfantis, Harris
Khan, Mohammed
Bowman, Elise
Trivers, Glennwood
Hussain, S.
Zanetti, Krista
Harris, Curtis
TI Inflammation is associated with aging and DNA damage response in
inflammatory bowel disease
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3493
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804112
ER
PT J
AU Sorbara, L
Kishawi, I
Pinsky, P
Meltzer, S
Franklin, W
Bemis, L
Gaston, S
Rom, W
Srivastava, S
AF Sorbara, Lynn
Kishawi, Iman
Pinsky, Paul
Meltzer, Stephen
Franklin, Wilbur
Bemis, Lynne
Gaston, Sandra
Rom, William
Srivastava, Sudhir
TI MicroRNA microarrays for biomarker discovery: Joint EDRN-Agilent project
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
Agilent Technol, Santa Clara, CA USA.
Johns Hopkins Univ, Baltimore, MD USA.
Univ Colorado, Denver, CO 80202 USA.
Harvard, Beth Israel Deaconess Med Ctr, Boston, MA USA.
NYU, Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5383
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701803344
ER
PT J
AU Sosa, MS
Yang, CF
Lopez-Haber, C
Klein-Szanto, A
Lemmon, M
Gutkind, JS
Kazanietz, M
AF Sosa, Maria Soledad
Yang, Chengfeng
Lopez-Haber, Cynthia
Klein-Szanto, Andres
Lemmon, Mark
Gutkind, J. Silvio
Kazanietz, Marcelo
TI The Rac-GEF P-Rex1is an essential mediator of Rac activation and
motility downstream of ErbB receptors in breast cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
Michigan State Univ, E Lansing, MI 48824 USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2497
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802489
ER
PT J
AU Sparano, J
Moulder, S
Kazi, A
Coppola, D
Negassa, A
Vandat, L
Li, TH
Christine, P
Fineberg, S
Munster, P
Malafa, M
David, L
Hoschander, S
Hopkins, U
Hershman, D
Wright, J
Kleer, C
Merjver, S
Sebti, S
AF Sparano, Joseph
Moulder, Stacy
Kazi, Aslamuzzaman
Coppola, Domenico
Negassa, Abdissa
Vandat, Linda
Li, Tianhong
Christine, Pellegrino
Fineberg, Susan
Munster, Pam
Malafa, Mokenge
David, Lee
Hoschander, Shira
Hopkins, Una
Hershman, Dawn
Wright, John
Kleer, Celina
Merjver, Sofia
Sebti, Said
TI Phase II trial of the farnesyl transferase inhibitor tipifarnib plus
neoadjuvant doxorubicin-cyclophosphamide in patients with clinical stage
IIB-IIIC breast cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Montefiore Einstein Canc Ctr, Bronx, NY USA.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
Weill Cornell Med Ctr, New York, NY USA.
Columbia Presbyterian Med Ctr, New York, NY 10032 USA.
NCI, CTEP, Bethesda, MD 20892 USA.
Univ Michigan, Ann Arbor, MI 48109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5624
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805372
ER
PT J
AU Stark, K
Shelton, P
Gorski, D
Ethier, S
Chen, A
Nguyen, B
Burger, A
AF Stark, Karri
Shelton, Phillip
Gorski, David
Ethier, Stephen
Chen, Alice
Binh Nguyen
Burger, Angelika
TI Vorinostat can sensitize triple negative breast cancer cell lines to
Aminoflavone Prodrug
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Wayne State Univ, Detroit, MI USA.
Univ Maryland, Baltimore, MD 21201 USA.
Wayne State Univ, Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
NCI, Canc Therapeut Evaluat Program, Bethesda, MD 20892 USA.
