Program Leader, Tumor Biology and Progression Research Program
Professor, Department of Laboratory Medicine and Pathology

mccar001@umn.edu
612-625-7454 — office
612-625-5453- lab
Preferred contact method: E-mail

Dr. McCarthy received his B.A. from Susquehanna University in 1974. He obtained his Ph.D. in 1981 from Catholic University in Washington, D.C. His graduate laboratory training was at the National Institute of Dental Research, in Bethesda Maryland, under the mentorship of Dr. Sharon M. Wahl. His graduate research topic focused on acute and chronic inflammation. His specific research emphasis was on identifying important signaling pathways in activated macrophages that regulate the expression of collagenolytic matrix metalloproteinases. He accepted a postdoctoral associate position in 1981 at the University of Minnesota. His postdoctoral research addressed mechanisms by which the extracellular matrix proteins fibronectin and laminin promote the adhesion, migration and invasion of metastatic tumor cells. His current research focuses on the importance of cell surface proteoglycans and glycosaminoglycans in mediating tumor adhesion, growth and metastasis. He is currently a professor of Laboratory Medicine and Pathology at the University of Minnesota in Minneapolis. Dr. McCarthy also serves as program leader for the Tumor Biology and Progression Research Program at the Masonic Cancer Center. He chairs the Tumor Progression and Metastasis Grants Review Panel at NIH and he also serves on the Research Council of the American Cancer Society.

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.

Selected Publications

Eisenmann, K.M., McCarthy, J.B., Simpson, M.A., Keely, P.J., Guan, J-L., Tachibana, K., Furcht, L.T., and J. Iida. 1999. Melanoma chondroitin sulfate proteoglycan signaling through cdc42, Ack-1 and p130cas regulates integrin-mediated cell spreading. Nat Cell Biol. 1:507-513.

Iida, J., Pei, D., Kang, T., Simpson, M.A., Herlyn, M., Furcht, L.T., and McCarthy, J.B. 2001. Melanoma chondroitin sulfate proteoglycan regulates matrix metalloproteinase-dependent human melanoma invasion into type I collagen. J. Biol. Chem. 276:18786-18794.

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

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):4569-4576.