Fig. 1
From: Crosstalk between DNA methylation and hypoxia in acute myeloid leukaemia
Common mutations in epigenetic regulators and their influence on DNA methylation in AML. In wild-type cells (black; top, left), the equilibrium between methylated (5mC) and unmodified (C) cytosines is governed by balanced DNMT3A and TET2 activity. IDH1/2 activity produces α-KG (orange), which is required for TET function. Loss of function DNMT3A mutations (green; bottom, left) lead to impaired DNMT3A activity and hypomethylation (purple). Conversely, loss of function TET2 (pink; top, right) or IDH1/2 (blue; bottom right) mutations result in hypermethylation (red). Mutations in IDH1/2 lead to the production of the oncometabolite 2-HG, which acts as a competitive inhibitor for TET2, resulting in decreased TET2 activity and hypermethylation (blue; bottom, right)