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Comment
. 2017 Jan;7(1):14-16.
doi: 10.1158/2159-8290.CD-16-1285.

Targeting HDAC3 in CREBBP-Mutant Lymphomas Counterstrikes Unopposed Enhancer Deacetylation of B-cell Signaling and Immune Response Genes

Uta E Höpken  1
Affiliations
Comment

Targeting HDAC3 in CREBBP-Mutant Lymphomas Counterstrikes Unopposed Enhancer Deacetylation of B-cell Signaling and Immune Response Genes

Uta E Höpken. Cancer Discov. 2017 Jan.

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.

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  • CREBBP Inactivation Promotes the Development of HDAC3-Dependent Lymphomas.
    Jiang Y, Ortega-Molina A, Geng H, Ying HY, Hatzi K, Parsa S, McNally D, Wang L, Doane AS, Agirre X, Teater M, Meydan C, Li Z, Poloway D, Wang S, Ennishi D, Scott DW, Stengel KR, Kranz JE, Holson E, Sharma S, Young JW, Chu CS, Roeder RG, Shaknovich R, Hiebert SW, Gascoyne RD, Tam W, Elemento O, Wendel HG, Melnick AM. Jiang Y, et al. Cancer Discov. 2017 Jan;7(1):38-53. doi: 10.1158/2159-8290.CD-16-0975. Epub 2016 Oct 12. Cancer Discov. 2017. PMID: 27733359 Free PMC article.

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