Incidence of the main genetic markers in glioblastoma multiforme is independent of tumor topology
Jazyk angličtina Země Slovensko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
17447852
Knihovny.cz E-zdroje
- MeSH
- amplifikace genu MeSH
- chromozomální aberace MeSH
- dospělí MeSH
- erbB receptory genetika MeSH
- genetické markery genetika MeSH
- genová dávka MeSH
- glioblastom genetika patologie MeSH
- hybridizace in situ fluorescenční MeSH
- hybridizace nukleových kyselin MeSH
- incidence MeSH
- karyotypizace MeSH
- lidé středního věku MeSH
- lidé MeSH
- lidské chromozomy, pár 10 genetika MeSH
- mapování chromozomů MeSH
- nádorové biomarkery genetika MeSH
- nádorový supresorový protein p53 genetika MeSH
- nádory mozku genetika patologie MeSH
- polymerázová řetězová reakce MeSH
- prognóza MeSH
- senioři MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- erbB receptory MeSH
- genetické markery MeSH
- nádorové biomarkery MeSH
- nádorový supresorový protein p53 MeSH
Glioblastoma multiforme (GBM) is the most common as well as the most aggressive type of primary brain tumor of astrocytic origin in adults. GBM is characterized by a high degree of intratumoral heterogeneity both in histomorphology and genetic changes. Trisomy/polysomy of chromosome 7, monosomy of chromosome 10, EGFR gene amplification and p53 deletion have been described as the typical genetic markers for tumor classification and prediction of possible response to therapy. Our work was based on detection of these four main genetic changes both in central and peripheral parts of the tumors to evaluate possible differences in the topological incidence of these genetic markers. Chromosomal abnormalities in tumor samples from a group of 21 patients surgically treated for GBM were characterized by means of the interphase-fluorescence in situ hybridization (I-FISH) technique using sets of centromere and locus-specific DNA probes. In addition, we performed a detailed analysis of one selected tumor sample using a genomic microarray system (GenoSensor Array 300) to characterize copy number changes of specific sequences and refine results obtained by I-FISH. However, the data show no significant differences in occurrence of the described genetic markers in either part of the tumor.
Low-level copy number changes of MYC genes have a prognostic impact in medulloblastoma