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Dr. Benjamin Ebert is the George P. Canellos, MD, and Jean S. Canellos Professor of Medicine at Harvard Medical School, Chair of Medical Oncology at the Dana-Farber Cancer Institute, a Howard Hughes Medical Institute Investigator, and an Institute Member of the Broad Institute.Dr. Ebert is an elected member of the National Academy of Medicine, the American Society for Clinical Investigation and the Association of American Physicians. He served as President of the American Society for Clinical Investigation. His awards include the Till and McCollough Award from the International Society of Experimental Hematopoiesis, the William Dameshek Prize from the American Society of Hematology, the Meyenburg Prize, and mentoring and teaching awards from Harvard Medical School.Dr. Ebert received a bachelor's degree from Williams College and a doctorate from Oxford University as a Rhodes Scholar where he worked with Peter Ratcliffe, who was subsequently awarded the Nobel Prize in Medicine. He completed an M.D. from Harvard Medical School, a residency in internal medicine at Massachusetts General Hospital, and a fellowship in hematology/oncology at the Dana-Farber Cancer Institute. He was on the faculty of Brigham and Women’s Hospital for 10 years before returning to the Dana-Farber.
The primary focus of the Ebert laboratory is the genetics, biology, and therapy of myeloid malignancies.The Ebert laboratory focuses on the molecular basis and treatment of hematologic malignancies and its non-malignant precursor conditions, with a particular focus on myelodysplastic syndromes (MDS) and clonal hematopoiesis of indeterminate potential (CHIP). The laboratory uses human genetics and a range of model systems to examine the genetics, biology, and clinical implications of MDS and CHIP. CHIP is a pre-malignant state that is associated with increased risk of hematologic malignancy, increased all-cause mortality, atherosclerotic cardiovascular disease, and changes in inflammatory markers. The lab studies the biological basis of transformation of hematopoietic cells by somatic mutations and has developed novel models to study myeloid malignancies.The Ebert laboratory demonstrated that lenalidomide, a derivative of thalidomide, binds the CRL4-CRBN E3 ubiquitin ligase and induces degradation of specific substrates, a novel mechanism of action for a drug. More broadly, thalidomide analogs have the potential to induce degradation of a broad array of zinc finger transcription factors and other proteins. Expanding the library of molecules that function by degrading disease-relevant proteins, many of which were previously considered “undruggable,” has potential for novel therapeutics.
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