The lack of histopathological separation has made it difficult to estimate the relative frequency at which both subsets of GB occur 6. However, histopathologically, primary and secondary GBs are indistinguishable with the presence of poorly differentiated, pleomorphic astrocytic tumour cells with marked nuclear atypia, brisk mitotic activity, prominent microvascular proliferation and/or necrosis 1. The secondary GBs developed in astrocytomas must be distinguished from primary GBs because these are probably responsible for most of the GBs of long clinical duration 1. Primary and secondary GBs constitute relatively distinct disease entities that evolve primarily through different genetic pathways and show different expression profiles 3 and are likely to differ in response to therapy but share a high frequency of LOH 10q, which is likely to be associated with the overall GB phenotype 3, 4, 5. Primary GB constitutes around 90 per cent of cases, whereas secondary GB constitutes 10 per cent of cases 1. p53 mutations occur in >65 per cent of secondary GBs 1. In contrast, secondary GB develops slowly in younger patients with a median age of 45 yr and arises from pre-existing low-grade astrocytoma. EGFR amplification occurs in 40 per cent of primary GBs 1. Primary GB occurs de novo in older patients with a median age of 62 yr, without recognizable precursor lesion. Among all these markers, p53 and EGFR were the most widely studied genes in the literature 2. The most common genetic alterations in GB include loss of heterozygosity on chromosome 10 (LOH 10), mutations in p53, amplification and rearrangements of epidermal growth factor receptor ( EGFR) gene, murine double minute 2 ( MDM2) amplification, phosphatase and tensin ( PTEN) homology mutations, tumour suppressor genes p16 INK4a/p14 ARF loss and retinoblastoma gene mutations 1. It manifests at any age, preferentially with peak incidence between 45 and 75 yr of age 1. Glioblastoma (GB) is the most frequent brain tumour, accounting for approximately 12-15 per cent of all intracranial neoplasms and 65-75 per cent of astrocytic tumours.
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