Fig. 1From: Emerging therapies for glioblastoma: current state and future directionsGenetic and epigenetic alterations in the genesis of gliomas. Shown are the relationships between the molecular lesions and pathobiology in the different types of gliomas. IDH, socitrate dehydrogenase; RELA, transcription factor p65; CDKN, cyclin-dependent kinase inhibitor; YAP1, YES-associated protein 1; PF, posterior fossa; NF2, neurofibromin 2; SEGA, subependymal giant cell astrocytoma; TSC, tuberous sclerosis; RTK, receptor tyrosine kinase; PDGFRA, platelet-derived growth factor receptor-α; TERT, telomerase reverse transcriptase; PTEN, phosphatase and tensin homologue; EGFR, epidermal growth factor receptor; H3F3A, histone H3.3; HIST1H3B, histone H3.1; ACVR1, activin A receptor 1; ATRX, α-thalassemia/mental retardation syndrome X-linked; TP53, tumour protein p53; PPM1D, protein phosphatase 1D; MGMT, O-6-methylguanine-DNA methyltransferase; g-CIMP, glioma CpG island methylator phenotype; Chr., chromosome; CIC, Drosophila homologue of capicua; Those IDH-mutant glioblastomas derived by progression from pre-existing lower grade astrocytomas (blue arrow) are tend to manifest in younger patients (≤50 years of age) compared with IDH wild-type tumorsBack to article page