title: -93G-->A polymorphism of hMLH1 and risk of primary lung cancer.
abstract: Polymorphisms in DNA repair genes may be associated with differences in the repair capacity of DNA damage and may thereby influence an individual's susceptibility to smoking-related cancer. We investigated the association between the -93G-->A polymorphism in the hMLH1 gene and the risk of lung cancer in a Korean population. The hMLH1 -93G-->A polymorphism was typed in 372 lung cancer patients and 371 healthy controls that were frequency-matched for age and sex. There was no significant association between the hMLH1 -93G-->A genotype and the risk for adenocarcinoma or small cell carcinoma. However, the AA genotype was associated with a significantly increased risk for squamous cell carcinoma compared with both the GG genotype (adjusted OR=2.02; 95% CI=1.15-3.55; p=0.014) and the combined GG and GA genotype (adjusted OR=1.83; 95% CI=1.24-2.71; p=0.003). When the subjects were stratified by smoking exposure, the AA genotype was associated with a significantly increased risk for squamous cell carcinoma in lighter smokers (< or = 39 pack-years; adjusted OR=1.95; 95% CI=1.03-3.66; p=0.039) compared with the combined GG and GA genotype, whereas there was no significant association in heavier smokers (> 39 pack-years; adjusted OR=1.47; 95% CI=0.82-2.61). These results suggest that the hMLH1 -93G-->A polymorphism could be used as a marker of genetic susceptibility to squamous cell carcinoma of the lung.
authors.affiliation: Cancer Research Institute, Kyungpook National University Hospital, Daegu, South Korea.
authors.forename: Sun Ha
authors.initials: SH
authors.lastname: Park
authors.forename: Ga Young
authors.initials: GY
authors.lastname: Lee
authors.forename: Hyo-Sung
authors.initials: HS
authors.lastname: Jeon
authors.forename: Su Jeong
authors.initials: SJ
authors.lastname: Lee
authors.forename: Kyung Mee
authors.initials: KM
authors.lastname: Kim
authors.forename: Sang Soo
authors.initials: SS
authors.lastname: Jang
authors.forename: Chang Ho
authors.initials: CH
authors.lastname: Kim
authors.forename: Won Kee
authors.initials: WK
authors.lastname: Lee
authors.forename: Sin
authors.initials: S
authors.lastname: Kam
authors.forename: Rang Woon
authors.initials: RW
authors.lastname: Park
authors.forename: In-San
authors.initials: IS
authors.lastname: Kim
authors.forename: Tae Hoon
authors.initials: TH
authors.lastname: Jung
authors.forename: Jae Yong
authors.initials: JY
authors.lastname: Park
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000368:Aged; D020137:Base Pair Mismatch; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics*; D002294:Carcinoma, Squamous Cell / Q000235:genetics*; D002352:Carrier Proteins; D016022:Case-Control Studies; D004249:DNA Damage; D004260:DNA Repair; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007723:Korea; D008175:Lung Neoplasms / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D000070957:MutL Protein Homolog 1; D009363:Neoplasm Proteins / Q000235:genetics*; D009687:Nuclear Proteins; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; C501486:MLH1 protein, human; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D000070957:MutL Protein Homolog 1