Vol 6, No 2 (2010)
Review paper
Published online: 2010-06-25
The molecular basis for treatment of gliomas
Onkol. Prak. Klin 2010;6(2):73-78.
Abstract
Gliomas are the most common of all primary tumours of the central nervous system and account for 70%
of them. Glioblastoma (GBM), the most frequent and the most lethal of all gliomas may develop de novo
(primary GBM) or by progression from grade II or anaplastic astrocytoma. Those two types of GBM are
distinct disease entities with clear differences in clinical outcome and molecular genetics. For example,
almost all secondary GBMs harbor mutations in IDH1 gene, whereas in primary GBMs these mutations are
very rarely seen. Primary GBMs form a very heterogenous group of tumours and are characterized by
many genetics alterations. One of such alteration is the expression of mutated EGFR gene. The most
common mutation is EGFR-vIII that constitutively activates the receptor. Advances in molecular biology of
gliomas may also help to select patients who better respond to conventional chemotherapy. Silencing of
MGMT gene by methylation of its promoter observed in 45% of GBMs is associated with better outcome of
patients treated with temozolomide. 1p/19q codeletion is a favourable prognostic factor in oligodendrogliomas
and also predicts response to PCV chemotherapy. However, so far in gliomas critical molecular
targets for novel drugs have not been recognized.
Onkol. Prak. Klin. 2010; 6, 2: 73-78
Onkol. Prak. Klin. 2010; 6, 2: 73-78
Keywords: gliomasmethylation of MGMT1p/19q codeletionIDH1 mutationsEGFR-vIII
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