Incidence of the main genetic markers in glioblastoma multiforme is independent of tumor topology
Language English Country Slovakia Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
17447852
Knihovny.cz E-resources
- MeSH
- Gene Amplification MeSH
- Chromosome Aberrations MeSH
- Adult MeSH
- ErbB Receptors genetics MeSH
- Genetic Markers genetics MeSH
- Gene Dosage MeSH
- Glioblastoma genetics pathology MeSH
- In Situ Hybridization, Fluorescence MeSH
- Nucleic Acid Hybridization MeSH
- Incidence MeSH
- Karyotyping MeSH
- Middle Aged MeSH
- Humans MeSH
- Chromosomes, Human, Pair 10 genetics MeSH
- Chromosome Mapping MeSH
- Biomarkers, Tumor genetics MeSH
- Tumor Suppressor Protein p53 genetics MeSH
- Brain Neoplasms genetics pathology MeSH
- Polymerase Chain Reaction MeSH
- Prognosis MeSH
- Aged MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- ErbB Receptors MeSH
- Genetic Markers MeSH
- Biomarkers, Tumor MeSH
- Tumor Suppressor 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