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Evaluation of BRD1 as a novel therapeutic target for diffuse large B cell lymphoma

Joel Pomerantz

Joel Pomerantz


The Johns Hopkins University School of Medicine

Project Term: July 1, 2019 - June 30, 2022

Antigen receptor signaling to NF-kappaB is frequently dysregulated in Diffuse Large B Cell Lymphoma (DLBCL) and required for lymphoma cell proliferation. Using a novel genome-wide loss-of-function screen, we identified the chromatin regulatory protein BRD1 as a factor required in this pathway. We propose to test our hypothesis that BRD1 is a novel therapeutic target for the treatment of DLBCL and other lymphomas that depend upon chronic antigen receptor signaling to NF-kappaB.

Lay Abstract

A key arm of the human immune system consists of B cells, white blood cells that sense the presence of an infection, secrete antibodies, and help recruit other cells in the immune system to help fight the infection. Several types of human lymphoma develop as a result of mutations that dysregulate the molecular machinery responsible for normal B cell function. Often in lymphoma, the dysregulated machinery makes the B cell grow and divide out of control, as if the cell is receiving a signal that an infection needs to be challenged. Our group has been studying this signaling machinery, trying to identify the component parts, figure out how they operate normally, and how mutations in human lymphoma disrupt the machinery and cause disease. We recently developed a new approach aimed at identifying previously undiscovered parts of this machinery, and identified BRD1, a gene regulatory protein that has not previously been studied in this context. In this application, we propose to test our hypothesis that BRD1 is a novel, “druggable” therapeutic target for the treatment of Diffuse Large B Cell lymphoma and other forms of Non-Hodgkin Lymphoma that depend on dysregulated signaling.

Translational Research Program
Grant Subprogram
TRP Basic
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