Tigris Pharmaceut, Bonita Springs, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2905
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802085
ER
PT J
AU Stepp, MA
Jurjus, R
Pal-Ghosh, S
Tadvalkar, G
Cataisson, C
Ryscavage, A
Yuspa, S
AF Stepp, Mary Ann
Jurjus, Rosalyn
Pal-Ghosh, Sonali
Tadvalkar, Gauri
Cataisson, Christophe
Ryscavage, Andrew
Yuspa, Stuart
TI Syndecan-1 is required for formation of cutaneous squamous cell
carcinomas after chemical carcinogenesis.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 George Washington Univ, Sch Med, Washington, DC USA.
NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2222
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702604093
ER
PT J
AU Stepp, MA
Jurjus, R
Pal-Ghosh, S
Tadvalkar, G
Cataisson, C
Ryscavage, A
Yuspa, S
AF Stepp, Mary Ann
Jurjus, Rosalyn
Pal-Ghosh, Sonali
Tadvalkar, Gauri
Cataisson, Christophe
Ryscavage, Andrew
Yuspa, Stuart
TI Syndecan-1 is required for formation of cutaneous squamous cell
carcinomas after chemical carcinogenesis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 George Washington Univ, Sch Med, Washington, DC USA.
NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2222
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702803101
ER
PT J
AU Stone, R
Nick, A
Spannuth, W
Bonome, T
Lutgendorf, S
De Geest, K
Merritt, W
Lin, Y
Gershenson, D
Coleman, R
Birrer, M
Sood, A
AF Stone, Rebecca
Nick, Alpa
Spannuth, Whitney
Bonome, Tomas
Lutgendorf, Susan
De Geest, Koen
Merritt, William
Lin, Yvonne
Gershenson, David
Coleman, Robert
Birrer, Michael
Sood, Anil
TI The clinical and biological significance of focal adhesion kinase
activation in ovarian carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 UT MD Anderson Canc Ctr, Houston, TX USA.
NIH, Cell & Canc Biol Branch, Bethesda, MD 20892 USA.
Univ Iowa, Dept Obstet & Gynecol, Iowa City, IA 52242 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3636
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702705166
ER
PT J
AU Stuelten, C
Busch, J
Tang, BW
Oshima, A
Sutton, E
Karpova, T
Roberts, A
Wakefield, L
Niederhuber, J
AF Stuelten, Christina
Busch, Johanna
Tang, Binwu
Oshima, Akira
Sutton, Emily
Karpova, Tatiana
Roberts, Anita
Wakefield, Lalage
Niederhuber, John
TI Transient tumor-fibroblast interactions durably increase tumor cell
malignancy by a TGF-beta mediated mechanism
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Stuelten, Christina; Busch, Johanna; Tang, Binwu; Oshima, Akira; Sutton, Emily; Karpova, Tatiana; Roberts, Anita; Wakefield, Lalage; Niederhuber, John] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3504
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804269
ER
PT J
AU Sudarshan, S
Sourbier, C
Kong, HS
Block, K
Romero, V
Yang, YF
Galindo, C
Mollapour, M
Scroggins, B
Goode, N
Lee, MJ
Gourlay, C
Trepel, J
Linehan, WM
Neckers, L
AF Sudarshan, Sunil
Sourbier, Carole
Kong, Hye-Sik
Block, Karen
Romero, Vladimir
Yang, Youfeng
Galindo, Cynthia
Mollapour, Mehdi
Scroggins, Bradley
Goode, Norman
Lee, Min-Jung
Gourlay, Campbell
Trepel, Jane
Linehan, W. Marston
Neckers, Len
TI Fumarate hydratase deficiency induces glycolytic addiction and a
HIF1-\#945; amplification loop stabilized by glucose dependent
generation of reactive oxygen species
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 UT Hlth Sci Ctr, San Antonio, TX USA.
NCI, Bethesda, MD 20892 USA.
