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 adjace...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. Hpyloriwas 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: Hpyloriwas 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% vs47%, P = 0.02). Hpylori infection was associated with E-cad methylation in nonneoplastic 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 Hpyloriinfection to promote the inactivation of CDH1, suggesting that Hpylori infection might affect GC in an initial stage because polymorphism is germ line.Mechanism of hypermethylation of CDH1 promoter in GC is complex, and Hpyloriinfection might affect it in an initial stage.展开更多
基金Supported by Clinical Research Fund of the Tri-Service General Hospital CY Foundation for Advancement of Education, Science and Medicine, Taipei, Taiwan, China
文摘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. Hpyloriwas 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: Hpyloriwas 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% vs47%, P = 0.02). Hpylori infection was associated with E-cad methylation in nonneoplastic 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 Hpyloriinfection to promote the inactivation of CDH1, suggesting that Hpylori infection might affect GC in an initial stage because polymorphism is germ line.Mechanism of hypermethylation of CDH1 promoter in GC is complex, and Hpyloriinfection might affect it in an initial stage.
