Assistant Professor, Health Disparity and Community Outreach Coordinator
Department of Biological Sciences
University of Delaware
Newark, DE 19716
Ph.D., Mississippi State University - 1998
M.S., Clark Atlanta University - 1992
B.S., Morehouse College - 1989
It is the preference of prostate cancer to spread (metastasize) to bone causing symptoms such as intense pain, bone fractures, and/or spinal cord compression. The molecular mechanisms for this metastatic pattern of advanced prostate cancer are not known and are under intense investigation. In order to metastasize to a particular organ, a cancer cell must first adhere to the endothelial cells lining the blood vessel (microvessel) that feeds the organ. Endothelial cells, derived from a specific organ’s microvessel, are distinct in their expression of cell adhesion molecules (CAMs). Previous studies have shown that prostate cancer cells adhered preferentially to human bone marrow endothelial cells (HBME) when compared to other endothelial cell types in vitro. This observation suggests that prostate cancer metastasis to bone is mediated partially by the preferential adhesion to HBME cells in the bone marrow.
The objective of my research is to identify the CAMs expressed on HBME cells inclusive of the respective ligands or counter-receptors found on prostate cancer cells that are involved in prostate cancer cell-HBME interaction. Once the CAM-ligand complex(es) responsible for prostate cancer cell adhesion to HBME cells is/are identified, the effect of bone-stromal factors on the expression of HBME-specific CAMs and prostate cancer- corresponding ligands will be examined. It is interesting to note that the activation of CAMs on prostate cancer cells by extracellular matrix components may contribute to the Akt (a kinase) activation of survival pathways and may allow the cancer cells to resist cytotoxic and hormonal therapies.