There is increasing awareness that AML is a widely heterogeneous disease, not only based on clinical characteristics and demographics of the patients we treat but also based on the genomics of the disease. Wider accessibility to next-generation DNA sequencing in AML has identified recurrent genetic abnormalities that drive disease biology, define overall prognosis, and predict for response to newly developed target-specific therapies. This knowledge has allowed the field to move away from a "one-size-fits-all" approach in newly diagnosed AML, to a more thoughtful, individualized approachy based on these factors. The first steps in realizing this new approach involve developing systems to efficiently obtain and analyze patient- and disease-related factors prior to starting therapy and having available clinical trials to address each subtype.
Keywords: Acute myeloid leukemia; FLT3; IDH1; IDH2; Secondary AML; TP53.