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Article: Concurrent hypermethylation of multiple tumor-related genes in gastric carcinoma and adjacent normal tissues

TitleConcurrent hypermethylation of multiple tumor-related genes in gastric carcinoma and adjacent normal tissues
Authors
Issue Date2001
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 2001, v. 91 n. 12, p. 2294-2301 How to Cite?
AbstractBACKGROUND. Transcriptional silencing by CpG-island hypermethylation now is believed to be an important mechanism of tumorigenesis. To date, studies on CpG-island hypermethylation in gastric carcinoma and adjacent normal tissues are few. METHODS. The authors examined 5 gastric carcinoma cell lines, 26 frozen gastric carcinoma tissues and their adjacent nontumor area for concurrent CpG-island hypermethylation in 6 tumor-related genes (p15, p16, E-cadherin, GST-pi, hMLH1, and VHL) by methylation-specific polymerase chain reaction. Nontumorous gastric tissues from 10 gastritis patients were used as controls. RESULTS. Hypermethylation was not detected in any tissue taken from gastritis patients but was identified in all 5 cell lines and in 24 (92.3%) gastric carcinoma patients. CpG-island methylation in tumor-related genes also was detected in 7 out of the 25 adjacent normal tissues from cancer patients. Hypermethylation of E-cadherin, p15, and p16 were detected more frequently than GST-pi and hMLH1, whereas aberrant methylation of VHL was not detected. Concurrent hypermethylation in 2 or more tumor-related genes was detected in 3 out of the 5 gastric carcinoma cell lines, 22 (84.6%) tumor samples, and 5 (20%) adjacent gastric tissues. Eighteen (69.2%) tumor samples showed hypermethylation in ≥ 3 genes. CONCLUSIONS. The current study showed that concurrent hypermethylation of multiple tumor-related genes is detected frequently in gastric carcinoma and adjacent normal tissues. Study findings suggested that a mechanism that leads to dysregulation in CpG-island methylation is likely to be involved in the early gastric carcinogenesis process. © 2001 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/162554
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorYu, Jen_US
dc.contributor.authorNg, EKWen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorMa, PKen_US
dc.contributor.authorLee, TLen_US
dc.contributor.authorGo, MYYen_US
dc.contributor.authorChung, Sen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:21:06Z-
dc.date.available2012-09-05T05:21:06Z-
dc.date.issued2001en_US
dc.identifier.citationCancer, 2001, v. 91 n. 12, p. 2294-2301en_US
dc.identifier.issn0008-543Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/162554-
dc.description.abstractBACKGROUND. Transcriptional silencing by CpG-island hypermethylation now is believed to be an important mechanism of tumorigenesis. To date, studies on CpG-island hypermethylation in gastric carcinoma and adjacent normal tissues are few. METHODS. The authors examined 5 gastric carcinoma cell lines, 26 frozen gastric carcinoma tissues and their adjacent nontumor area for concurrent CpG-island hypermethylation in 6 tumor-related genes (p15, p16, E-cadherin, GST-pi, hMLH1, and VHL) by methylation-specific polymerase chain reaction. Nontumorous gastric tissues from 10 gastritis patients were used as controls. RESULTS. Hypermethylation was not detected in any tissue taken from gastritis patients but was identified in all 5 cell lines and in 24 (92.3%) gastric carcinoma patients. CpG-island methylation in tumor-related genes also was detected in 7 out of the 25 adjacent normal tissues from cancer patients. Hypermethylation of E-cadherin, p15, and p16 were detected more frequently than GST-pi and hMLH1, whereas aberrant methylation of VHL was not detected. Concurrent hypermethylation in 2 or more tumor-related genes was detected in 3 out of the 5 gastric carcinoma cell lines, 22 (84.6%) tumor samples, and 5 (20%) adjacent gastric tissues. Eighteen (69.2%) tumor samples showed hypermethylation in ≥ 3 genes. CONCLUSIONS. The current study showed that concurrent hypermethylation of multiple tumor-related genes is detected frequently in gastric carcinoma and adjacent normal tissues. Study findings suggested that a mechanism that leads to dysregulation in CpG-island methylation is likely to be involved in the early gastric carcinogenesis process. © 2001 American Cancer Society.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_US
dc.relation.ispartofCanceren_US
dc.subject.meshAdaptor Proteins, Signal Transducingen_US
dc.subject.meshCadherins - Geneticsen_US
dc.subject.meshCarcinoma - Geneticsen_US
dc.subject.meshCarrier Proteinsen_US
dc.subject.meshCell Cycle Proteinsen_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P15en_US
dc.subject.meshGenes, P16 - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMethylationen_US
dc.subject.meshNeoplasm Proteins - Geneticsen_US
dc.subject.meshNuclear Proteinsen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshStomach Neoplasms - Geneticsen_US
dc.subject.meshTranscription Factors - Geneticsen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshTumor Suppressor Proteinsen_US
dc.titleConcurrent hypermethylation of multiple tumor-related genes in gastric carcinoma and adjacent normal tissuesen_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.doi10.1002/1097-0142(20010615)91:12<2294::AID-CNCR1261>3.0.CO;2-Gen_US
dc.identifier.pmid11413518-
dc.identifier.scopuseid_2-s2.0-0035876138en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035876138&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume91en_US
dc.identifier.issue12en_US
dc.identifier.spage2294en_US
dc.identifier.epage2301en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridYu, J=35351306800en_US
dc.identifier.scopusauthoridNg, EKW=7201647539en_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridMa, PK=18836911500en_US
dc.identifier.scopusauthoridLee, TL=35292432600en_US
dc.identifier.scopusauthoridGo, MYY=7101882939en_US
dc.identifier.scopusauthoridChung, S=19642462800en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US

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