Aml: Deacetylases

Abstract

Human malignancies, including acute myeloid leukemia (AML), are driven by genetic lesions that result in loss of function of tumor suppressor genes and/or activation of oncogenes. In addition to changes in the genome, we now understand that aberrations to the epigenome, either through mutation of genes encoding epigenetic regulators, or inappropriate recruitment of epigenetic enzymes to genetic loci by oncogenic fusion proteins commonly found in AML, can lead to neoplastic transformation. Alterations in the function, expression, or localization of histone acetyltransferases (HATS) and histone deacetylases (HDACs) have been shown to be important for the development of AML. Compounds that targ..