RESUMEN
Acute myeloid leukemia (AML) is considered to be an irreversible change of gene function caused by certain genetic changes, resulting in abnormal proliferation, differentiation disorder, and abnormal apoptosis of leukemia cells, leading to the occurrence and development of leukemia. Epigenetics refers to the change of heritable gene expression but the gene does not change in sequence. A large number of studies have shown that the pathogenesis of AML is closely related to the regulation of epigenetics. The regulation of epigenetic modification in the cellular metabolism, immune microenvironment and immune response of AML has been received increasing attention. This review will describe the regulation of epigenetics in the cellular metabolism, immune microenvironment and immune response of AML and the advances in the targeted intervention measures.
RESUMEN
Acute myeloid leukemia (AML) is a kind of genetic heterogeneous clonal hematopoietic stem cell disorder.Although there were improvements in the outcomes of selected younger patients and those with specific cytogenetic and molecular genetic characteristics,the overall survival for older patients remains dismal.In the last few years,next-generation sequencing technologies have identified recurrent mutations in genes encoding proteins involved in the epigenetic regulation of transcription in most patients with AML.This discovery has led to new insights into the role of the epigenome in AML and opens the possibility of epigenetically targeted therapies.This article will review the most important recurrent mutations in epigenetic regulatory genes and highlight the current and future treatment strategies that attempt to exploit epigenetic targets with the use of hypomethylating agents,which were reported on the 56th American Society of Hematology annual congress in 2014.