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
AUTHORS (14)
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
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