title: Targeting HDAC3 in CREBBP-Mutant Lymphomas Counterstrikes Unopposed Enhancer Deacetylation of B-cell Signaling and Immune Response Genes.
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. Cancer Discov; 7(1); 14-6. ©2017 AACRSee related article by Jiang et al., p. 38.
authors.affiliation: Max Delbrück Center for Molecular Medicine, Berlin, Germany. uhoepken@mdc-berlin.de.
authors.forename: Uta E
authors.initials: UE
authors.lastname: Höpken
mesh_terms: D001402:B-Lymphocytes; D004268:DNA-Binding Proteins / Q000235:genetics; D018858:Germinal Center; D006801:Humans; D016393:Lymphoma, B-Cell / Q000235:genetics; D016403:Lymphoma, Large B-Cell, Diffuse / Q000235:genetics; D051560:Proto-Oncogene Proteins c-bcl-6 / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; D051560:Proto-Oncogene Proteins c-bcl-6