Richard M. Stone, MD
Program Director, Adult Leukemia
Professor of Medicine, Harvard Medical School
Office phone: 617-632-1906
Preferred contact method: email
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Leukemia, Myelodysplastic syndromes, Myeloproliferative disorders
Area of ResearchTherapy for Acute Leukemias and Related Disorders
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA 02215
BiographyDr. Stone received his MD in 1981 from Harvard Medical School, his internal medicine residency training at Brigham and Women's Hospital, and his hematology-oncology fellowship at DFCI. He has performed numerous laboratory and clinical studies on acute leukemia and related disorders, and frequently participates in grand rounds worldwide. He is currently the Director of the Adult Acute Leukemia Program at DFCI, serves on the Medical Oncology Board of the American Board of Internal Medicine, and is vice chair of the Leukemia Core Committee for the national cooperative trials group Cancer and Leukemia Group B.
- Dana-Farber Cancer Institute Medical Oncology Teaching Award
ResearchTherapy for Acute Leukemias and Related Disorders
The primary focus of our clinical team is patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), myelodysplastic syndromes (MDS), and myeloproliferative disorders. Our practice is located in the Center for Hematologic Malignancies in the ambulatory clinic at DFCI, but we also see inpatients at Brigham and Women's Hospital. In addition to seeing patients with refractory leukemia and advanced myelodysplasia, we see others with complex or difficult cases who have been referred from outside New England and from other countries. Our goal is to provide the highest level of clinical care and improve the outcome for all patients.
Our research involves identifying novel targets involved in the pathophysiology of acute leukemia and myelodysplastic syndrome. Inhibition of the FLT3 tyrosine kinase, for example, may offer benefits in AML patients - especially those whose blasts have an activating mutation in the enzyme - similar to the success of imatinib in the treatment of patients with chronic myeloid leukemia (CML). After conducting several trials with FLT3 inhibitors as single agents in myeloid malignancies, we are now focusing on combining these drugs with chemotherapeutic agents. Our laboratory continues to explore the mechanism of leukemic transformation via mutated FLT3, especially regarding activation of downstream pathways such as protein kinase A or AKT, which may be involved in key aspects of leukemogenesis such as prevention of apoptosis and promotion of self-renewal.
Other areas of clinical research include targeted therapy in T cell ALL, based on inhibition of NOTCH activation, a common survival mechanism in such cells; application of intensive "pediatric-type" strategies in adults with ALL; and many novel drugs in AML in AML and MDS including histone deacetylase inhibitors, NEDD-8 inhibitors, HSP90 inhibitors, MEK inhibitors and others.
- Cools J, Stover EH, Boulton CL, Gotlib J, Legare RD, Amaral SM, Curley DP, Duclos N, Rowan R, Kutok JL, Lee BH, Williams IR, Coutre SE, Stone RM, DeAngelo DJ, Marynen P, Manley PW, Meyer T, Fabbro D, Neuberg D, Weisberg E, Griffin JD, Gilliland DG. PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRalpha-induced myeloproliferative disease. Cancer Cell 2003;3:459-69.
- Sekeres MA, Stone RM, Zahrieh D, Neuberg D, Morrison V, DeAngelo DJ, Galinsky I, Lee SJ. Decision-making and quality of life in older adults with acute myeloid leukemia or advanced myelodysplastic syndrome. Leukemia 2004;18:809-16.
- Sekeres MA, Peterson B, Dodge RK, Mayer RJ, Moore JO, Lee EJ, Kolitz J, Baer MR, Schiffer CA, Carroll AJ, Vardiman JW, Davey FR, Bloomfield CD, Larson RA, Stone RM, Cancer and Leukemia Group B. Differences in prognostic factors and outcomes in African Americans and whites with acute myeloid leukemia.
- Stone RM, DeAngelo DJ, Klimek V, Galinsky I, Estey E, Nimer SD, Grandin W, Lebwohl D, Wang Y, Cohen P, Fox EA, Neuberg D, Clark J, Gilliland DG, Griffin J. Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412. Blood 2005;105:54-60.
- Stone RM, DeAngelo DJ, Janosova A, Galinsky I, Canning C, Ritz J, Soiffer RJ. Low dose interleukin-2 following intensification therapy with high dose cytarabine for acute myelogenous leukemia in first complete remission. Am J Hematol. 2008;83:771-777.
- Stone R, Donohue K, Stock W, Hars V, Linker C, Shea T, DeAngelo D, Marcucci G, Bloomfield C, Larson R. A phase II study of continuous infusion homoharringtonine and cytarabine in newly diagnosed patients with chronic myeloid leukemia: CALGB Study 19804. Cancer Chemotherapy Pharmacology 2009;63:859.
- Bar-Natan, Michal, MD
- Motyckova, Gabi, MD, PHD