Abstract
Acute myeloid leukemia (AML) is a heterogeneous clonal disorder, characterized by malignant proliferation of immature abnormal myeloid precursors. Both cytogenetic and molecular genetic mutations are recognized to have an impact on prognosis of AML. Recently, several recurrent mutations in epigenetic machinery have been linked to abnormal gene expression as a leading cause in initiation and progression of AML. These alterations include key proteins involved in DNA methylation, posttranslational histone modification, chromatin remodeling, and microRNAs. Unlike genetic events, epigenetic effects may be targeted and reversed pharmacologically, resulting in the potential change of a specific epigenetic state. The promising results of combination clinical trials with DNA methylation inhibitors and histone deacetylase inhibitors have highlighted their potential use in AML therapy. However, the precise function of the epigenetic framework in AML pathogenesis and the molecular mechanisms underlying the efficacy of epigenetic compounds have not yet been fully elucidated. Here, we illustrate the key players in epigenetic networks, and their aberrant role in AML. In addition, we examine epigenetic therapies currently under investigation that have shown promise in treating AML.
Published Version
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