Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/16930
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dc.contributor.authorPapadopoulou, A.en
dc.contributor.authorTrangas, T.en
dc.contributor.authorTeixeira, M. R.en
dc.contributor.authorHeim, S.en
dc.contributor.authorDimitriadis, E.en
dc.contributor.authorTsarouha, H.en
dc.contributor.authorAndersen, J. A.en
dc.contributor.authorEvangelou, E.en
dc.contributor.authorIoannidis, P.en
dc.contributor.authorAgnantis, N. J.en
dc.contributor.authorPandis, N.en
dc.date.accessioned2015-11-24T18:34:24Z-
dc.date.available2015-11-24T18:34:24Z-
dc.identifier.issn1522-8002-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/16930-
dc.rightsDefault Licence-
dc.subjecttelomeraseen
dc.subjectgenetic alterationsen
dc.subjectbreast canceren
dc.subjectcghen
dc.subjectcytogeneticsen
dc.subjectcomparative genomic hybridizationen
dc.subjectcanceren
dc.subjectcellsen
dc.subjectexpressionen
dc.subjectassociationen
dc.subjecttumorsen
dc.subjectgrowthen
dc.subjectmiceen
dc.titleTelomerase activity and genetic alterations in primary breast carcinomasen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondary<Go to ISI>://000181739100009-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιώνel
heal.publicationDate2003-
heal.abstractIt has been proposed that the structural and numerical chromosome abnormalities recorded in breast cancer could be the result of telomere dysfunction and that telomerase is activated de novo to provide a survival mechanism curtailing further chromosomal aberrations. However, recent in vivo and in vitro data show that the ectopic expression of telomerase promotes tumorigenesis via a telomere length-independent mechanism. In this study, the relation between telomerase expression and the extent of chromosomal aberrations was investigated in 62 primary breast carcinomas. Telomerase activity was measured using a polymerase chain reaction-based telomeric repeat amplification protocol assay and 92% of the tumors were found to express telomerase with a relative activity ranging from 0 to 3839.6. Genetic alterations were determined by G-banding and comparative genomic hybridization analysis and 97% of the tumors exhibited chromosomal aberrations ranging from 0 to 44 (average: 10.98). In the overall series, the relationship between telomerase activity levels and genetic changes could be best described by a quadratic model, whereas in tumors with below-average genetic alteration numbers, a significant positive association was recorded between the two variables (coefficient=0.374, P=.017). The relationship between telomerase activity levels and the extent of genetic alteration may reflect the complex effect of telomerase activation upon tumor progression in breast carcinomas.en
heal.journalNameNeoplasiaen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
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