Fig. 1

Genetic 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 tumors