<i>CREBBP</i> Inactivation Promotes the Development of HDAC3-Dependent Lymphomas

2016266 citationsJournal Articlegreen Open Access

Authors

Yanwen Jiang · Cornell University

Ana Ortega-Molina · Memorial Sloan Kettering Cancer Center

Huimin Geng · University of California, San Francisco

Hsia-Yuan Ying · Cornell University

Katerina Hatzi · Memorial Sloan Kettering Cancer Center

Sara Parsa · Memorial Sloan Kettering Cancer Center

Dylan McNally

Abstract

Our findings establish the tumor suppressor function of CREBBP in GC lymphomas in which CREBBP mutations disable acetylation and result in unopposed deacetylation by BCL6/SMRT/HDAC3 complexes at enhancers of B-cell signaling and immune response genes. Hence, inhibition of HDAC3 can restore the enhancer histone acetylation and may serve as a targeted therapy for CREBBP-mutant lymphomas. Cancer Discov; 7(1); 38-53. ©2016 AACR.See related commentary by Höpken, p. 14This article is highlighted in the In This Issue feature, p. 1.

Topics & Keywords

Histone Deacetylase Inhibitors Research Protein Degradation and Inhibitors Ubiquitin and proteasome pathways

UN Sustainable Development Goals

Good health and well-being

Publication Details

Published in: Cancer Discovery

Volume 7, Issue 1, pp. 38-53

DOI: 10.1158/2159-8290.cd-16-0975

Field-Weighted Citation Impact: 13.25