title: Epigenetics in acute myeloid leukemia.
abstract: Acute myeloid leukemia (AML) is a disease characterized by uncontrolled proliferation of clonal neoplastic hematopoietic precursor cells. This leads to the disruption of normal hematopoiesis and bone marrow failure. Major breakthroughs in the past have contributed to our understanding of the genetic failures and the changed biology in AML cells that underlie the initiation and progression of the disease. It is now recognized that not only genetic but also epigenetic alterations are similarly important in this process. Since these alterations do not change the DNA sequences and are pharmacologically reversible, they have been regarded as optimal targets for what is now known as epigenetic therapy. In this review, we will discuss our current understanding of normal epigenetic processes, outline our knowledge of epigenetic alterations in AML, and discuss how this information is being used to improve current therapy of this disease.
authors.affiliation: German Cancer Research Center, Division of Toxicology and Cancer Risk Factors, Heidelberg, Germany. c.plass@dkfz.de <c.plass@dkfz.de>
authors.forename: Christoph
authors.initials: C
authors.lastname: Plass
authors.forename: Christopher
authors.initials: C
authors.lastname: Oakes
authors.forename: William
authors.initials: W
authors.lastname: Blum
authors.forename: Guido
authors.initials: G
authors.lastname: Marcucci
mesh_terms: D042002:Chromatin Assembly and Disassembly; D002844:Chromatium / Q000502:physiology; D019175:DNA Methylation; D044127:Epigenesis, Genetic; D020868:Gene Silencing; D056572:Histone Deacetylase Inhibitors; D006657:Histones / Q000502:physiology; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000628:therapy; D022661:RNA, Untranslated / Q000502:physiology
chemical_list: D056572:Histone Deacetylase Inhibitors; D006657:Histones; D022661:RNA, Untranslated