{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T21:29:50Z","timestamp":1789594190654,"version":"build-2803163510"},"reference-count":29,"publisher":"BMJ","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    E-cadherin methylation is important in gastric carcinogenesis. Reversing hypermethylation may halt the carcinogenic process. We have previously reported that\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    infection is associated with E-cadherin methylation in chronic gastritis patients.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Aim:<\/jats:bold>\n                    To examine if eradication of\n                    <jats:italic>H pylori<\/jats:italic>\n                    could reverse E-cadherin methylation.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    Patients with dyspepsia and positive for\n                    <jats:italic>H pylori<\/jats:italic>\n                    infection, with a mucosal biopsy showing chronic active gastritis, were randomised to receive\n                    <jats:italic>H pylori<\/jats:italic>\n                    eradication therapy (group 1, n\u200a=\u200a41) or no treatment (group 2, n\u200a=\u200a40), 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\n                    <jats:italic>H pylori<\/jats:italic>\n                    infection (n\u200a=\u200a22) and without (n\u200a=\u200a19) were retrieved for methylation analysis. Methylation was assessed using methylation specific polymerase chain reaction and sequencing.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    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\u200a=\u200a0.004); 78.9% (15\/19) of specimens were unmethylated after eradication of\n                    <jats:italic>H pylori<\/jats:italic>\n                    . 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\u200a=\u200a0.5). Gastric mucosal biopsy showed persistent chronic active gastritis in all cases. Methylation frequency did not differ in\n                    <jats:italic>H pylori<\/jats:italic>\n                    positive or negative intestinal metaplastic specimens (72.7%\n                    <jats:italic>v<\/jats:italic>\n                    63%; p\u200a=\u200a0.5).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    <jats:italic>H pylori<\/jats:italic>\n                    eradication therapy could reverse methylation in patients with chronic gastritis. This demonstrates an environmental effect on methylation.\n                  <\/jats:p>","DOI":"10.1136\/gut.2005.077776","type":"journal-article","created":{"date-parts":[[2006,1,20]],"date-time":"2006-01-20T20:32:45Z","timestamp":1137789165000},"page":"463-468","source":"Crossref","is-referenced-by-count":148,"title":["Eradication of\n                    <i>Helicobacter pylori<\/i>\n                    infection reverses E-cadherin promoter hypermethylation"],"prefix":"10.1136","volume":"55","author":[{"given":"A O O","family":"Chan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J Z","family":"Peng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S K","family":"Lam","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K C","family":"Lai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M F","family":"Yuen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H K L","family":"Cheung","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y L","family":"Kwong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Rashid","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C K","family":"Chan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B C-Y","family":"Wong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2006,1,20]]},"reference":[{"key":"2025121306055612000_55.4.463.1","first-page":"3554","volume":"48","year":"1988","journal-title":"Cancer Res"},{"key":"2025121306055612000_55.4.463.2","unstructured":"IARC working group on the evaluation of carcinogenic risks to humans, schistosomes, liver flukes, helicobacter pylori. 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