Abstract
Recent progress in the molecular genetics of acute myeloid leukemia (AML) has shown this disease to be more heterogeneous than previously realized. Recurrent cytogenetic and mutational changes in leukemic blasts have been confirmed to have high prognostic significance. High-throughput techniques to analyze the AML genome in greater depth have revealed novel mutations with putative roles in leukemogenesis. The use of prognostic biomarkers has allowed for a more detailed categorization of AML based on risk. Despite this tremendous progress, the understanding of the mechanisms by which these changes influence leukemia growth and response to treatment is still limited, which in turn has hindered the development of rationally targeted therapies for AML. The integration of clinical, cytogenetic and molecular data will be essential to translate the current research momentum into better outcomes for patients with AML.
Financial & competing interests disclosure
CA Schiffer has received research funding from Ambit, Ariad, Celgene, Novartis, Pfizer, BMS and Micromet. He has also served as a consultant for Ambit, Ariad, Celgene, Eisai, Micromet, BMS and Pfizer. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.