Univ Kent, Canterbury CT2 7NZ, Kent, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5302
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802198
ER
PT J
AU Takikita, M
Hu, N
Giffen, C
Taylor, P
Hewitt, S
AF Takikita, Mikiko
Hu, Nan
Giffen, Carol
Taylor, Philip
Hewitt, Stephen
TI Cytokeratin 14 and fascin are associated with histological
differentiation in esophageal squamous cell carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Tissue Array Res Program, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
Informat Management Serv Inc, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1010
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801484
ER
PT J
AU Tanaka, H
Yamamoto, M
Miyakoshi, M
Tamakawa, S
Tokusashi, Y
Yaginuma, Y
Ogawa, K
AF Tanaka, Hiroki
Yamamoto, Masahiro
Miyakoshi, Masaaki
Tamakawa, Susumu
Tokusashi, Yoshihiko
Yaginuma, Yuji
Ogawa, Katsuhiro
TI Rapamycin induces necrosis in mouse hepatocellular carcinomas by
antiangiogenic activity, but also activates cap-independent translation
of HIF-1\#945; in hepatocellular carcinoma cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 LSU Hlth Sci Ctr, Shreveport, LA USA.
Asahikawa Med Coll, Asahikawa, Hokkaido 078, Japan.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 125
PG 2
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702602471
ER
PT J
AU Tasevska, N
Cross, A
Dodd, K
Ziegler, R
Caporaso, N
Sinha, R
AF Tasevska, Natasa
Cross, Amanda
Dodd, Kevin
Ziegler, Regina
Caporaso, Neil
Sinha, Rashmi
TI The effect of meat consumption, meat cooking preferences, meat mutagens
and heme iron on lung cancer risk in the Prostate, Lung, Colorectral,
and Ovarian Cancer Screening Trial (PLCO)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Tasevska, Natasa; Cross, Amanda; Dodd, Kevin; Ziegler, Regina; Caporaso, Neil; Sinha, Rashmi] NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 62
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704401
ER
PT J
AU Terzuoli, E
Uranchimeg, B
Rapisarda, A
Burger, A
Ziche, M
Melillo, G
AF Terzuoli, Erika
Uranchimeg, Badarch
Rapisarda, Annamaria
Burger, Angelika
Ziche, Marina
Melillo, Giovanni
TI Modulation of HIF-1\#945; mRNA processing by Aminoflavone: a novel
mechanism of HIF-1\#945; inhibition in breast cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Siena, Dept Mol Biol, I-53100 Siena, Italy.
NCI, Frederick, MD 21701 USA.
Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 266
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804074
ER
PT J
AU Truong, T
Sauter, W
McKay, J
Hosgood, D
Boffetta, P
Brennan, P
Hung, R
AF Therese Truong
Sauter, Wiebke
McKay, James
Hosgood, Dean
Boffetta, Paolo
Brennan, Paul
Hung, Rayjean
CA Int Lung Canc Consort
TI Coordinated association study of 10 potential lung cancer susceptibility
variants by the International Lung Cancer Consortium (ILCCO)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Int Agcy Res Canc, F-69372 Lyon, France.
Helmholtz Zentrum Munich, German Res Ctr Environm Hlth, Inst Epidemiol, Neuherberg, Germany.
NCI, DCEG, Bethesda, MD 20892 USA.
Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1914
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603173
ER
PT J
AU Tian, S
Bank, A
Huang, JQ
Yoshimura, T
Zeng, X
AF Tian, Song
Bank, Alexander
Huang, Jiaqiang
Yoshimura, Teizo
Zeng, Xiao
TI siRNA array study identified the NFkB pathway as an important controller
for high CCL2 expression in glioma cell line U105MG
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 SABiosciences Corp, Frederick, MD USA.
NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1545
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804346
ER
PT J
AU Tosca, P
Merrill, J
Ryan, M
Knostman, K
Johnson, J
Peggins, J
Tomaszewski, J
AF Tosca, Patricia
Merrill, John
Ryan, Michael
Knostman, Katherine
Johnson, Jerry
Peggins, James
Tomaszewski, Joseph
TI A comparative neurotoxicity study of Breflate and six Brefeldin-A
prodrugs administered IV to male Fischer 344 rats
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Battelle Mem Inst, Columbus, OH USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5102
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801216
ER
PT J
AU Trempus, C
Wei, SJ
Humble, M
Dang, H
Bortner, C
Williams, J
Morris, R
Tennant, R
AF Trempus, Carol
Wei, Sung-Jen
Humble, Margaret
Dang, Hong
Bortner, Carl
Williams, Jason
Morris, Rebecca
Tennant, Raymond
TI Overexpression of the T-box transcription factor, Tbx1, abrogates
cellular transformation in culture and delays tumor growth in mice
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
Alpha Gamma Technol Inc, Raleigh, NC USA.
Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2375
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701800178
ER
PT J
AU Tripathi, V
Zimonjic, D
Popescu, N
AF Tripathi, Veenu
Zimonjic, Drazen
Popescu, Nicholas
TI DLC1 associates with cell-cell adhesion complex and induces expression
of E-cadherin in GAP dependent manner
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Tripathi, Veenu; Zimonjic, Drazen; Popescu, Nicholas] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 619
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804418
ER
PT J
AU Tsai, HT
Caporaso, N
Kyle, R
Katzmann, J
Dispenzieri, A
Hayes, R
Marti, G
Albitar, M
Ghia, P
Rajkumar, V
Landgren, O
AF Tsai, Huei-Ting
Caporaso, Neil
Kyle, Robert
Katzmann, Jerry
Dispenzieri, Angela
Hayes, Richard
Marti, Gerald
Albitar, Maher
Ghia, Paolo
Rajkumar, Vincent
Landgren, Ola
TI Evidence of immune disruption up to 9.8 years prior to diagnosis of
chronic lymphocytic leukemia: A prospective study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
Mayo Clin, Div Hematol & Internal Med, Rochester, MN USA.
Mayo Clin, Div Clin Biochem & Immunol, Rochester, MN USA.
Mayo Clin, Lab Med & Pathol, Rochester, MN USA.
NIH, Ctr Biol Evaluat & Res, US FDA, Bethesda, MD 20892 USA.
Quest Diagnost, Nichols Inst, San Juan Capistrano, CA USA.
Univ Vita Salute San Raffaele, Dept Oncol, Unit & Lab Lymphoid Malignancies, Milan, Italy.
Ist Sci San Raffaele, Milan, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1680
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702702330
ER
PT J
AU Tsang, P
Cheuk, A
Chen, QR
Khan, J
AF Tsang, Patricia
Cheuk, Adam
Chen, Qing-Rong
Khan, Javed
TI High throughput siRNA screening identifies NF-kB as a target for
combination therapy in neuroblastoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Tsang, Patricia; Cheuk, Adam; Chen, Qing-Rong; Khan, Javed] NIH, Gaithersburg, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 5677
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804366
ER
PT J
AU Uzturk, G
Chatterjee, C
Ginsburg, E
Rheey, J
Vonderhaar, B
Berg, P
AF Uzturk, Gizem
Chatterjee, Cynthia
Ginsburg, Erika
Rheey, Jinguen
Vonderhaar, Barbara
Berg, Patricia
TI Prolactin stimulates pBP1, a homeotic protein frequently activated in
breast cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 George Washington Univ, Washington, DC USA.
NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3349
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801274
ER
PT J
AU van der Watt, P
Maske, C
Hendricks, D
Parker, I
Denny, L
Govender, D
Birrer, M
Leaner, V
AF van der Watt, Pauline
Maske, Christopher
Hendricks, Denver
Parker, Iqbal
Denny, Lynette
Govender, Dhirendra
Birrer, Michael
Leaner, Virna
TI The Karyopherin proteins, Crm1 and Karyopherin \#946;1, are
overexpressed in cervical cancer and critical for cancer cell survival
and proliferation.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Cape Town, ZA-7925 Cape Town, South Africa.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 535
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701802184
ER
PT J
AU Varticovski, L
Pine, S
Salcido, C
Robles, A
Ryan, B
LaRochelle, A
Harris, C
AF Varticovski, Lyuba
Pine, Sharon
Salcido, Crystal
Robles, Ana
Ryan, Brid
LaRochelle, Andre
Harris, Curtis
TI Identification of cancer stem cells in small cell lung cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 LHC CCR NCI NIH, Bethesda, MD USA.
