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

Authors

  • U.E. Hoepken

Journal

  • Cancer Discovery

Citation

  • Canc Discov 7 (1): 14-16

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.


DOI

doi:10.1158/2159-8290.CD-16-1285