Targeting HDAC3 in CREBBP-mutant lymphomas counterstrikes unopposed enhancer deacetylation of B-cell signaling and immune response genes

Item Type:	Editorial
Title:	Targeting HDAC3 in CREBBP-mutant lymphomas counterstrikes unopposed enhancer deacetylation of B-cell signaling and immune response genes
Creators Name:	Höpken, U.E.
Abstract:	The cellular phenotype of B-cell lymphomas arising from B cells undergoing germinal center reactions, such as follicular lymphoma and diffuse large B-cell lymphoma, is strongly shaped by mutations in chromatin-modifying genes. The work presented by Jiang and colleagues addresses how somatic mutations in CREBBP disable acetylation and cause unopposed deacetylation by BCL6/SMRT/HDAC3 complexes on enhancers of B-cell signaling and immune response genes. This opens a therapeutic avenue toward targeted inhibition of CREBBP-mutant lymphomas by HDAC inhibitors.
Keywords:	B-Cell Lymphoma, B-Lymphocytes, Diffuse Large B-Cell Lymphoma, DNA-Binding Proteins, Germinal Center, Proto-Oncogene Proteins C-bcl-6
Source:	Cancer Discovery
ISSN:	2159-8274
Publisher:	American Association for Cancer Research
Volume:	7
Number:	1
Page Range:	14-16
Date:	January 2017
Official Publication:	https://doi.org/10.1158/2159-8290.CD-16-1285
PubMed:	View item in PubMed

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