Oncogenic mutations in ABC-DLBCL

Dr James Wang, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA

Activated B cell like diffuse large B cell lymphoma (ABC-DLBCL) is an aggressive and incurable form of B cell malignancy. A hallmark of ABC-DLBCL is the constitutive activation of NFkB transcription factors, attributed by part to mutations in CARD11, MYD88, CD79B and TNFAIP3. Each mutation’s role in the pathogenesis of ABC-DLBCL is confounded by the accumulation of many other protein damaging mutations in the malignant cells. Here we analyze the effects of these mutations in otherwise normal B cells by using retroviral gene transfer and by using ENU-mutated mice. I will discuss the consequences of B cells acquiring these mutations, and propose mechanism for how these mutations interact in ABC-DLBCL. These data provide novel understand to the pathogenesis of lymphomas and will benefit the search for new therapeutic approaches.

James graduated in biomedical science with first class honors from the University of Melbourne. He then completed his PhD under the supervision of Professor Christopher Goodnow and Dr Keisuke Horikawa in the Department of Immunology at the John Curtin School of Medical Research from 2011 to 2015. He joined Dr Louis Staudt’s laboratory at the National Cancer Institute in 2016, and was awarded an NHMRC overseas early career fellowship in 2017 to develop new animal models of diffuse large B cell lymphoma.

Dr Wang is the winner of the 2016 Dewar-Milne Prize in Immunology.