Table 1.

Subclassification in glioblastoma.

Classical	Mutated in EGFR with high expression. Lacks P53 mutation. CDKN2A deleted which causes inactivation of the RB pathway. Amplification of chromosome 7 and deletion of chromosome 10. Classical O-6-methylguanine-DNA methyltransferase (MGMT)-methylated tumours respond significantly better to aggressive treatment as compared with non-MGMT-methylated classical tumours. Astrocytic-like.
Mesenchymal	Mutated in NF which activates the PI3K/Akt pathway. Mutated in PTEN which activates the RAS pathway. Expression of YKL-40 and MET which can cause epithelial-to-mesenchymal transition. Inflammatory and necrotic. MGMT-methylated mesenchymal tumours seem to respond better to aggressive treatment than non-MGMT-methylated tumours, but this is not significant. Astrocytic-like.
Proneural	Mutated in PDGFRA which activates the PI3K pathway and the RAS pathway. Mutated in P53, IDH and PDGFRA. If PDGFRA is mutated, then IDH will not be mutated and opposite. No difference in response to aggressive treatment when stratified for MGMT status. Often secondary glioblastoma. Oligodendrocytic-like.

Modified and simplified from Verhaak et al,5 Cancer Genome Atlas Research Network,9 Murat et al,32