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

Official URL:https://doi.org/10.1158/2159-8290.CD-16-1285
PubMed:View item in PubMed
Creators Name:Hoepken, U.E.
Journal Title:Cancer Discovery
Journal Abbreviation:Cancer Discov
Volume:7
Number:1
Page Range:14-16
Date:January 2017
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.
ISSN:2159-8274
Publisher:American Association for Cancer Research (U.S.A.)
Item Type:Editorial

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