- Centers & Specialties
- Clinical Interests
- Benign hematology
- Myeloproliferative diseases
- Thrombosis and hemostasis
- Medical Education
- MD, PhD, UC San Diego School of Medicine
- Residency, Massachusetts General Hospital
- Fellowship, Dana Farber Cancer Institute
- Board Certifications
- Internal Medicine
- Medical Oncology
- Foreign Languages
- Boston: Massachusetts General Hospital
- Insurances Accepted
- Aetna Health Inc.
- Beech Street
- Blue Cross Blue Shield - Blue Care 65
- Blue Cross Blue Shield - Indemnity
- Blue Cross Blue Shield - Managed Care
- Blue Cross Blue Shield - Partners Plus
- Cigna (PAL #'s)
- Fallon Community HealthCare
- Great-West Healthcare (formally One Health Plan)
- Harvard Pilgrim Health Plan - ACD
- Harvard Pilgrim Health Plan - PBO
- Health Care Value Management (HCVM)
- Humana/Choice Care PPO
- Medicare - ACD
- Neighborhood Health Plan - ACD
- Neighborhood Health Plan - PBO
- OSW - Maine
- OSW - New Hampshire
- OSW - Vermont
- Private Health Care Systems (PHCS)
- Senior Whole Health
- Tufts Health Plan
- United Healthcare (non-HMO) - ACD
- United Healthcare (non-HMO) - PBO
Note: This provider may accept more insurance plans than shown; please call the practice to find out if your plan is accepted.
- Patient Age Group
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.
- Research Summary
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.
55 Fruit Street
Boston, MA 02114-2696