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Article: Promoter methylation of E-cadherin gene in gastric mucosa associated with Helicobacter pylori infection and in gastric cancer

TitlePromoter methylation of E-cadherin gene in gastric mucosa associated with Helicobacter pylori infection and in gastric cancer
Authors
Issue Date2003
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
Citation
Gut, 2003, v. 52 n. 4, p. 502-506 How to Cite?
AbstractBackground: E-cadherin is an adhesion molecule involved in tumour invasion/metastasis. Silencing of E-cadherin by promoter CpG methylation has been shown in both familial and sporadic gastric cancers. Helicobacter pylori is a class I carcinogen in gastric cancer. Aims: This study was undertaken to investigate the association between methylation of E-cadherin and H pylori in gastric mucosa from dyspeptic patients, and in intestinal metaplasia and primary and meta-static adenocarcinoma from surgical specimens of patients with gastric cancer. Methods: E-cadherin methylation was studied using methylation specific polymerase chain reaction in microdissected tissue from biopsies or surgical resection specimens. E-cadherin expression was studied by immunohistochemistry. Results: E-cadherin methylation was present in 31% (11/35) of gastric mucosae from dyspeptic patients, and was associated with H pylori infection (p=0.002), but was independent of the age of the patient or presence or absence of gastritis. E-cadherin methylation was present in 0% (0/8) of normal mucosa, 57% (12/21) of intestinal metaplasias, and 58% (15/26) of primary and 65% (21/32) of metastatic cancers. E-cadherin methylation status was concordant in 92% (11/12) of intestinal metaplasias and primary cancers, and in 85% (17/20) of primary and metastatic cancers from the same resected specimen. E-cadherin methylation in gastric cancer was associated with depth of tumour invasion (p=0.02) and regional nodal metastasis (p=0.05). Conclusion: E-cadherin methylation is an early event in gastric carcinogenesis, and is initiated by H pylori infection.
Persistent Identifierhttp://hdl.handle.net/10722/43098
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.authorLam, SKen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorYeung, YHen_HK
dc.contributor.authorHui, WMen_HK
dc.contributor.authorRashid, Aen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2007-03-23T04:38:48Z-
dc.date.available2007-03-23T04:38:48Z-
dc.date.issued2003en_HK
dc.identifier.citationGut, 2003, v. 52 n. 4, p. 502-506en_HK
dc.identifier.issn0017-5749en_HK
dc.identifier.urihttp://hdl.handle.net/10722/43098-
dc.description.abstractBackground: E-cadherin is an adhesion molecule involved in tumour invasion/metastasis. Silencing of E-cadherin by promoter CpG methylation has been shown in both familial and sporadic gastric cancers. Helicobacter pylori is a class I carcinogen in gastric cancer. Aims: This study was undertaken to investigate the association between methylation of E-cadherin and H pylori in gastric mucosa from dyspeptic patients, and in intestinal metaplasia and primary and meta-static adenocarcinoma from surgical specimens of patients with gastric cancer. Methods: E-cadherin methylation was studied using methylation specific polymerase chain reaction in microdissected tissue from biopsies or surgical resection specimens. E-cadherin expression was studied by immunohistochemistry. Results: E-cadherin methylation was present in 31% (11/35) of gastric mucosae from dyspeptic patients, and was associated with H pylori infection (p=0.002), but was independent of the age of the patient or presence or absence of gastritis. E-cadherin methylation was present in 0% (0/8) of normal mucosa, 57% (12/21) of intestinal metaplasias, and 58% (15/26) of primary and 65% (21/32) of metastatic cancers. E-cadherin methylation status was concordant in 92% (11/12) of intestinal metaplasias and primary cancers, and in 85% (17/20) of primary and metastatic cancers from the same resected specimen. E-cadherin methylation in gastric cancer was associated with depth of tumour invasion (p=0.02) and regional nodal metastasis (p=0.05). Conclusion: E-cadherin methylation is an early event in gastric carcinogenesis, and is initiated by H pylori infection.en_HK
dc.format.extent215201 bytes-
dc.format.extent28672 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
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.rightsGut. Copyright © B M J Publishing Group.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCadherins - genetics - metabolismen_HK
dc.subject.meshHelicobacter infections - complications - genetics - metabolismen_HK
dc.subject.meshHelicobacter pylorien_HK
dc.subject.meshPromoter regions (genetics) - geneticsen_HK
dc.subject.meshStomach neoplasms - genetics - metabolism - microbiologyen_HK
dc.titlePromoter methylation of E-cadherin gene in gastric mucosa associated with Helicobacter pylori infection and in gastric canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0017-5749&volume=52&issue=4&spage=502&epage=506&date=2003&atitle=Promoter+methylation+of+E-cadherin+gene+in+gastric+mucosa+associated+with+Helicobacter+pylori+infection+and+in+gastric+canceren_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1136/gut.52.4.502en_HK
dc.identifier.pmid12631658-
dc.identifier.pmcidPMC1773595-
dc.identifier.scopuseid_2-s2.0-0037537477en_HK
dc.identifier.hkuros77693-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037537477&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume52en_HK
dc.identifier.issue4en_HK
dc.identifier.spage502en_HK
dc.identifier.epage506en_HK
dc.identifier.isiWOS:000181828100010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridYeung, YH=7006608758en_HK
dc.identifier.scopusauthoridHui, WM=7103196477en_HK
dc.identifier.scopusauthoridRashid, A=7102299914en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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