Background:E-cadherin methylation is important in gastric carcinogenesis.Reversing hypermethylation may halt the carcinogenic process.We have previously reported that Helicobacter pylori infection is associated with E...Background:E-cadherin methylation is important in gastric carcinogenesis.Reversing hypermethylation may halt the carcinogenic process.We have previously reported that Helicobacter pylori infection is associated with E-cadherin methylation in chronic gastritis patients.Aim:To examine if eradication of H pylori could reverse E-cadherin methylation.Methods:Patients with dyspepsia and positive for H pylori infection,with a mucosal biopsy showing chronic active gastritis,were randomised to receive H pylori eradication therapy(group 1,n = 41)or no treatment(group 2,n = 40),and were followed up prospectively.Gastric mucosae were taken for methylation assay at week 0(before treatment)and week 6(after treatment).Archived specimens of intestinal metaplasia with H pylori infection(n = 22)and without(n = 19)were retrieved for methylation analysis.Methylation was assessed using methylation specific polymerase chain reaction and sequencing.Results:Methylation at E-cadherin was detected in 46%(19/41)and 17%(7/41)of patients at weeks 0 and 6,respectively,in group 1(p = 0.004);78.9%(15/19)of specimens were unmethylated after eradication of H pylori.Mucosal biopsy showed chronic inactive gastritis in 35 patients,intestinal metaplasia in one,and normal mucosa in five at week 6.Methylation was detected in 47.5%(19/40)and 52.5%(21/40)of patients at weeks 0 and 6,respectively,in group 2(P = 0.5).Gastric mucosal biopsy showed persistent chronic active gastritis in all cases.Methylation frequency did not differ in H pylori positive or negative intestinal metaplastic specimens(72.7%v 63%;p = 0.5).Conclusion:H pylori eradication therapy could reverse methylation in patients with chronic gastritis.This demonstrates an environmental effect on methylation.展开更多
文摘Background:E-cadherin methylation is important in gastric carcinogenesis.Reversing hypermethylation may halt the carcinogenic process.We have previously reported that Helicobacter pylori infection is associated with E-cadherin methylation in chronic gastritis patients.Aim:To examine if eradication of H pylori could reverse E-cadherin methylation.Methods:Patients with dyspepsia and positive for H pylori infection,with a mucosal biopsy showing chronic active gastritis,were randomised to receive H pylori eradication therapy(group 1,n = 41)or no treatment(group 2,n = 40),and were followed up prospectively.Gastric mucosae were taken for methylation assay at week 0(before treatment)and week 6(after treatment).Archived specimens of intestinal metaplasia with H pylori infection(n = 22)and without(n = 19)were retrieved for methylation analysis.Methylation was assessed using methylation specific polymerase chain reaction and sequencing.Results:Methylation at E-cadherin was detected in 46%(19/41)and 17%(7/41)of patients at weeks 0 and 6,respectively,in group 1(p = 0.004);78.9%(15/19)of specimens were unmethylated after eradication of H pylori.Mucosal biopsy showed chronic inactive gastritis in 35 patients,intestinal metaplasia in one,and normal mucosa in five at week 6.Methylation was detected in 47.5%(19/40)and 52.5%(21/40)of patients at weeks 0 and 6,respectively,in group 2(P = 0.5).Gastric mucosal biopsy showed persistent chronic active gastritis in all cases.Methylation frequency did not differ in H pylori positive or negative intestinal metaplastic specimens(72.7%v 63%;p = 0.5).Conclusion:H pylori eradication therapy could reverse methylation in patients with chronic gastritis.This demonstrates an environmental effect on methylation.
