LAUSR

Although tumourigenesis occurs due to genetic mutations, the role of epigenetic dysregulations in cancer is also well established. Epigenetic dysregulations in cancer may occur as a result of mutations in genes encoding histone/DNA-modifying enzymes and chromatin remodellers or mutations in histone protein itself. It is also true that misregulated gene expression without genetic mutations in these factors could also support tumour initiation and progression. Interestingly, metabolic rewiring has emerged as a hallmark of cancer due to gene mutations in specific metabolic enzymes or dietary/environmental factors. Recent studies report an intricate cross-talk between epigenetic and metabolic reprogramming in cancer. This review discusses the role of epigenetic and metabolic dysregulations and their cross-talk in tumourigenesis with a special focus on gliomagenesis. We also discuss the role of recently developed human embryonic stem cells/induced pluripotent stem cells-derived organoid models of gliomas and how these models are proving instrumental in uncovering human-specific cellular and molecular complexities of gliomagenesis.