alexa IKZF2 Driving Self-Renewal and Inhibiting Myeloid Differentiation Through Chromatin Accessibility | OMICS International| Abstract
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Journal of Molecular and Genetic Medicine
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  • Short Communication   
  • J Mol Genet Med 2019, Vol 13(2): 419

IKZF2 Driving Self-Renewal and Inhibiting Myeloid Differentiation Through Chromatin Accessibility

Wu M1, Tan Z1, Ma M1, Tao S1, Zheng H1* and Liu X2*
1Department of Pathophysiology, Anhui Medical University, Hefei, Anhui, P.R. China
2Department of Pharmacology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
*Corresponding Author (s) : Dr. Zheng H, Department of Pathophysiology, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, 23032, P.R. China, Tel: 86-55165161129, Email: [email protected]
Dr. Liu X, Department of Pharmacology, Northwestern University, Chicago, IL 60611, USA, Tel: 86-55165161129, Email: [email protected]

Received Date: Mar 26, 2019 / Accepted Date: Apr 09, 2019 / Published Date: Apr 16, 2019

Abstract

Control of myeloid differentiation and leukemia stem cell (LSC) self-renewal involves genetic and epigenetic regulators and mechanisms. Genetic regulation in leukemia has been highlighted as a novel way for maintaining the LSC program. Translocations of histone methyltransferases, such as the mixed-lineage leukemia (MLL) genes including Hoxa9, Myc, and Ikzf2, give rise to one of the most aggressive subtypes of acute myeloid leukemia (AML). Uncontrolled expansion of immature myeloid cells coupled with leukemia stem cell self-renewal and a block in differentiation are some of the characteristic traits of AML.

Keywords: Leukemia; Genetic and epigenetic regulators; Cellular metabolism

Citation: Wu M, Tan Z, Ma M, Tao S, Liu X, et al. (2019) IKZF2 Driving Self-Renewal and Inhibiting Myeloid Differentiation Through Chromatin Accessibility. J Mol Genet Med 13:419.

Copyright: © 2019 Wu M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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