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Nucleotide excision repair gene polymorphisms and risk of advanced colorectal adenoma: XPC polymorphisms modify smoking-related risk

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dc.contributor.authorHuang, Wen-Yi-
dc.contributor.authorBerndt, Sonja I.-
dc.contributor.authorKang, Daehee-
dc.contributor.authorChatterjee, Nilanjan-
dc.contributor.authorChanock, Stephen J.-
dc.contributor.authorYeager, Meredith-
dc.contributor.authorWelch, Robert-
dc.contributor.authorBresalier, Rober S.-
dc.contributor.authorWeissfeld, Joel L.-
dc.contributor.authorHayes, Richard B.-
dc.date.accessioned2010-01-07T05:32:54Z-
dc.date.available2010-01-07T05:32:54Z-
dc.date.issued2006-02-24-
dc.identifier.citationCancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):306-11.en
dc.identifier.issn1055-9965 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16492920-
dc.identifier.urihttps://hdl.handle.net/10371/28303-
dc.description.abstractOBJECTIVES: Nucleotide excision repair enzymes remove bulky damage caused by environmental agents, including carcinogenic polycyclic aromatic hydrocarbons found in cigarette smoke, a risk factor for colorectal adenoma. Among participants randomized to the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we studied the risk of advanced colorectal adenoma in relation to cigarette smoking and selected single nucleotide polymorphisms (SNP) in the nucleotide excision repair pathway.METHODS: Cases (n = 772) were subjects with left-sided advanced adenoma (>1 cm in size, high-grade dysplasia, or villous characteristics). Controls (n = 777) were screen-negative for left-sided polyps by sigmoidoscopy. DNA was extracted from blood samples and 15 common nonsynonymous SNPs in seven-nucleotide excision repair genes [XPC, RAD23B (hHR23B), CSB (ERCC6), XPD (ERCC2), CCNH, XPF (ERCC4), and XPG (ERCC5)] were genotyped.RESULTS: None of the studied SNPs were independently associated with advanced adenoma risk. Smoking was related to adenoma risk and XPC polymorphisms (R492H, A499V, K939Q) modified these effects (P(interaction) from 0.03-0.003). Although the three XPC variants were in linkage disequilibrium, a multivariate logistic regression tended to show independent protective effects for XPC 499V (P(trend) = 0.06), a finding supported by haplotype analysis (covariate-adjusted global permutation P = 0.03).CONCLUSIONS: Examining a spectrum of polymorphic variants in nucleotide excision repair genes, we found evidence that smoking-associated risks for advanced colorectal adenoma are modified by polymorphisms in XPC, particularly haplotypes containing XPC 499V.en
dc.language.isoenen
dc.publisherAmerican Association for Cancer Researchen
dc.subjectAdenoma/*geneticsen
dc.subjectAgeden
dc.subjectAllelesen
dc.subjectCase-Control Studiesen
dc.subjectColorectal Neoplasms/*geneticsen
dc.subjectDNA Helicases/geneticsen
dc.subjectDNA Repair/*geneticsen
dc.subjectDNA-Binding Proteins/*geneticsen
dc.subjectFemaleen
dc.subjectGenotypeen
dc.subjectHumansen
dc.subjectLinkage Disequilibriumen
dc.subjectLogistic Modelsen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectMultivariate Analysisen
dc.subjectRisk Factorsen
dc.subjectSmoking/adverse effects/*geneticsen
dc.subjectPolymorphism, Single Nucleotide-
dc.titleNucleotide excision repair gene polymorphisms and risk of advanced colorectal adenoma: XPC polymorphisms modify smoking-related risken
dc.typeArticleen
dc.contributor.AlternativeAuthor강대희-
dc.identifier.doi10.1158/1055-9965.EPI-05-0751-
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