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Conference Paper: Methylation of E-cadherin gene in gastric cancer and in normal gastric mucosa from patients with and without Helicobacter pylori infection

TitleMethylation of E-cadherin gene in gastric cancer and in normal gastric mucosa from patients with and without Helicobacter pylori infection
Authors
Issue Date2002
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
The 2002 Digestive Disease Week and the 103rd Annual Meeting of the American Gastroenterological Association (AGA), San Francisco, CA., 19-22 May 2002. In Gastroenterology, 2002, v. 122 suppl. 4, p. A238, abstract no. M935 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, versus 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.
Persistent Identifierhttp://hdl.handle.net/10722/101841
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170

 

DC FieldValueLanguage
dc.contributor.authorChan, AOO-
dc.contributor.authorLam, SK-
dc.contributor.authorWong, BCY-
dc.contributor.authorHui, WM-
dc.contributor.authorKwong, YL-
dc.date.accessioned2010-09-25T20:06:33Z-
dc.date.available2010-09-25T20:06:33Z-
dc.date.issued2002-
dc.identifier.citationThe 2002 Digestive Disease Week and the 103rd Annual Meeting of the American Gastroenterological Association (AGA), San Francisco, CA., 19-22 May 2002. In Gastroenterology, 2002, v. 122 suppl. 4, p. A238, abstract no. M935-
dc.identifier.issn0016-5085-
dc.identifier.urihttp://hdl.handle.net/10722/101841-
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, versus 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.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro-
dc.relation.ispartofGastroenterology-
dc.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.titleMethylation of E-cadherin gene in gastric cancer and in normal gastric mucosa from patients with and without Helicobacter pylori infection-
dc.typeConference_Paper-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0016-5085&volume=122 &issue=4 suppl 1&spage=A238&epage=&date=2002&atitle=Methylation+of+E-cadherin+gene+in+gastric+cancer+and+in+normal+gastric+mucosa+from+patients+with+and+without+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_subscribed_fulltext-
dc.identifier.doi10.1016/S0016-5085(02)83883-5-
dc.identifier.hkuros73081-
dc.identifier.volume122-
dc.identifier.issuesuppl. 4-
dc.identifier.spageA238, abstract no. M935-
dc.identifier.epageA238, abstract no. M935-
dc.publisher.placeUnited States-

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