NCI CCR, Bethesda, MD USA.
NHBLI, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 176
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603206
ER
PT J
AU Vora, M
Calcagno, A
Ambudkar, S
Gottesman, M
Gillet, JP
AF Vora, Meena
Calcagno, Anna
Ambudkar, Suresh
Gottesman, Michael
Gillet, Jean-Pierre
TI Characterization of multidrug resistance-linked gene signatures from
TaqMan low density arrays, microarray gene expression and cellular
assays for the NCI-60 panel using an integrative data analysis system,
SIMUSITE (TM)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Biophase Syst, Fremont, CA USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2466
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801063
ER
PT J
AU Wali, A
Cavallo-Medved, D
Lonardo, F
Lei, J
Wang, Y
Rishi, A
Carbone, M
Sloane, B
Ruckdeschel, J
Pass, H
AF Wali, Anil
Cavallo-Medved, Dora
Lonardo, Fulvio
Lei, Jing
Wang, Ying
Rishi, Arun
Carbone, Michele
Sloane, Bonnie
Ruckdeschel, John
Pass, Harvey
TI Gene expression pattern and clinical significance of cathepsin B in
malignant pleural mesothelioma.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Wayne State Univ, Dept Surg, John D Dingell VA Med Ctr, Detroit, MI USA.
Wayne State Univ, Dept Pathol, John D Dingell VA Med Ctr, Detroit, MI 48202 USA.
Wayne State Univ, Dept Pharmacol, John D Dingell VA Med Ctr, Detroit, MI 48201 USA.
Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
Canc Res Ctr Hawaii, Thorac Oncol Program, Honolulu, HI USA.
NYU, Sch Med, Dept Cardiothorac Surg, New York, NY USA.
NCI, Ctr Canc, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2602
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804193
ER
PT J
AU Walker, A
Kotz, H
Minasian, L
Venkatasen, A
Turkbey, B
Houston, N
Kohn, E
Annunziata, C
AF Walker, Amanda
Kotz, Herbert
Minasian, Lori
Venkatasen, Aradhana
Turkbey, Baris
Houston, Nicole
Kohn, Elise
Annunziata, Christina
TI Phase II study of clinical activity and proteomic profiling of the
VEGFR2 inhibitor vandetanib in women with relapsed or refractory
epithelial ovarian, fallopian tube, or primary peritoneal cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Walker, Amanda; Kotz, Herbert; Minasian, Lori; Venkatasen, Aradhana; Turkbey, Baris; Houston, Nicole; Kohn, Elise; Annunziata, Christina] NCI, Bethesda, MD 20892 USA.
RI Annunziata, Christina/L-3219-2016
OI Annunziata, Christina/0000-0003-2033-6532
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3581
PG 2
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701805335
ER
PT J
AU Wang, F
Yang, XP
Burnett, J
Friedman, J
Lu, H
Cohen, J
Chen, Z
Van Waes, C
AF Wang, Frederick
Yang, Xinping
Burnett, Jeffrey
Friedman, Jay
Lu, Hai
Cohen, Jonah
Chen, Zhong
Van Waes, Carter
TI TGF-\#946; receptor Ill is downregulated by \#916;Np63 and methylation
and contributes to altered TGF-\#946; and NF -\#954;B signaling and the
malignant phenotype in head and neck squamous cell cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NIH, HHMI, Res Scholars Program, Bethesda, MD 20892 USA.
Natl Inst Deafness & Other Commun Disorders, Tumor Biol Sect, Head & Neck Surg Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA LB-13
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801239
ER
PT J
AU Wang, SQ
Tsutsumi, S
Xu, WP
Neckers, L
AF Wang, Suiquan
Tsutsumi, Shinji
Xu, Wanping
Neckers, Len
TI Cancer cells harboring MET gene amplification are sensitive to Hsp90
inhibitor 17-AAG
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wang, Suiquan; Tsutsumi, Shinji; Xu, Wanping; Neckers, Len] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 1853
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702802176
ER
PT J
AU Wang, XY
Lu, JC
Penalva, L
Okano, H
Linnoila, R
Glazer, R
AF Wang, Xiao-Yang
Lu, Jiachun
Penalva, Liuz
Okano, Hideyuki
Linnoila, R.
