CREBBP inactivation promotes the development of HDAC3-dependent lymphomas Academic Article uri icon

Overview

MeSH Major

  • Isolated Noncompaction of the Ventricular Myocardium
  • Magnetic Resonance Imaging, Cine
  • Referral and Consultation

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.

publication date

  • January 2017

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC5300005

Digital Object Identifier (DOI)

  • 10.1158/2159-8290.CD-16-0975

PubMed ID

  • 27733359

Additional Document Info

start page

  • 38

end page

  • 53

volume

  • 7

number

  • 1