Promoter methylation status of hMLH1, MGMT, and CDKN2A/p16 in colorectal adenomas

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dc.contributor.authorPsofaki, V.en
dc.contributor.authorKalogera, C.en
dc.contributor.authorTzambouras, N.en
dc.contributor.authorStephanou, D.en
dc.contributor.authorTsianos, E.en
dc.contributor.authorSeferiadis, K.en
dc.contributor.authorKolios, G.en
dc.date.accessioned2015-11-24T18:56:05Z
dc.date.available2015-11-24T18:56:05Z
dc.identifier.issn1007-9327-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18981
dc.rightsDefault Licence-
dc.subjectAdaptor Proteins, Signal Transducing/*geneticsen
dc.subjectAdenoma/*genetics/physiopathologyen
dc.subjectAgeden
dc.subjectColorectal Neoplasms/*genetics/physiopathologyen
dc.subjectCpG Islands/geneticsen
dc.subjectCyclin-Dependent Kinase Inhibitor p16/*geneticsen
dc.subjectDNA Methylation/*physiologyen
dc.subjectDNA Modification Methylases/*geneticsen
dc.subjectDNA Repair Enzymes/*geneticsen
dc.subjectDisease Progressionen
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectMicrosatellite Repeats/geneticsen
dc.subjectMiddle Ageden
dc.subjectNuclear Proteins/*geneticsen
dc.subjectPromoter Regions, Genetic/*geneticsen
dc.subjectTumor Suppressor Proteins/*geneticsen
dc.titlePromoter methylation status of hMLH1, MGMT, and CDKN2A/p16 in colorectal adenomasen
heal.abstractAIM: To investigate aberrant DNA methylation of CpG islands and subsequent low- or high-level DNA microsatellite instability (MSI) which is assumed to drive colon carcinogenesis. METHODS: DNA of healthy individuals, adenoma (tubular or villous/tubulovillous) patients, and colorectal carcinoma patients who underwent colonoscopy was used for assessing the prevalence of aberrant DNA methylation of human DNA mismatch repair gene mutator L homologue 1 (hMLH1), Cyclin-dependent kinase inhibitor 2A (CDKN2A/p16), and O-6-methylguanine DNA methyltransferase (MGMT), as well as their relation to MSI. RESULTS: The frequency of promoter methylation for each locus increased in the sequence healthy tissue/adenoma/carcinoma. MGMT showed the highest frequency in each group. MGMT and CDKN2A/p16 presented a statistically significant increase in promoter methylation between the less and more tumorigenic forms of colorectal adenomas (tubular vs tubullovillous and villous adenomas). All patients with tubulovillous/villous adenomas, as well as all colorectal cancer patients, showed promoter methylation in at least one of the examined loci. These findings suggest a potentially crucial role for methylation in the polyp/adenoma to cancer progression in colorectal carcinogenesis. MSI and methylation seem to be interdependent, as simultaneous hMLH1, CDKN2A/p16, and MGMT promoter methylation was present in 8/9 colorectal cancer patients showing the MSI phenotype. CONCLUSION: Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/20653064-
heal.journalNameWorld J Gastroenterolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2010-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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