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Signalling through the B cell receptor (BCR) is central to the development and maintenance of B cells. In light of the numerous proliferative and survival pathways activated downstream of the BCR, it comes as no surprise that malignant B cells would co-opt this receptor to promote their own growth and survival. However, direct evidence for BCR signalling in human lymphoma has only come to light recently. Roles for antigen-dependent and antigen-independent, or tonic, BCR signalling have now been described for several different lymphoma subtypes. Furthermore, correlative data implicate antigen-dependent BCR signalling in many other forms of lymphoma. A host of therapeutic agents targeting effectors of the BCR signalling pathway are now in clinical trials and have shown initial success against multiple forms of lymphoma.
Dr. Staudt received his B.A. from Harvard College and his M.D. and Ph.D. degrees from the University of Pennsylvania School of Medicine. Following Internal Medicine training, he joined Nobel Laureate David Baltimore's laboratory at the Whitehead Institute as a Jane Coffin Childs postdoctoral fellow. In 1988, he established his laboratory at the National Cancer Institute (NCI), which focuses on the molecular basis for human lymphoid malignancies and the development of targeted therapies for these cancers. Dr. Staudt is Co-Chief of the Lymphoid Malignancies Branch and Director of the NCI Center for Cancer Genomics, which oversees large-scale programs studying the genomic aberrations in cancer. He has received numerous awards for his research, including the 2009 Dameshek Prize from the American Society of Hematology, the 2015 San Salvatore Prize, the 2016 C. Chester Stock Award Lectureship from Memorial Sloan Kettering Cancer Center, the 2017 Princess Takamatsu Memorial Award from the American Association for Cancer Research, and election to the National Academy of Sciences in 2013.