Aml: Deacetylases

Margherita Ghisi; Ricky W Johnstone

doi:10.1007/978-1-4939-1393-0_21

Aml: Deacetylases

Margherita Ghisi, Ricky W Johnstone

Research output: Chapter in Book/Report/Conference proceeding › Chapter (Book) › Other › peer-review

1 Citation (Scopus)

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 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 language	English
Title of host publication	Targeted Therapy of Acute Myeloid Leukemi
Editors	Michael Andreeff
Place of Publication	New York NY USA
Publisher	Springer
Pages	411-439
Number of pages	29
ISBN (Electronic)	9781493913930
ISBN (Print)	9781493913923
DOIs	https://doi.org/10.1007/978-1-4939-1393-0_21
Publication status	Published - 1 Jan 2015
Externally published	Yes

Keywords

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

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10.1007/978-1-4939-1393-0_21

Cite this

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AB - 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.

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Aml: Deacetylases

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Keywords

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