Glazer, Robert
TI Musashi1 regulates breast cancer stem cell self-renewal and is a
predictor of human breast cancer survival
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
Guangzhou Med Univ, Guangzhou, Guangdong, Peoples R China.
Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
Keio Univ, Sch Med, Tokyo, Japan.
Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3059
PG 1
WC Oncology
SC Oncology
GA V43TB
UT WOS:000209702603131
ER
PT J
AU Wang, Y
Ozawa, A
Agarwal, S
Marx, S
AF Wang, Yan
Ozawa, Atsushi
Agarwal, Sunita
Marx, Stephen
TI Menin regulates the AKT signaling pathway through its interaction with
AKT
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wang, Yan; Ozawa, Atsushi; Agarwal, Sunita; Marx, Stephen] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 3832
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804431
ER
PT J
AU Warren, K
Gururangan, S
Balis, F
Berg, S
Blaney, S
Wallace, D
Boyett, J
Kun, L
AF Warren, Katherine
Gururangan, Sri
Balis, Frank
Berg, Stacey
Blaney, Susan
Wallace, Dana
Boyett, James
Kun, Larry
TI Phase II Trial of 06-Benzylguanine and temozolomide in pediatric
patients with recurrent or progressive high-grade gliomas and brainstem
gliomas (BSG): A Pediatric Brain Tumor Consortium (PBTC) Study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Duke Univ, Med Ctr, Durham, NC USA.
Texas Childrens Canc Ctr, Houston, TX USA.
St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4056
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702702198
ER
PT J
AU Warren, K
Gururangan, S
Balis, F
Berg, S
Blaney, S
Wallace, D
Boyett, J
Kun, L
AF Warren, Katherine
Gururangan, Sri
Balis, Frank
Berg, Stacey
Blaney, Susan
Wallace, Dana
Boyett, James
Kun, Larry
TI Phase II Trial of O6-Benzylguanine and temozolomide in pediatric
patients with recurrent or progressive high-grade gliomas and brainstem
gliomas (BSG): A Pediatric Brain Tumor Consortium (PBTC) Study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Duke Univ, Med Ctr, Durham, NC USA.
Texas Childrens Canc Ctr, Houston, TX USA.
St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4056
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804058
ER
PT J
AU Watters, J
Park, Y
Hollenbeck, A
Schatzkin, A
Albanes, D
AF Watters, Joanne
Park, Yikyung
Hollenbeck, Albert
Schatzkin, Arthur
Albanes, Demetrius
TI Cigerette smoking and prostate cancer in a prospective US cohort study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
AARP, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2130
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702704072
ER
PT J
AU Wei, BR
Hoover, S
Spehalski, E
Zhou, WD
Edwards, J
Tessitore, A
Ross, M
Risinger, J
Goldsmith, P
Alvord, W
Quinones, O
Woolard, K
Liotta, L
Petricoin, E
Simpson, RM
AF Wei, Bih-Rong
Hoover, Shelley
Spehalski, Elizabeth
Zhou, Weidong
Edwards, Jennifer
Tessitore, Alessandra
Ross, Mark
Risinger, John
Goldsmith, Paul
Alvord, W.
Quinones, Octavio
Woolard, Kevin
Liotta, Lance
Petricoin, Emanuel
Simpson, R. Mark
TI Mass spectrometry driven discovery proteomics of serum from mice with
human ovarian cancer resulted in identification of a potential
cancer-origin biomarker that correlates with peritoneal tumor burden
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Mol Pathol Unit, LCBG, Bethesda, MD 20892 USA.
NCI, Antibody & Prot Purificat Unit, CCR, Bethesda, MD 20892 USA.
