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Article: Eradication of Helicobacter pylori infection reverses E-cadherin promoter hypermethylation

TitleEradication of Helicobacter pylori infection reverses E-cadherin promoter hypermethylation
Authors
Issue Date2006
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
Citation
Gut, 2006, v. 55 n. 4, p. 463-468 How to Cite?
AbstractBackground: 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.
Persistent Identifierhttp://hdl.handle.net/10722/44964
ISSN
2015 Impact Factor: 14.921
2015 SCImago Journal Rankings: 6.474
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorPeng, JZen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorLai, KCen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorCheung, HKLen_HK
dc.contributor.authorKwong, YLen_HK
dc.contributor.authorRashid, Aen_HK
dc.contributor.authorChan, CKen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2007-10-30T06:14:33Z-
dc.date.available2007-10-30T06:14:33Z-
dc.date.issued2006en_HK
dc.identifier.citationGut, 2006, v. 55 n. 4, p. 463-468en_HK
dc.identifier.issn0017-5749en_HK
dc.identifier.urihttp://hdl.handle.net/10722/44964-
dc.description.abstractBackground: 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.en_HK
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dc.format.extent125545 bytes-
dc.format.extent9342 bytes-
dc.format.extent2057 bytes-
dc.format.mimetypeapplication/pdf-
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dc.languageengen_HK
dc.publisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/en_HK
dc.relation.ispartofGuten_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsGut. Copyright © B M J Publishing Group.en_HK
dc.subject.meshCadherins-geneticsen_HK
dc.subject.meshGastritis-geneticsen_HK
dc.subject.meshHelicobacter-Infections-geneticsen_HK
dc.subject.meshHelicobacter-pylorien_HK
dc.subject.meshPromoter-Regions-Genetics-geneticsen_HK
dc.titleEradication of Helicobacter pylori infection reverses E-cadherin promoter hypermethylationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0017-5749&volume=55&issue=4&spage=463&epage=468&date=2006&atitle=Eradication+of+Helicobacter+pylori+infection+reverses+E-cadherin+promoter+hypermethylationen_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1136/gut.2005.077776en_HK
dc.identifier.pmid16428266-
dc.identifier.pmcidPMC1856151-
dc.identifier.scopuseid_2-s2.0-33645119366en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645119366&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume55en_HK
dc.identifier.issue4en_HK
dc.identifier.spage463en_HK
dc.identifier.epage468en_HK
dc.identifier.isiWOS:000236561900012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridPeng, JZ=12796973500en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridLai, KC=7402135595en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridCheung, HKL=7201839335en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.scopusauthoridRashid, A=7102299914en_HK
dc.identifier.scopusauthoridChan, CK=7404813824en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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