Department of Biological Sciences: Leading the way to Prominence

Carlton R. Cooper, Ph.D.

Assistant Professor

Cooper

Phone: (302) 831-6062
Fax: (302) 831-2281
Email: crcooper@udel.edu
Office: 324 Wolf Hall

Address:
Department of Biological Sciences
Wolf Hall
University of Delaware
Newark, DE 19716

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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 625* - Cancer Biology

*Course web site available through MyCourses

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.

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.

Current Projects

Differential activation of the Rho GTPases in prostate motility, invasion and metastasis. PI: Dr. Kenneth van Golen, University of Michigan; Co PIs: Dr. Carlton R. Cooper and Dr. Timothy M. Ritty, Washington University in St. Louis. Funded by Department of Defense (DoD) new investigator award, 2004-2007.
Analysis of the role of TGF-β in prostate cancer metastasis to bone using computer modeling. Funded in part by DoD, 2005-2007.
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 contribution of endothelial progenitor cells to the progression of end-stage renal disease.
The functional differences between human umbical vein endothelial cells (HUVEC) and bone marrow endothelial cell (BMEC).
The role of nitric oxide and RhoA GTPases in cancer cell extravasation of BMEC under shear-stress.

Research Group

Bianca Graves, M.S. - Lab Manager (M.S., Clark Atlanta University). Grant and manuscript administrator, cell culture coordinator.
Linda Sequeira, B.S. - Research Specialist (B.S., Trinity College). The role of nitric oxide and RhoA GTPase in cancer cell extravasation through BMECs.
Fayth Miles, M.S. - Ph.D. Graduate Student (M.S., Johns Hopkins University). Analysis of the role of TGF-β in prostate cancer metastasis to bone using computer modeling. Dr. Robert A. Sikes (advisor) and Dr. Carlton R. Cooper (co-advisor).
J. Matthew (Matt) Kuczmarki, B.S. - M.S. Graduate Student (B.S., University of Delaware). Isolation and Charactization of endothelial progentor cells AND functional differences between HUVEC and BMEC. Dr. David Edwards (advisor) and Dr. Carlton R. Cooper (co-advisor).
Charles Drummer - UNCF MERCK Undergraduate Fellow. Prostate cancer resistance mediated by extracellular matrix components.
Val Mechanik - Undergraduate Research Assistant. Development and Characterization of Endothelial cells from African-American and functional differences between HUVECs and BMECs.
Chris Mandala - Undergraduate Research Assistanct. Development and Characterization of Endothelial cells from African-American.

