Functional polymorphisms in FAS/FASL system contribute to the risk of occurrence but not progression of gastric cardiac adenocarcinoma

Hepatogastroenterology. 2012 Jan-Feb;59(113):141-6. doi: 10.5754/hge11300.

Abstract

Background/aims: Loss of FAS and gain of aberrant FASL expression are common features of malignant transformation. This study was designed to investigate whether the functional polymorphisms of FAS-1377 G/A (rs2234767) and FASL-844 T/C (rs763110) have an effect on the occurrence and progression of gastric cardiac adenocarcinoma (GCA).

Methodology: Associations of the FAS and FASL polymorphisms with GCA were estimated by OR and their 95% confidence intervals using logistic regression.

Results: In this study, as compared with the wild type homozygote and heterozygote, either the FAS-1377 AA or FASL-844 CC genotype was associated with increased risk of GCA (OR=1.78; 95% CI, 1.19-2.64 and OR=1.92; 95% CI, 1.46-2.54, respectively). Furthermore, individuals with both the FAS-1377 AA and FASL-844 CC genotypes have a higher risk of GCA (OR=4.09; 95% CI, 2.27-7.37) compared to those with the FAS-1377 GG and FASL-844 TT genotypes. Moreover, the FAS-1377 AA genotype increased the risk of GCA among smokers (OR=1.88; 95% CI, 1.11-3.20) but not among non-smokers, suggesting a potential gene-smoking interaction.

Conclusions: This current study suggests that functional polymorphisms in the apoptotic pathway genes FAS and FASL may significantly contribute to the occurrence of GCA.

MeSH terms

  • Adenocarcinoma / genetics*
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology
  • Adult
  • Aged
  • Cardia / metabolism*
  • Cardia / pathology
  • Case-Control Studies
  • China
  • Disease Progression
  • Fas Ligand Protein / genetics*
  • Fas Ligand Protein / metabolism
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease
  • Heterozygote
  • Homozygote
  • Humans
  • Logistic Models
  • Male
  • Middle Aged
  • Odds Ratio
  • Phenotype
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic
  • Risk Assessment
  • Risk Factors
  • Smoking / adverse effects
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology
  • fas Receptor / genetics*
  • fas Receptor / metabolism

Substances

  • FAS protein, human
  • FASLG protein, human
  • Fas Ligand Protein
  • fas Receptor