The aim of the present study was to investigate the relative expression of hTERT (relhTERT) and its transcripts A+B+ (contained in the full-length product), Adel and Bdel in astrocytic gliomas (grades I-IV, n=38). relhTERT was assessed by duplex reverse transcription-PCR and the expression profile of Adel, Bdel and A+B+ transcripts by nested real time-PCR. relhTERT and A+B+ presence correlated well with each other ( P<0.001) and with histological grading [grades I-II (low) vs III-IV (high), P(relhTERT)=0.002 and P(A+B+)<0.001].
Using a miRNA array, miR-519d and miR-4758 were found to be upregulated in gangliogliomas (n=26) compared to control cortex (n=17), peritumoural tissue (n=7), dysembryoplastic neuroepithelial tumours (n=9) and astrocytomas (grade I-IV; subependymal giant cell astrocytomas, n=10; pilocytic astrocytoma, n=15; diffuse astrocytoma grade II, n=10; grade III, n=14 and glioblastoma n=15).
Quantitative real time PCR (qRT-PCR) of 148 astrocytomas samples (grades I-IV) showed that SAA1 mRNA was significantly higher in GBM when compared to AGI-III and NN samples (p < 0.0001).
Specimens of astrocytoma World Health Organisation (WHO) grade I-IV in 14 patients and control brain tissue obtained from three normal persons were studied.
We have analysed 57 paediatric astrocytoma (WHO grades I-IV) using comparative genomic hybridisation in order to identify common regions of abnormality.
The aim of the study was to assess the localization of Polysialic acid (polySia) and Neural cell adhesion molecule (NCAM) in grade I-IVastrocytomas by confocal microscopy, and also to clarify and compare their relationship to conventional clinicopathological features in these tumors.
Glioma is one of the most prevalent types of primary intracranial carcinoma with varying malignancy grades I-IV and histological subtypes, including astrocytomas, glioblastoma multiform (GBM), oligodendrogliomas and mixed tumors.
Tissues from 44 astrocytomas corresponding to Grades I-IV of the World Health Organization (WHO) classification were analyzed for the presence of mutations in exons 5, 7, and 8 of the p53 gene using single strand conformation polymorphism (SSCP) and sequence analysis of DNA amplified by the polymerase chain reaction.