Publication details

Studium polyzomie chromozomu 7, monozomie chromozomu 10, amplifikace genu EGFR a delece genu p53 u multiformního glioblastomu pomocí metody fluorescenční in situ hybridizace (FISH)

Title in English Study of polysomy of chromosome 7, monosomy of chromosome 10, EGFR amplification and p53 deletion in glioblastoma multiforme using fluorescent in situ hybridization
Authors

NEČESALOVÁ Eva KUGLÍK Petr CEJPEK Pavel VESELSKÁ Renata VRANOVÁ Vladimíra PEŠÁKOVÁ Martina RELICHOVÁ Jiřina

Year of publication 2006
Type Article in Periodical
Magazine / Source Klinická onkologie
MU Faculty or unit

Faculty of Science

Citation
Field Genetics and molecular biology
Keywords Glioblastoma multiforme; chromosomal abnormalities; fluorescence in situ hybridization; polysomy of chromosome 7; monosomy of chromosome 10; gene EGFR amplification; gene p53 deletion
Description Backgrounds. Glioblastoma multiforme (GBM, astrocytoma grade IV) is the most common adult primary brain tumor with high genetic and histomorphological variability. Cytogenetic diagnostic methods form an integral part of glioblastoma diagnostics recently. Different types of glioblastomas are associated with distinct chromosomal aberrations that may provide useful information with respect to tumor classification, prediction prognosis and response to therapy. Methods and results. In this study, we present the molecular cytogenetic results of tumor specimens from 27 patients with glioblastoma multiforme diagnosis. We investigated chromosomal abnormalities in touch preparations from central and periphery parts of the tumor by interphase-fluorescence in situ hybridization (I-FISH). This metod was used to detect the incidence of the most frequent genetic abnormalities as the polysomy of chromosome 7, monosomy of chromosome 10, the EGFR gene amplification, and p53 deletion. The results of I-FISH analyses showed monosomy 10 in 100 % of cases, polysomy 7 (3–5 copy of chromosome 7) in 93 % of cases, EGFR gene amplification was present in 26 % of tumors and p53 gene deletion in 22 % of cases. Conclusions. Our results confirm high frequency of cytogenetic abnormalities involved in pathogenetic process of GBM which can be used as specific diagnostic and predictive markers.
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