|Ph.D., 1981, Cell Biology, Columbia University|
|Postdoctoral research: Center for Cancer Research at Massachusetts Institute of Technology|
|Office:||University of Massachusetts Medical School
364 Plantation Street, LRB-428
Worcester, MA 01605
We are interested in the initiation and progression of epithelial-derived tumors (carcinomas), especially aggressive, poorly differentiated tumors. Our research projects emphasize molecular cell biology but they derive from the analysis and clinical behavior of carcinomas. Our goal is to identify mechanisms that account for the loss of differentiation and the highly aggressive behavior of these tumors, and to exploit these mechanisms to improve prognosis and therapy. A major focus of this work is to define mechanisms that control the genesis and function of cancer stem cells with an emphasis on the role of integrin and VEGF signaling.
Regulation and Function of Integrins: The lab has a long-standing interest in the a6 integrins (a6b1 and a6b4), which function as receptors for the laminins, a family of extracellular matrix proteins. We seek to understand how these integrins contribute to tumor initiation with an emphasis on cancer stem cells and on the role of laminins in the cancer stem cell niche.
VEGF Function and Signaling in Carcinoma Cells: This project is based on the hypothesis that VEGF receptors expressed on carcinoma cells mediate VEGF signaling and that VEGF signaling in epithelial cells contributes to tumor initiation. This hypothesis challenges the notion that the function of VEGF in cancer is limited to angiogenesis and that therapeutic approaches based on the inhibition of VEGF and its receptors target only angiogenesis. We are focused on understanding the nature of VEGF signaling in cancer stem cells and developing strategies to target this signaling therapeutically.