The Laboratory for Prostate Cancer Research

Selected Publications

Cooper CR, Graves B, Pruitt F, et al. Novel surface expression of reticulocalbin 1 on bone endothelial cells and human prostate cancer cells is regulated by TNF-alpha. J Cell Biochem. 2008;104(6):2298–2309.
Cooper CR, Gurski L, Satcher R, van Golen KL. Mechanisms of metastasis to bone: the role of bone marrow endothelium. In: Bronner F, Farach-Carson M, eds. Bone and Cancer. Vol. 5. Springer; 2008:in press. Topics in Bone Biology.
Lyles RH, Poindexter C, Evans A, Brown M, Cooper CR. Nonlinear model-based estimates of IC(50) for studies involving continuous therapeutic dose-response data. Contemp Clin Trials. 2008;29(6):878–886.
Miles FL, Pruitt FL, van Golen KL, Cooper CR. Stepping out of the flow: capillary extravasation in cancer metastasis. Clin Exp Metastasis. 2008;25(4):305–324.
Sequeira L, Dubyk CW, Riesenberger TA, Cooper CR, van Golen KL. Rho GTPases in PC-3 prostate cancer cell morphology, invasion and tumor cell diapedesis. Clin Exp Metastasis. 2008;25(5):569–579.
Barwe SP, Maul RS, Christiansen JJ, et al. Preferential association of prostate cancer cells expressing prostate specific membrane antigen to bone marrow matrix. Int J Oncol. 2007;30(4):899–904.
Sikes RA, Cooper CR, Beck GL, Pruitt F, Brown ML, Balian G. Bone stromal cells as therapeutics targets in osseous metastasis. In: Meadows GG, ed. Integration/Interaction of Oncologic Growth. Vol. 15. Boston, MA: Kluwer Academic Publishers; 2005:369–386. Cancer Growth and Progression.
Brennen WN, Cooper CR, Capitosti S, Brown ML, Sikes RA. Thalidomide and analogues: current proposed mechanisms and therapeutic usage. Clin Prostate Cancer. 2004;3(1):54–61.
Cooper CR, Sikes RA, Nicholson BE, Sun Y-X, Pienta KJ, Taichman RS. Cancer cells homing to bone: the significance of chemotaxis and cell adhesion. Cancer Treat Res. 2004;118:291–309.
Stewart DA, Cooper CR, Sikes RA. Changes in extracellular matrix (ECM) and ECM-associated proteins in the metastatic progression of prostate cancer. Reprod Biol Endocrinol. 2004;2:2.
Cooper CR, Chay CH, Gendernalik JD, et al. Stromal factors involved in prostate carcinoma metastasis to bone. Cancer. 2003;97(3 Suppl):739–747.
Lee H-L, Pienta KJ, Kim W-J, Cooper CR. The effect of bone-associated growth factors and cytokines on the growth of prostate cancer cells derived from soft tissue versus bone metastases in vitro. Int J Oncol. 2003;22(4):921–926.
Snider TG 3rd, Coats KS, Storts RW, et al. Natural bovine lentivirus type 1 infection in Holstein dairy cattle. II. Lymphoid tissue lesions. Comp Immunol Microbiol Infect Dis. 2003;26(1):1–15.
Snider TG 3rd, Hoyt PG, Coats KS, et al. Natural bovine lentiviral type 1 infection in Holstein dairy cattle. I. Clinical, serological, and pathological observations. Comp Immunol Microbiol Infect Dis. 2003;26(2):89–101.
Chay CH, Cooper CC, Hellerstedt BA, Pienta KJ. Antimetastatic drugs in prostate cancer. Clin Prostate Cancer. 2002;1(1):14–19.
Chay CH, Cooper CR, Gendernalik JD, et al. A functional thrombin receptor (PAR1) is expressed on bone-derived prostate cancer cell lines. Urology. 2002;60(5):760–765.
Cooper CR, Bhatia JK, Muenchen HJ, et al. The regulation of prostate cancer cell adhesion to human bone marrow endothelial cell monolayers by androgen dihydrotestosterone and cytokines. Clin Exp Metastasis. 2002;19(1):25–33.
Taichman RS, Cooper C, Keller ET, Pienta KJ, Taichman NS, McCauley LK. Use of the stromal cell-derived factor-1/CXCR4 pathway in prostate cancer metastasis to bone. Cancer Res. 2002;62(6):1832–1837.
Donald CD, Cooper CR, Harris-Hooker S, Emmett N, Scanlon M, Cooke DB 3rd. Cytoskeletal organization and cell motility correlates with metastatic potential and state of differentiation in prostate cancer. Cell Mol Biol (Noisy-le-Grand). 2001;47(6):1033–1038.
Keller ET, Zhang J, Cooper CR, et al. Prostate carcinoma skeletal metastases: cross-talk between tumor and bone. Cancer Metastasis Rev. 2001;20(3-4):333–349.
Cooper CR, McLean L, Walsh M, et al. Preferential adhesion of prostate cancer cells to bone is mediated by binding to bone marrow endothelial cells as compared to extracellular matrix components in vitro. Clin Cancer Res. 2000;6(12):4839–4847.
Cooper CR, Hanson LA, Diehl WJ, Pharr GT, Coats KS. Natural selection of the Pol gene of bovine immunodeficiency virus. Virology. 1999;255(2):294–301.
Cooper CR, Emmett N, Harris-Hooker S, Patterson R, Cooke DB 3rd. Biometric assessment of prostate cancer's metastatic potential. World J Urol. 1994;12(6):304–307.
Cooper CR, Donald C, Emmett N, Harris-Hooker S, Cooke DB 3rd. Adhesion and invasion potential of rat prostatic cancer cells: correlation with metastatic potential. Invasion Metastasis. 1993;13(4):178–184.