Aml: Deacetylases

Margherita Ghisi, Ricky W Johnstone

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Otherpeer-review

1 Citation (Scopus)


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 target these epigenetic regulators have now been developed and therefore offer a new therapeutic option for patients with AML driven by alterations to the epigenome.

Original languageEnglish
Title of host publicationTargeted Therapy of Acute Myeloid Leukemi
EditorsMichael Andreeff
Place of PublicationNew York NY USA
Number of pages29
ISBN (Electronic)9781493913930
ISBN (Print)9781493913923
Publication statusPublished - 1 Jan 2015
Externally publishedYes


  • Acute myeloid leukemia
  • Deacetylases
  • Epigenetic regulators
  • Epigenetic therapy
  • Epigenetics
  • HDAC inhibitors
  • Histone-modifying enzymes

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