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Conference Paper: Reversal of E-Cadherin Promoter Hypermethylation Status after Helicobacter pylori Eradication

TitleReversal of E-Cadherin Promoter Hypermethylation Status after Helicobacter pylori Eradication
Authors
Issue Date2004
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
The 2004 Digestive Disease Week and the 105th Annual Meeting of the American Gastroenterological Association (AGA), New Orleans, LA., 15-20 May 2004. In Gastroenterology, 2004, v. 126 n. 4 suppl. 2, p. A38, abstract no. 333 How to Cite?
AbstractBACKGROUND: E-cadherin hypermethylation plays an important role in gastric carcinogenesis. Reversing hypermethyation may halt carcinogenic process. We have previously reported that Helicobacter pylon infection is an independent factor for predicting E-cadherin methylation in chronic gastritis in patients without gastric cancer. AIM: to examine if eradication of H. pylori could reverse E-cadherin methylation. METHODS: Patients with dyspepsia and H. pylori infection were randomized to receive H. pylori eradication therapy (Group 1, n = 41) or no treatment (Group 2, n = 40) and followed up prospectively. Gastric mucosae were taken for methylation assay at Week 0 (before treatment) and Week 6 (after treatment). Archived specimens with intestinal metaplasia with H. pylori infection (n = 22) and without (n = 19) were also retrieved for methylation analysis. Methylation was assessed using methylation specific PCR. RESULTS: Methylation was detected in 46% (19/41) and 17% (7/41) at Week 0 and 6, respectively in Group 1 (P = 0.004). 78.9% (15/19) specimens turned un-methylated after eradicating H. pylori. The disappearing of methylation did not depend on the reversal of chronic gastritis to normal mucosa, as only one chronic gastritis specimen with positive methylation reversed to normal mucosa and showed negative methylation after H. pylon eradication. Methylation was detected in 47.5% (19/40) and 52.5% (21/40) at Week 0 and 6, respectively in Group 2 (P = 0.5). Methylation frequency did not differ in H. pylori positive or negative intestinal metaplastic specimens (72.7% vs 63%, P = 0.5). CONCLUSION: H. pylon eradication therapy could reverse methylation in patients with chronic gastritis and may halt the process of gastric carcinogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/102913
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170

 

DC FieldValueLanguage
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorPeng, JZen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorHui, WMen_HK
dc.contributor.authorWong, RWMen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorKwong, YLen_HK
dc.contributor.authorRashid, Aen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-25T20:49:56Z-
dc.date.available2010-09-25T20:49:56Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 2004 Digestive Disease Week and the 105th Annual Meeting of the American Gastroenterological Association (AGA), New Orleans, LA., 15-20 May 2004. In Gastroenterology, 2004, v. 126 n. 4 suppl. 2, p. A38, abstract no. 333en_HK
dc.identifier.issn0016-5085en_HK
dc.identifier.urihttp://hdl.handle.net/10722/102913-
dc.description.abstractBACKGROUND: E-cadherin hypermethylation plays an important role in gastric carcinogenesis. Reversing hypermethyation may halt carcinogenic process. We have previously reported that Helicobacter pylon infection is an independent factor for predicting E-cadherin methylation in chronic gastritis in patients without gastric cancer. AIM: to examine if eradication of H. pylori could reverse E-cadherin methylation. METHODS: Patients with dyspepsia and H. pylori infection were randomized to receive H. pylori eradication therapy (Group 1, n = 41) or no treatment (Group 2, n = 40) and followed up prospectively. Gastric mucosae were taken for methylation assay at Week 0 (before treatment) and Week 6 (after treatment). Archived specimens with intestinal metaplasia with H. pylori infection (n = 22) and without (n = 19) were also retrieved for methylation analysis. Methylation was assessed using methylation specific PCR. RESULTS: Methylation was detected in 46% (19/41) and 17% (7/41) at Week 0 and 6, respectively in Group 1 (P = 0.004). 78.9% (15/19) specimens turned un-methylated after eradicating H. pylori. The disappearing of methylation did not depend on the reversal of chronic gastritis to normal mucosa, as only one chronic gastritis specimen with positive methylation reversed to normal mucosa and showed negative methylation after H. pylon eradication. Methylation was detected in 47.5% (19/40) and 52.5% (21/40) at Week 0 and 6, respectively in Group 2 (P = 0.5). Methylation frequency did not differ in H. pylori positive or negative intestinal metaplastic specimens (72.7% vs 63%, P = 0.5). CONCLUSION: H. pylon eradication therapy could reverse methylation in patients with chronic gastritis and may halt the process of gastric carcinogenesis.-
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_HK
dc.relation.ispartofGastroenterologyen_HK
dc.titleReversal of E-Cadherin Promoter Hypermethylation Status after Helicobacter pylori Eradicationen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0016-5085&volume=126&issue=4 Suppl 2&spage=333&epage=&date=2004&atitle=Reveral+of+E-Cadherin+Promoter+Hypermethylation+Status+after+Helicobacter+pylori+Eradicationen_HK
dc.identifier.emailChan, AOO: aoochan@hku.hken_HK
dc.identifier.emailLam, SK: deanmed@hku.hken_HK
dc.identifier.emailHui, WM: hrmehwm@hkucc.hku.hken_HK
dc.identifier.emailWong, RWM: wmwongg@hku.hken_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.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0016-5085(04)80007-6-
dc.identifier.hkuros86058en_HK
dc.identifier.volume126en_HK
dc.identifier.issue4 suppl. 2en_HK
dc.identifier.spageA38, abstract no. 333en_HK
dc.identifier.epageA38, abstract no. 333-

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