Similarly, epigenetics plays an important role in leukaemogenesis and AML disease biology (Wouters & Delwel, 2016). Partly, aberrant DNA methylomes with resulting gene expression deregulation in AML can be explained by recurrent aberrations in epigenetic regulators, such as DNMT3A, ASXL1, TET2, KMT2A, IDH1 and IDH2 (Wouters & Delwel, 2016). However, even in the absence of said somatic aberrations, distinct classes, defined by their DNA methylome, are discernible and of prognostic relevance (Figueroa et al., 2010). Further research into the epigenome could lead to improved classification — especially in cases for which no leukaemia‐driving (cyto‐)genetic event can be identified. Epigenetic compounds (e.g. hypomethylating agents) are already an integral part of the therapeutic arsenal and AML diagnostics would be likely to benefit from inclusion of epigenetic analytics. However, there is, as of yet, no prospect of epigenetic analysis in the clinical routine.
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