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Conference Paper: Methylation of E-cadherin gene in gastric cancer and in normal gastric mucosa from patients with and wihtout Helicobacter pylori infection

TitleMethylation of E-cadherin gene in gastric cancer and in normal gastric mucosa from patients with and wihtout Helicobacter pylori infection
Authors
Issue Date2003
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH
Citation
The 2003 Asia Pacific Digestive Week (APDW 2003) and 18th Annual Scientific Meeting of the Gastroenterological Society of Singapore, Singapore, 12-16 April 2003. In Journal of Gastroenterology and Hepatology, 2003, v. 18 n. suppl. 1, p. A27, abstract no. 6 How to Cite?
AbstractINTRODUCTION: E(epithelial)-cadherin is an important homotypic adhesion molecule which plays important role in tumor invasion/metastasis. Silencing of E-cadherin by CpG island methylation has been identified to be an important mechanism in both familial and sporadic gastric cancer. AIM: We investigated methylation of E-cadherin in normal gastric mucosa from normal subjects, and intestinal metaplasia, adenocarcinoma, and metastatic lymph nodes from patients with gastric cancer. METHODS: Methylation at E-cadherin was studied by methylation-specific polymerase chain reaction (MSP) and expression of E-cadherin by immunohistochemical staining. All statistical studies were two-sided. Results CpG island methylation was identified in 30% of normal gastric mucosa. Significant association between methylation and Helicobacter pylori was observed: 90% of methylated mucosa were H. pylori + ve, vs. 65% of unmethylated mucosa were H. pylori—ve (P = 0.002). Methylation in mucosa increases with age (P = 0.04). Methylation was observed in 59% of intestinal metaplasia, 58% of tumorous tissues, and 60% of metastatic lymph nodes. Concordancy rate of methylation status between different stages in the same patient was 83%. Methylation at E-cadherin correlated with lymph node metastasis (P = 0.046), and was observed more frequently in mucinous and signet ring cell tumors (P = 0.0058). CONCLUSION: A possible link exists among E-cadherin methylation, Helicobacter pylori and aging. This may provide clue for the initiating mechanism of methylation.
DescriptionThis free journal suppl. entitled: Abstracts from the Asia Pacific Digestive Week (APDW 2003)
Persistent Identifierhttp://hdl.handle.net/10722/102381
ISSN
2015 Impact Factor: 3.322
2015 SCImago Journal Rankings: 1.190

 

DC FieldValueLanguage
dc.contributor.authorChan, AOO-
dc.contributor.authorLam, SK-
dc.contributor.authorWong, BCY-
dc.contributor.authorHui, WM-
dc.contributor.authorKwong, YL-
dc.date.accessioned2010-09-25T20:28:21Z-
dc.date.available2010-09-25T20:28:21Z-
dc.date.issued2003-
dc.identifier.citationThe 2003 Asia Pacific Digestive Week (APDW 2003) and 18th Annual Scientific Meeting of the Gastroenterological Society of Singapore, Singapore, 12-16 April 2003. In Journal of Gastroenterology and Hepatology, 2003, v. 18 n. suppl. 1, p. A27, abstract no. 6-
dc.identifier.issn0815-9319-
dc.identifier.urihttp://hdl.handle.net/10722/102381-
dc.descriptionThis free journal suppl. entitled: Abstracts from the Asia Pacific Digestive Week (APDW 2003)-
dc.description.abstractINTRODUCTION: E(epithelial)-cadherin is an important homotypic adhesion molecule which plays important role in tumor invasion/metastasis. Silencing of E-cadherin by CpG island methylation has been identified to be an important mechanism in both familial and sporadic gastric cancer. AIM: We investigated methylation of E-cadherin in normal gastric mucosa from normal subjects, and intestinal metaplasia, adenocarcinoma, and metastatic lymph nodes from patients with gastric cancer. METHODS: Methylation at E-cadherin was studied by methylation-specific polymerase chain reaction (MSP) and expression of E-cadherin by immunohistochemical staining. All statistical studies were two-sided. Results CpG island methylation was identified in 30% of normal gastric mucosa. Significant association between methylation and Helicobacter pylori was observed: 90% of methylated mucosa were H. pylori + ve, vs. 65% of unmethylated mucosa were H. pylori—ve (P = 0.002). Methylation in mucosa increases with age (P = 0.04). Methylation was observed in 59% of intestinal metaplasia, 58% of tumorous tissues, and 60% of metastatic lymph nodes. Concordancy rate of methylation status between different stages in the same patient was 83%. Methylation at E-cadherin correlated with lymph node metastasis (P = 0.046), and was observed more frequently in mucinous and signet ring cell tumors (P = 0.0058). CONCLUSION: A possible link exists among E-cadherin methylation, Helicobacter pylori and aging. This may provide clue for the initiating mechanism of methylation.-
dc.languageeng-
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH-
dc.relation.ispartofJournal of Gastroenterology and Hepatology-
dc.rightsPreprint This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article]. Authors are not required to remove preprints posted prior to acceptance of the submitted version. Postprint This is the accepted version of the following article: [full citation], which has been published in final form at [Link to final article].-
dc.titleMethylation of E-cadherin gene in gastric cancer and in normal gastric mucosa from patients with and wihtout Helicobacter pylori infection-
dc.typeConference_Paper-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0815-9319&volume=18&issue=9 suppl&spage=&epage=&date=2003&atitle=Methylation+of+E-cadherin+gene+in+gastric+cancer+and+in+normal+gastric+mucosa+from+patients+with+and+wihtout+Helicobacter+pylori+infectionen_HK
dc.identifier.emailChan, AOO: aoochan@hku.hk-
dc.identifier.emailLam, SK: hrmelsk@hkucc.hku.hk-
dc.identifier.emailWong, BCY: bcywong@hku.hk-
dc.identifier.emailHui, WM: hrmehwm@hkucc.hku.hk-
dc.identifier.emailKwong, YL: ylkwong@hku.hk-
dc.identifier.authorityWong, BCY=rp00429-
dc.identifier.authorityKwong, YL=rp00358-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1046/j.1440-1746.18.s1.1.x-
dc.identifier.hkuros99257-
dc.identifier.volume18-
dc.identifier.issuesuppl. 1-
dc.identifier.spageA27, abstract no. 6-
dc.identifier.epageA27, abstract no. 6-
dc.publisher.placeAustralia-

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