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Article: Promoter hypermethylation of tumor-related genes in gastric intestinal metaplasia of patients with and without gastric cancer

TitlePromoter hypermethylation of tumor-related genes in gastric intestinal metaplasia of patients with and without gastric cancer
Authors
Issue Date2002
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2002, v. 102 n. 6, p. 623-628 How to Cite?
AbstractPromoter hypermethylation is an alternative mechanism of gene silencing in human cancers including gastric cancer. While intestinal metaplasia (IM) is generally regarded as a precancerous lesion of the stomach, our study examines the presence of gene promoter hypermethylation in IM of patients with and without gastric cancer. We examined 31 samples of gastric cancer, 36 gastric IM (21 associated with gastric cancer and 15 from noncancer patients) and 10 normal gastric biopsies. Tissues containing foci of IM were carefully microdissected from paraffin-embedded section. Bisulfite-modifiedDNA was examined for gene promoter hypermethylation in DAP-kinase, E-cadherin, GSTP1, p14, p15, p16, RASSFIA and hMLH1 by methylation-specific-PCR. None of the control gastric tissues had hypermethylation detected, but gene promoter hypermethylation was frequently detected in gastric cancer and IM. The mean number of methylated genes in cancer and IM was 3.0 and 1.4, respectively (p < 0.0001). Methylation in IM from cancer patients was all associated with concurrent methylation in the corresponding tumor samples. The numbers of methylated genes were similar in IM obtained from cancer and noncancer patients. By examining the methylation patterns of these genes, 3 differential methylation patterns were recognized: hypermethylation was more frequent in cancer than in IM (DAP-kinase, p14, p15 and p16); comparable frequencies of methylation in cancer and IM (E-cadherin and hMLH1); and no methylation (GSTP1). Aberrant methylation in tumor-related genes is frequently detected in gastric IM of both cancer and noncancer patients, suggesting their early involvement in the multistep progression of gastric carcinogenesis. © 2002 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/162660
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTo, KFen_US
dc.contributor.authorLeung, WKen_US
dc.contributor.authorLee, TLen_US
dc.contributor.authorYu, Jen_US
dc.contributor.authorTong, JHMen_US
dc.contributor.authorChan, MWYen_US
dc.contributor.authorNg, EKWen_US
dc.contributor.authorChung, SCSen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:22:09Z-
dc.date.available2012-09-05T05:22:09Z-
dc.date.issued2002en_US
dc.identifier.citationInternational Journal Of Cancer, 2002, v. 102 n. 6, p. 623-628en_US
dc.identifier.issn0020-7136en_US
dc.identifier.urihttp://hdl.handle.net/10722/162660-
dc.description.abstractPromoter hypermethylation is an alternative mechanism of gene silencing in human cancers including gastric cancer. While intestinal metaplasia (IM) is generally regarded as a precancerous lesion of the stomach, our study examines the presence of gene promoter hypermethylation in IM of patients with and without gastric cancer. We examined 31 samples of gastric cancer, 36 gastric IM (21 associated with gastric cancer and 15 from noncancer patients) and 10 normal gastric biopsies. Tissues containing foci of IM were carefully microdissected from paraffin-embedded section. Bisulfite-modifiedDNA was examined for gene promoter hypermethylation in DAP-kinase, E-cadherin, GSTP1, p14, p15, p16, RASSFIA and hMLH1 by methylation-specific-PCR. None of the control gastric tissues had hypermethylation detected, but gene promoter hypermethylation was frequently detected in gastric cancer and IM. The mean number of methylated genes in cancer and IM was 3.0 and 1.4, respectively (p < 0.0001). Methylation in IM from cancer patients was all associated with concurrent methylation in the corresponding tumor samples. The numbers of methylated genes were similar in IM obtained from cancer and noncancer patients. By examining the methylation patterns of these genes, 3 differential methylation patterns were recognized: hypermethylation was more frequent in cancer than in IM (DAP-kinase, p14, p15 and p16); comparable frequencies of methylation in cancer and IM (E-cadherin and hMLH1); and no methylation (GSTP1). Aberrant methylation in tumor-related genes is frequently detected in gastric IM of both cancer and noncancer patients, suggesting their early involvement in the multistep progression of gastric carcinogenesis. © 2002 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_US
dc.relation.ispartofInternational Journal of Canceren_US
dc.subject.meshAgeden_US
dc.subject.meshApoptosis Regulatory Proteinsen_US
dc.subject.meshCadherins - Geneticsen_US
dc.subject.meshCalcium-Calmodulin-Dependent Protein Kinases - Geneticsen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshFemaleen_US
dc.subject.meshGastric Mucosa - Pathologyen_US
dc.subject.meshGlutathione S-Transferase Pien_US
dc.subject.meshGlutathione Transferase - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshIsoenzymes - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMetaplasiaen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshStomach Neoplasms - Genetics - Pathologyen_US
dc.titlePromoter hypermethylation of tumor-related genes in gastric intestinal metaplasia of patients with and without gastric canceren_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/ijc.10783en_US
dc.identifier.pmid12448005-
dc.identifier.scopuseid_2-s2.0-0037146740en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037146740&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume102en_US
dc.identifier.issue6en_US
dc.identifier.spage623en_US
dc.identifier.epage628en_US
dc.identifier.isiWOS:000179306200012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridLee, TL=35292432600en_US
dc.identifier.scopusauthoridYu, J=35351306800en_US
dc.identifier.scopusauthoridTong, JHM=7202724564en_US
dc.identifier.scopusauthoridChan, MWY=7402597788en_US
dc.identifier.scopusauthoridNg, EKW=7201647539en_US
dc.identifier.scopusauthoridChung, SCS=19642462800en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US

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