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David completed his undergraduate training in Biochemistry at the University of Alberta in Edmonton, Canada. He entered the Medical Scientist Training Program (M.D., Ph.D.) at the University of California San Diego and carried out his Ph.D. research with Dr. Mark Kamps. David did his internship and residency at the Massachusetts General Hospital as well as a year as a Chief Medical Resident in the Department of Internal Medicine. He was a Hematology and Oncology fellow in the combined Dana-Farber Cancer Institute, MGH Cancer Center fellowship program. David joined the MGH Cancer Center as an attending in benign hematology. He splits his time between the laboratory (80% research) and clinic (20% direct patient care). He sees patients with all diagnoses with a focus on patients with myeloproliferative disorders. David has a special interest in rare hematologic conditions. In 2011 he defined a new syndrome - the TEMPI syndrome - which affects only 9 identified patients worldwide. David's research involves understanding and identifying new treatments for acute myeloid leukemia. His research is currently being carried out in the lab of Dr. David Scadden. He is focused on designing drugs for patients with acute myeloid leukemia that trigger differentiation, or maturation, of the leukemic cells.
Acute myeloid leukemia (AML) is a devastating disease with a5-year survival rate of 25%. One success story has been the discovery of drugswhich trigger differentiation in the 10% of patients with acute promyelocyticleukemia. Differentiation therapies, including all-trans retinoic acid, arewell-tolerated and extremely effective, leading to 5-year survival ratesapproaching 80% in the small subset of patients with acute promyelocyticleukemia. Differentiation therapy is unfortunately not available for theremaining 90% of patients with AML.
HoxA9 is a critical mediator of normal hematopoiesis. Theexpression of HoxA9 is normally downregulated as cells mature along the myeloidlineage. The inappropriate expression of HoxA9 has been demonstrated in themajority (>70%) of AML. Furthermore, those leukemias which contain MLLfusion oncoproteins are dependent upon HoxA9 for their proliferation andsurvival. These observations make HoxA9 and its downstream effectors attractivecandidates for drug targeting. The gene targets of HoxA9 and the mechanism bywhich HoxA9 establishes differentiation arrest in leukemia are not known.
I am interested in understanding how HoxA9 establishes differentiation arrest in acute myeloid leukemia. Furthermore, I am interested in identifying new compounds which can overcome this differentiation arrest and which will be active in treating human leukemia.
View my most recent publications at PubMed
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