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 CitationMeyer, Sara E., "From EMT to HSC to AML: ZEB2 is a cell fate switch." (2017). Department of Cancer Biology Faculty Papers. Paper 112.