Abstract
AIM: To study Helicobacter pylori (H. pylori) infection in relation to E-cadherin (E-cad) promoter polymorphism and hypermethylation in GCs. METHODS: Specimens were taken from representative cancerous lesions and adjacent non-cancerous epithelia of 67 resected GCs. H. pylori was detected by real-time PCR of the cagA gene from non-neoplastic epithelium. E-cad promoter polymorphism and hypermethylation were determined by restriction fragment length polymorphism analysis and methylation-specific PCR, respectively. Expression of E-cad protein was determined by immunohistochemistry. RESULTS: H. pylori was found in 57% of patients with GC. H. pylori infection was more frequently found in tumors with the -160C/C genotype than those with the -160C/A and -160A/A genotypes (74% vs 47%, P = 0.02). H. pylori infection was associated with E-cad methylation in non-neoplastic epithelium; however, no significant difference in H. pylori was observed between methylated and unmethylated cancerous lesions. CONCLUSION: Patients with the -160C/C genotype might require H. pylori infection to promote the inactivation of CDH1, suggesting that H. pylori infection might affect GC in an initial stage because polymorphism is germ line. Mechanism of hypermethylation of CDH1 promoter in GC is complex, and H. pylori infection might affect it in an initial stage.