Acquired CARD11 mutation promotes BCR independence in Diffuse Large B Cell Lymphoma.


Type
Article
Change log
Authors
Caeser, Rebecca 
Walker, Ieuan 
Gao, Jie 
Shah, Nimish 
Rasso-Barnett, Livia 
Abstract

Diffuse large B cell lymphoma (DLBCL) is an aggressive non-Hodgkin lymphoma that is molecularly and clinically heterogeneous. Gene expression studies have revealed how DLBCL can be divided into germinal center (GC) and activated B cell (ABC) subtypes. The ABC subtype is associated with constitutive activation of the NF-κB pathway, commonly as a consequence of genetic activation of the B cell receptor (BCR) pathway1. Components of the BCR pathway that are activated by mutation include CD79B, MYD88 and CARD11. Chronic stimulation of the BCR in ABC DLBCL may also result from engagement of the BCR by self antigens in the tumor microenvironment. These preclinical observations suggest a role for the targeted inhibitors of the BCR pathway in the treatment of DLBCL1.

Description
Keywords
Aged, B-Cell Activation Factor Receptor, CARD Signaling Adaptor Proteins, Female, Guanylate Cyclase, Humans, Lymphoma, Large B-Cell, Diffuse, Male, Mutation
Journal Title
JCO Precis Oncol
Conference Name
Journal ISSN
2473-4284
2473-4284
Volume Title
5
Publisher
American Society of Clinical Oncology (ASCO)
Sponsorship
Medical Research Council (MR/M008584/1)
Wellcome Trust (203151/Z/16/Z)
Medical Research Council (MC_PC_17230)
D.H. was supported by a Clinician Scientist Fellowship from the Medical Research Council (MR/M008584/1) and a project grant from the Kay Kendall Leukaemia Fund. The Hodson laboratory receives core funding from Wellcome and MRC to the Wellcome-MRC Cambridge Stem Cell Institute and from the CRUK Cambridge Cancer Centre.