Louis M. Staudt

National Institutes of Health

Election Year: 2013
Primary Section: 43, Immunology and Inflammation
Secondary Section: 41, Medical Genetics, Hematology, and Oncology
Membership Type: Member


Louis M. Staudt is Director of the Center for Cancer Genomics at the National Cancer Institute and also serves as Co-Chief of the Lymphoid Malignancies Branch. He is a cancer biologist who is known for his development of methods in genomics to define molecular subtypes of cancer and identify new targets for therapy. His particular focus is on the pathogenesis and treatment of lymphoma. Staudt was born in Michigan in 1955 and received his B.A. from Harvard College in 1976. He was awarded a Medical Scientist Training Program fellowship at the University of Pennsylvania School of Medicine and received his MD and PhD degrees in 1982. Following Internal Medicine training, he joined Nobel Laureate David Baltimore's laboratory at the Whitehead Institute as a Jane Coffin Childs Fellow. In 1988, he established his laboratory at the National Cancer Institute, and in 2011, he received the honorary title of NIH Distinguished Investigator. He has received numerous awards for his research, including the 2009 Dameshek Prize from the American Society of Hematology for outstanding contribution in hematology.

Research Interests

Staudt investigates the pathogenesis of human lymphomas and devises new treatment strategies using insights from functional and structural genomics. Using gene expression profiling, he established that diffuse large B cell lymphoma (DLBCL) is comprised of two molecular subtypes, termed activated B cell-like (ABC) and germinal center B cell-like (GCB). These subtypes are now viewed as molecularly distinct diseases that arise from different stages of normal B cell development, require separate genetic abnormalities to become malignant, have divergent cure rates with chemotherapy, and respond differentially to targeting agents. Staudt utilizes loss-of-function genetic screens and cancer genome resequencing to discover essential regulatory pathways that govern the proliferation and survival of lymphoma cells. Using these methods he showed that the survival of ABC DLBCL cells relies on constitutive signals from the B cell receptor and from MyD88, an adaptor in Toll-like receptor signaling. To attack B cell receptor signaling therapeutically, Staudt initiated clinical trials in DLBCL of ibrutinib, an inhibitor of the kinase BTK. Ibrutinib produces a high response rate in relapsed/refractory ABC DLBCL with minimal side effects, while GCB DLBCL tumors rarely respond. Staudt currently aims to develop combinations of targeted agents that will cure patients with lymphoma.

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