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The genes encoding the histone acetyltransferases (HATs) CREBB-binding protein (CREBBP) and EP300 are commonly mutated in germinal-center-derived B cell lymphomas, and their inactivation is thought to contribute to lymphomagenesis. In this issue of Immunity, Meyer et al. (2019) demonstrate that the somatic inactivation of one histone modifying enzyme might leave lymphomas uniquely sensitive to antagonists of the other.

Original publication

DOI

10.1016/j.immuni.2019.08.018

Type

Journal article

Journal

Immunity

Publication Date

09/2019

Volume

51

Pages

420 - 423

Addresses

MRC Human Immunology Unit, Nuffield Department of Medicine, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS, UK. Electronic address: oliver.bannard@ndm.ox.ac.uk.

Keywords

Germinal Center, B-Lymphocytes, Humans, Carrier Proteins, Epigenesis, Genetic, E1A-Associated p300 Protein, CREB-Binding Protein, Lymphoma, Large B-Cell, Diffuse