title: Interactions between cigarette smoking and XPC-PAT genetic polymorphism             enhance bladder cancer risk.
abstract: Inherited polymorphisms in the XPC gene that lead to a reduction in DNA             repair capacity may increase susceptibility to bladder cancer. We investigated             three polymorphisms of the XPC gene (PAT, Ala499Val and Lys939Gln) in 600 subjects             with bladder cancer and in 609 healthy controls by a polymerase chain reaction-restriction             fragment length polymorphism (PCR-RFLP) assay in a Chinese Han population. Smoking             was associated with a significant increase in the risk for bladder cancer (OR,             2.48; 95% CI, 1.91-3.21). The risk was greater among heavy smokers (OR, 3.09,             95% CI, 2.24-4.25) compared to light smokers (OR, 1.91, 95% CI, 1.37-2.68). In             three polymorphisms of XPC, only the XPC-PAT variant genotype exhibited a significantly             increased risk for bladder cancer. When the total smoking exposure-gene interaction             was examined, the three polymorphisms did not exhibit any significant effect in             never smokers but a significant dose-response association in light or heavy smokers.             Especially, the bladder cancer risk was significantly elevated among the polymorphisms             of XPC-PAT(+/-) (OR, 2.56, 95% CI, 1.56-4.21, p<0.001; OR, 3.41, 95% CI, 2.19-5.29,             p<0.001) and XPC-PAT(+/+) (OR, 3. 00, 95% CI, 1.31-6.88, p=0.009; OR, 6. 78,             95% CI, 3.00-15.54, p<0.001) with either light or heavy smoking exposure, respectively.             XPC-PAT polymorphisms contribute to the risk for developing bladder cancer and             an elevated risk of bladder cancer was significantly associated with the gene-environment             (smoking) interaction in a Chinese Han population.
authors.affiliation: Urology Institute of PLA, Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, PR China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Liu
authors.forename: Huanhuan
authors.initials: H
authors.lastname: Wang
authors.forename: Tianxin
authors.initials: T
authors.lastname: Lin
authors.forename: Quanfang
authors.initials: Q
authors.lastname: Wei
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhi
authors.forename: Fang
authors.initials: F
authors.lastname: Yuan
authors.forename: Bo
authors.initials: B
authors.lastname: Song
authors.forename: Jin
authors.initials: J
authors.lastname: Yang
authors.forename: Zhiwen
authors.initials: Z
authors.lastname: Chen
mesh_terms: D000368:Aged; D019943:Amino Acid Substitution; D002295:Carcinoma, Transitional Cell / Q000209:etiology / Q000235:genetics*; D016022:Case-Control Studies; D004268:DNA-Binding Proteins / Q000235:genetics*; D005260:Female; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D008957:Models, Genetic; D015999:Multivariate Analysis; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D001749:Urinary Bladder Neoplasms / Q000209:etiology / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; C086984:XPC protein, human