A study of loss of heterozygosity at 70 loci in anaplastic astrocytoma and glioblastoma multiforme with implications for tumor evolution

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dc.contributor.authorWooten, E. C.en
dc.contributor.authorFults, D.en
dc.contributor.authorDuggirala, R.en
dc.contributor.authorWilliams, K.en
dc.contributor.authorKyritsis, A. P.en
dc.contributor.authorBondy, M. L.en
dc.contributor.authorLevin, V. A.en
dc.contributor.authorO'Connell, P.en
dc.date.accessioned2015-11-24T19:38:59Z
dc.date.available2015-11-24T19:38:59Z
dc.identifier.issn1522-8517-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24202
dc.rightsDefault Licence-
dc.subjectAstrocytoma/*genetics/pathologyen
dc.subjectBrain Neoplasms/*genetics/pathologyen
dc.subjectCell Lineen
dc.subjectChromosome Mappingen
dc.subjectChromosomes, Human/genetics/ultrastructureen
dc.subjectDNA, Neoplasm/geneticsen
dc.subjectDisease Progressionen
dc.subjectGenetic Markersen
dc.subjectGlioblastoma/*genetics/pathologyen
dc.subjectHumansen
dc.subject*Loss of Heterozygosityen
dc.subjectPolymerase Chain Reactionen
dc.titleA study of loss of heterozygosity at 70 loci in anaplastic astrocytoma and glioblastoma multiforme with implications for tumor evolutionen
heal.abstractCancers that arise from astrocytes in the adult CNS present as either anaplastic astrocytomas (AAs) or as more aggressive glioblastomas multiforme (GBMs). GBMs either form de novo or progress from AAs. We proposed to examine the molecular genetic relationship between these CNS tumors by conducting a genome-wide allelic imbalance analysis that included 70 loci on examples of AA and GBM. We found significant loss of heterozygosity (LOH) at 13 discrete chromosomal loci in both AAs and GBMs. Loss was significant in both AAs and GBMs at 9 of these loci. AAs show the highest rates of LOH at chromosomes 1p, 4q, 6p, 9p, 11p, 11q, 13q, 14q, 15p, 17p, 17q, and 19q. GBMs showed the greatest losses at 1p, 6q, 8p, 9p, 10p, 10q, 11p, 13q, 17p, 17q, 18p, 18q, and 19q. GBMs also demonstrated significant amplification at the epidermal growth factor receptor locus (7p12). These data suggest that there are three classes of loci involved in glioma evolution. First are loci that are likely involved in early events in the evolution of both AAs and GBMs. The second class consists of AA-specific loci, typified by higher LOH frequency than observed in GBMs (4q, 6p, 17p, 17q, 19q). The third class consists of GBM-specific loci (6q, 8p, 10, 18q). Damage at these loci may either lead to de novo GBMs or permit existing AAs to progress to GBMs. Glioma-related LOH profiles may have prognostic implications that could lead to better diagnosis and treatment of brain cancer patients.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11550311-
heal.journalNameNeuro Oncolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate1999-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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