James B. McCarthy, Ph.D. Professor Department of Laboratory Medicine and Pathology Catholic University, 1981, Ph.D. mccar001@tc.umn.edu 612-625-7454 - office 612-625-5453 - lab

Research Interests:

Tumor cell adhesion, invasion, metastasis

The research in the McCarthy Laboratory focuses on understanding the importance of changes in the relationships between tumor cells and the surrounding extracellular matrix in tumor progression and metastasis. The research in the laboratory is organized into two major areas related to specific tumors. Melanoma, a malignant tumor of the skin, constitutes one of these research focus areas. Ongoing studies in the laboratory address the mechanisms by which an early progression antigen, termed Melanoma Chondroitin Sulfate Proteoglycan (MCSP) enhances adhesion, survival, growth and invasion of primary and metastatic melanomas. MCSP is a transmembrane proteoglycan that can enhance the adhesion and invasion of melanoma cells. Projects related to MCSP-mediated signal transduction, tumor cell survival, and activation of specific proteases important for tumor invasion are currently in progress. Additionally, related studies in prostate cancer are also ongoing in the laboratory. These studies focus on understanding the mechanism by which specific chemotactic cytokines (termed chemokines) stimulate prostate tumor invasion. Research projects are also in progress to study the importance of hyaluronan synthesis in prostate tumor growth, invasion, and metastasis to bone and other organs..

Recent Publications:

• Iida, J., Wilhelmson, K.L., Pei, D., Furcht, L.T., and McCarthy, J.B.  2004.  MT1-MMP promotes human melanoma invasion and growth.  J. Invest. Dermatol. 122:167-176.

• Yang, J., Price, M., Neudauer, C., Xia, H., Simpson, M., and McCarthy, J.B. 2004. Melanoma chondroitin sulfate proteoglycan activates FAK and ERK via separate integrin-dependent mechanisms.  J. Cell Biol. 165:881-891.

• Kim HR, Wheeler MA, Wilson CM, Iida J, Eng D, Simpson MA, McCarthy JB, Bullard KM. 2004. Hyaluronan facilitates invasion of colon carcinoma cells in vitro via interaction with CD44. Cancer Res. 64(13):4569-76.

• Bullard, K. M., Kim, H. R., Wheeler, M. A., Wilson, C. M., Neudauer, C. L., Simpson, M. A., McCarthy, J. B. 2003. Hyaluronan synthase-3 is upregulated in metastatic colon carcinoma cells and manipulation of expression alters matrix retention and cellular growth. Int. J. Cancer. 107: 739-46.

• Simpson, M.A., Wilson, C.M., Furcht, L.T., Spicer, A.P., Oegema, T.R., McCarthy, J.B.  2002. Manipulation of hyaluronan synthase expression in prostate adenocarcinoma cells alters pericellular matrix retention and adhesion to bone marrow endothelial cells. J. Biol. Chem. 277:10050-10057.

• Simpson, M.A., Wilson, C.M, Furcht, L.T. 2002. Inhibition of prostate tumor hyaluronan synthesis impairs subcutaneous growth and vascularization in immunocompromised mice. Am. J. Path. 161: 849-857.

• Iida, J.,Pei, D.,Kang, T.,Simpson, M. A.,Herlyn, M., Furcht, L. T.,McCarthy, J. B. 2001. Melanoma chondroitin sulfate proteoglycan regulates matrix metalloproteinase-dependent human melanoma invasion into type I collagen. J Biol Chem. 276:18786-94.

• Simpson, M. A., Reiland, J., Burger, S. R., Furcht, L. T., Spicer, A. P., Oegema, T. R., Jr., McCarthy, J. B. 2001. Hyaluronan synthase elevation in metastatic prostate carcinoma cells correlates with hyaluronan surface retention, a prerequisite for rapid adhesion to bone marrow endothelial cells. J Biol Chem. 276:17949-57.

Last modified on: Tuesday, August 22, 2006 9:45 AM