Harnessing the potential of epigenetic therapies for childhood acute myeloid leukemia

Acute myeloid leukemia (AML) results from clonal expansion of primitive myeloid cells that are incapable of differentiation. These clones have acquired genetic and epigenetic alterations that cause uncontrolled proliferation at the expense of normal hematopoiesis, leading to bone marrow exhaustion. The recent identification and characterization of many of these alterations [1] create the opportunity for the development of targeted treatments. Cancer genome consortiums have identified genes commonly mutated in AML, many of which are associated with epigenetic regulation [2 –5], indicating that chromatin modifiers play key roles in malignant transformation and exposing novel epigenetic targets for cancer drug discovery.

Source: Experimental Hematology - March 30, 2018 Category: Hematology Authors: Ashley A. Newcombe, Brenda E.S. Gibson, Karen Keeshan Tags: Review Source Type: research