Source:http://linkedlifedata.com/resource/pubmed/id/17447852
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2007-4-23
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| pubmed:abstractText |
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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Genetic Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Markers, Biological,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53
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| pubmed:status |
MEDLINE
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| pubmed:issn |
0028-2685
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
54
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
212-8
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:17447852-Adult,
pubmed-meshheading:17447852-Aged,
pubmed-meshheading:17447852-Brain Neoplasms,
pubmed-meshheading:17447852-Chromosome Aberrations,
pubmed-meshheading:17447852-Chromosome Mapping,
pubmed-meshheading:17447852-Chromosomes, Human, Pair 10,
pubmed-meshheading:17447852-Female,
pubmed-meshheading:17447852-Gene Amplification,
pubmed-meshheading:17447852-Gene Dosage,
pubmed-meshheading:17447852-Genetic Markers,
pubmed-meshheading:17447852-Glioblastoma,
pubmed-meshheading:17447852-Humans,
pubmed-meshheading:17447852-In Situ Hybridization, Fluorescence,
pubmed-meshheading:17447852-Incidence,
pubmed-meshheading:17447852-Karyotyping,
pubmed-meshheading:17447852-Male,
pubmed-meshheading:17447852-Middle Aged,
pubmed-meshheading:17447852-Nucleic Acid Hybridization,
pubmed-meshheading:17447852-Polymerase Chain Reaction,
pubmed-meshheading:17447852-Prognosis,
pubmed-meshheading:17447852-Receptor, Epidermal Growth Factor,
pubmed-meshheading:17447852-Tumor Markers, Biological,
pubmed-meshheading:17447852-Tumor Suppressor Protein p53
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| pubmed:year |
2007
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| pubmed:articleTitle |
Incidence of the main genetic markers in glioblastoma multiforme is independent of tumor topology.
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| pubmed:affiliation |
Department of Biology, Masaryk University, Bruno, Czech Republic.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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