In situ detection of telomeres by fluorescence in situ hybridization and telomerase activity in glioblastoma multiforme: Correlation with p53 status, EGFR, c-myc, MIB1, and Topoisomerase IIα protein expression

Adult Adolescent Brain Neoplasms Tartrate-Resistant Acid Phosphatase Acid Phosphatase Middle Aged DNA-Binding Proteins ErbB Receptors Isoenzymes Proto-Oncogene Proteins c-myc DNA Topoisomerases, Type II Ki-67 Antigen Antigens, Neoplasm Image Processing, Computer-Assisted Humans Child Glioblastoma Cell Division In Situ Hybridization, Fluorescence Polymorphism, Single-Stranded Conformational
DOI: 10.3892/ijo.23.6.1529 Publication Date: 2014-03-10T07:29:29Z
ABSTRACT
Aberrations of genes/proteins regulating cell cycle and growth, increased proliferation telomerase activity (TA) are documentable in glioblastoma multiforme. TA is more frequently detectable secondary glioblastoma, which also characterized by p53 mutation/overexpression. Discordant telomere (Te) length values have been reported glioblastomas with without TA. In 31 glioblastomas, pre-existing astrocytoma was not documented, we compared cases for the expression p53, EGFR, c-Myc, MIB-1 Topoisomerase IIalpha; mutations were investigated SSCP-PCR. Correlations made Te parameters [TePs: number (TeNo), area] as evaluated image analysis interphase nuclei fluorescence situ hybridization (FISH)-processed sections. We found no differences proteins TePs, except Te/nuclear area %, significantly lower TA+ (p=0.02). TePs were, instead, inversely correlated (p=0.0001). positively MIB1 staining index (p=0.033), showed a positive correlation between TeNo EGFR (p=0.042), trend towards negative (p=0.05). Tumors overexpressing had shorter lifetime seems to be tumor
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (0)
CITATIONS (0)