George Mason Univ, Ctr Appl Prote & Mol Med, Manassas, VA USA.
Mem Hlth Univ Med Ctr Inc, Anderson Canc Inst, Savannah, GA USA.
NCI, Data Management Serv Inc, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 4480
PG 1
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702701142
ER
PT J
AU Wei, J
Johansson, P
Chen, QR
Song, Y
Durinck, S
Wen, XY
Cheuk, A
Ludwig, A
Shohet, J
Smith, M
Houghton, P
Morton, C
Badgett, T
Khan, J
AF Wei, Jun
Johansson, Peter
Chen, Qingrong
Song, Young
Durinck, Steffen
Wen, Xinyu
Cheuk, Adam
Ludwig, Andrew
Shohet, Jason
Smith, Malcolm
Houghton, Peter
Morton, Christopher
Badgett, Thomas
Khan, Javed
TI microRNA profiling identifies cancer specific and prognostic signatures
in pediatric malignancies
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
Baylor Coll Med, Houston, TX 77030 USA.
St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2594
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701804104
ER
PT J
AU Wen, XY
Chen, QR
Wei, J
Song, Y
Guo, X
Khan, J
AF Wen, Xinyu
Chen, Qing-Rong
Wei, Jun
Song, Young
Guo, Xiang
Khan, Javed
TI The Oncogenomics Data Center: an integrated, multi-platform,
multifunctional database system
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wen, Xinyu; Chen, Qing-Rong; Wei, Jun; Song, Young; Guo, Xiang; Khan, Javed] NCI, NIH, SAIC Frederick, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2471
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801069
ER
PT J
AU White, R
Lu, SL
Bornstein, S
Salter, K
Olson, S
Anderson, P
Reh, D
Malkoski, S
Deng, CX
Wang, XJ
AF White, Ruth
Lu, Shi-Long
Bornstein, Sophia
Salter, Kelli
Olson, Susan
Anderson, Peter
Reh, Douglas
Malkoski, Steven
Deng, Chuxia
Wang, Xiao-Jing
TI Smad4 deletion leads to spontaneous head and neck cancer formation
associated with genomic instability
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
Univ Colorado, Hlth Sci Ctr, Aurora, CO USA.
NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2084
PG 1
WC Oncology
SC Oncology
GA V43TD
UT WOS:000209702804385
ER
PT J
AU Wilkinson, S
Fernandez, D
Chan, W
Gascoyne, R
Campo, E
Jaffe, E
Staudt, L
Delabie, J
Rosenwald, A
Rimsza, L
AF Wilkinson, Sarah
Fernandez, Diane
Chan, Wing
Gascoyne, Randy
Campo, Elias
Jaffe, Elaine
Staudt, Louis
Delabie, Jan
Rosenwald, Andreas
Rimsza, Lisa
TI MHC class II loss in diffuse large B-cell lymphoma is inversely
correlated with MUM1/IRF4 expression
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 Univ Arizona, Tucson, AZ USA.
Univ Nebraska Med Ctr, Omaha, NE USA.
British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
Univ Barcelona, Barcelona, Spain.
NCI, Bethesda, MD 20892 USA.
Norwegian Radium Hosp, Oslo, Norway.
Univ Wurzburg, D-97070 Wurzburg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 2712
PG 2
WC Oncology
SC Oncology
GA V43TC
UT WOS:000209702702112
ER
PT J
AU Williams, J
Ji, P
Zhou, H
Rigas, B
Kopelovich, L
AF Williams, Jennie
Ji, Ping
Zhou, Hui
Rigas, Basil
Kopelovich, Levy
TI Nitric oxide-donating aspirin S-nitrosylates signaling proteins in human
cancer cells: implications for its mechanism of action
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 SUNY Stony Brook, Stony Brook, NY 11794 USA.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2009
VL 69
SU 9
MA 20
PG 1
WC Oncology
SC Oncology
GA V43ST
UT WOS:000209701801004
ER
EF