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Richard M. Stone, MD

Professor, Department of Medicine, Harvard Medical School

Clinical Director, Adult Leukemia Program, Dana-Farber Cancer Institute

Associate Physician, Medicine, Brigham And Women's Hospital

Contact Info

Richard Stone
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: D-840
Phone: 617-632-2214
Fax: 617-632-2933


Susie Crowley
Administrative Assistant
Adult Leukemia Program
Dana-Farber Cancer Institute
44 Binney Street
Boston, MA, 02115
Phone: 617-632-2168
Fax: 617-632-2933

DF/HCC Program Affiliation

Leukemia, Co-Leader
Translational Pharmacology and Early Therapeutic Trials

DF/HCC Associations

Member, Center Scientific Council

Research Abstract

I am engaged in developmental therapeutics for patients with bone marrow stem cell disorders including the acute leukemias, myelodysplasia, and the myeloproliferative disorders. The areas of differentiation-based therapy, as well as cell signal modicifcation therapy (kinase inhibitors) currently with agents which act on protein kinase-C and immunologically-based therapy involving transduction of pro-inflammatory genes into leukemia cells and dendritic cell/leukemia cell fusions, represent an important current translocational focus. From a clinical standpoint we are involved in several large trials designed to improve the care of patients with acute leukemia: including immunotherapy with IL-2 as late post-remission therapy for the adults with AML (CALGB) and use of a bcl-2 antisense oligonucleotide in older adults with AmL (CALGB). We are also testing the feasibility of adding a FLT3 inhibitor to chemotherapy in newly dignosed patietns with AML and using a pediatric-like regimen to treat adults with ALL.We also have protocols employing novel agents in AML and MDS including:troxacitibine, cloretazine, gefitnib, and gamma secretase inhibitors. We also continue to be heavily involved with clinico-genetic correlates such as our work describing the frequency of JAK2 mutations in the myeloproliferative disorders and the pathophysiological significance or FIP1L1-PDGFRA fusions in the hypereosinophilic syndrome.


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