Title

From EMT to HSC to AML: ZEB2 is a cell fate switch.

Authors

Sara E. Meyer, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

1-26-2017

Comments

This article has not been peer reviewed. It is the authors' manuscript version prior to publication in Blood.

Volume 129, Issue 4, January 2017, Pages 400-401.

The published version is available at DOI: 10.1182/blood-2016-11-748186. Copyright © American Society of Hematology

Abstract

In this issue of Blood, complimentary studies by J. Li et al¹ and H. Li et al² identify the transcription factor ZEB2 as a critical regulator of multilineage differentiation in both normal and malignant hematopoiesis. In particular, these studies show that ZEB2 is an inhibitor of normal granulocyte production, and in acute myeloid leukemia (AML), antagonizing ZEB2 function releases the granulocytic differentiation block, creating an antileukemic therapeutic effect.

Recommended Citation

Meyer, Sara E., "From EMT to HSC to AML: ZEB2 is a cell fate switch." (2017). Department of Cancer Biology Faculty Papers. Paper 112.
https://jdc.jefferson.edu/cbfp/112

PubMed ID

28126955