بررسی ارتباط پلی مرفیسم ژن Fas/CD95 و آدنوکارسینوم معده

Background and purpose: Apoptosis is a physiological mechanism of programmed cell death that dysregulation in this process may lead to carcinogenesis. Functional gene polymorphism in Fas can alter transcriptional activities and thus change the risks of cancer. A to G substitution in Fas -670 promoter region disrupts the binding site of STAT1 transcription factor. This study aimed to assess the association of genetic variants of Fas -A670G polymorphism with the potential risk of gastric cancer. Materials and methods: Genomic DNA was extracted from 159 patients with gastric adenocarcinoma and 170 healthy people as control group. Two groups had similar age, sex and ethnic background. Gastric cancer was diagnosed based on clinical and endoscopic findings, and pathological confirmations. Genotyping was done according to PCR-RFLP method. The association of genotypes or allele with disease was analyzed by logistic regression model and odd ratio was obtained at confidence level of 0.05. Results: Results showed that the mean age of patients was not significantly different with that of control group. (62.14 + 12, and 58.93 + 14.2, P= 0.9). Also, allele frequency in the patients and controls was not significantly different (58.6% vs. 61.8%, P=0.47). Meanwhile, the genotype frequencies of –A670G polymorphism were significantly different in two groups. The A/G heterozygosity was significantly less frequent in the patients than that of controls (42.4% vs. 51.8%, P=0.041). On the other hand, the presence of heterozygous A670G decreased the cancer risk (R= 0.5 and CI 0.26-0.94). Conclusion: Our findings indicated that A670G polymorphism in Fas promoter region might be associated with the risk of gastric cancer. Therefore, genetic variation in Fas/FasL system may contribute to etiology of gastric cancer due to corruption in apoptotic process.