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James A. DeCaprio, MD

Associate Professor, Department of Medicine, Harvard Medical School

Faculty Director, DFCI Monoclonal Antibody Core, Dana-Farber Cancer Institute

Active Staff and Clinical Associate in Medicine, Medical Oncology, Dana-Farber Cancer Institute

Associate Professor of Medicine, Medical Oncology, Dana-Farber Cancer Institute

Active Staff and Associate Physician, Medicine, Brigham And Women's Hospital

Contact Info

James DeCaprio
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: Mayer 440
Phone: 617-632-3825
Fax: 617-582-8601


Not Available.

DF/HCC Program Affiliation

Cancer Genetics
Cancer Cell Biology

Research Abstract

A major area of interest of our laboratory is viral induced cancers. In particular, we study how oncogenic viral proteins enable the transformation of normal cells into cancer. We have found that expression of viral proteins has significant impact on the normal physiology of the cells including the cell cycle, signaling, and survival pathways. We are searching for additional mechanisms of viral induced transformation using a variety of approaches including identification of viral-host protein-protein interactions. We focus primarily on the small DNA tumor viruses especially SV40 and Merkel cell polyomavirus. We also study the contribution of Merkel cell polyomavirus to Merkel cell carcinoma, a highly aggressive and frequently lethal skin cancer.

Another important interest of our laboratory is the mammalian cell cycle with a particular focus on the role of the retinoblastoma family of tumor suppressors. The retinoblastoma family includes pRb (RB1), p107 (RBL1) and p130 (RBL2). We recently identified the DREAM complex that contains DP1, Rb-related protein p130, E2F4 and the MuvB core complex of five proteins (LIN9, LIN37, LIN52 LIN54 and RBBP4). We have demonstrated that the DREAM complex serves as a master coordinator of cell cycle gene expression. We use mass-spectroscopy, expression profiling, chromatin immunoprecipitation and additional genomic approaches to understand how cell cycle dependent gene expression is regulated. We strive to combine these molecular insights with genomic analysis of human cancers to identify novel therapeutic opportunities.


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