-93G-->A polymorphism of hMLH1 and risk of primary lung cancer

Int J Cancer. 2004 Nov 20;112(4):678-82. doi: 10.1002/ijc.20359.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Aged
  • Base Pair Mismatch
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Squamous Cell / genetics*
  • Carrier Proteins
  • Case-Control Studies
  • DNA Damage*
  • DNA Repair
  • Female
  • Genetic Predisposition to Disease*
  • Humans
  • Korea
  • Lung Neoplasms / genetics*
  • Male
  • Middle Aged
  • MutL Protein Homolog 1
  • Neoplasm Proteins / genetics*
  • Nuclear Proteins
  • Odds Ratio
  • Polymorphism, Genetic*
  • Risk Factors

Substances

  • Adaptor Proteins, Signal Transducing
  • Carrier Proteins
  • MLH1 protein, human
  • Neoplasm Proteins
  • Nuclear Proteins
  • MutL Protein Homolog 1