Carlton R. Cooper

Biological Sciences

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Carlton Cooper's Google Scholar Publications

Carlton R. Cooper

Associate Professor

crcooper@udel.edu

302-831-6062

Office: 405 Harker ISE Lab

Education

B.S. - Morehouse College
M.S. - Clark Atlanta University
Ph.D. - Mississippi State University
Postdoctoral - University of Michigan

Teaching

BISC 300 - Introduction to Microbiology
BISC 300 - Introduction to Microbiology
BISC 625 - Cancer Biology
UNIV 100 - First Year Experience

Research Interests

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.

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In addition to serving as an adhesive substrate for circulating prostate cancer cells, bone endothelial cells are recruited to growing prostate tumors in the bone during a process called angiogenesis. Angiogenesis is required for tumor expansion. We are also interested in testing novel compounds for their ability to inhibit endothelial cell growth and migration, activities necessary for angiogenesis. Compounds capable of doing this have immense clinical potential to prevent or treat bone metastases in prostate cancer patients.

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.

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Current Projects

Analysis of the role of TGF-β in prostate cancer metastasis to bone using computer modeling.
The functional role of cell surface reticulocalbin 1 on bone-marrow endothelial cells.
The isolation and characterization of endothelial cell derived from African-American.
The role of nitric oxide and RhoA GTPases in cancer cell extravasation of BMEC under shear-stress.