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James D. Griffin, MD

Professor, Department of Medicine, Harvard Medical School

Chair, Medical Oncology, Dana-Farber Cancer Institute

Director, Medical Oncology, Brigham And Women's Hospital

Contact Info

James Griffin
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: Mayer 540
Phone: 617-632-3360
Fax: 617-632-2260
Email not available

Assistant

Lisa Lewis
Administrative Assistant
Medical Oncology
Dana-Farber Cancer Institute
44 Binney Street
Boston, MA, 02115
Mailstop: D1608
Phone: 617-632-2266
Fax: 617-632-2260
lisa_lewis@dfci.harvard.edu

DF/HCC Program Affiliation

Leukemia

DF/HCC Associations

Member, Center Scientific Council
Deputy Associate Director, Clinical Science, Executive Committee
Member, Clinical Science Coordinating Committee

Research Abstract

Dr. Griffin's laboratory is focused on understanding the genetic events that cause leukemia. The major laboratory interests can be divided into three broad areas: 1. Mechanisms of transformation by the BCR/ABL oncogene. The product of the BCR/ABL oncogene is an activated tyrosine kinase which induces a myeloproliferative syndrome in humans and mice. p210BCR/ABL transforms hematopoietic cells at least in part by constitutively activating signal transduction pathways which are normally tightly regulated by growth factors such as IL-3 or GM-CSF, such as those involved in blocking apoptosis. Several critical targets of BCR/ABL have been identified, including CRKL, SHP2, PI3K, SHIP, and RAS. Defining the individual contribution of each pathway to CML is underway, as are gene discovery approaches to identifying novel targets. 2. Mechanisms of transformation by the FLT3 oncogene and development of targeted therapies against FLT3. FLT3 is mutated in about 35% of all cases of AML. The lab has developed a small molecule tyrosine kinase inhibitor that blocks signaling from FLT3, which is currently being tested in clinical trials. In vitro studies of mechanism and murine models are being used to develop the next generation of AML therapies using this inhibitor as part of the therapy. 3.Signaling of the Notch receptor in hematopoietic and epithelial cells. We have recently cloned a several nes members of the Notch signaling pathway, a family of transcriptional regulators (mastermind-like genes) that modulates expression of Notch regulated genes in a variety of cell lineages. One family member, MAML2, has recently been shown to be mutated in mucoepidermoid cancer and appears to be the cause of that neoplasm.

Publications

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