| | |

Murray Korc, M.D.

Contact Information:

Professional Interests:

Molecular biology of pancreatic cancer; abnormal gain of function through negative pathways; resistance of cancer cells to apoptosis; genetic mouse models of pancreatic cancer; tumor angiogenesis; role of microRNAs in pancreatic cancer.

Dr. Korc completed his undergraduate studies at Brooklyn College in 1968, majoring in Biology. He received his medical degree in 1974 from Albany Medical College. In 1977, he completed a residency in internal medicine at Albany Medical Center. In 1979, he completed training in endocrinology, diabetes and metabolism at University of California, San Francisco. He also completed three years of postdoctoral training at the same Institution in 1981. He then joined the faculty of the Department of Medicine at the University of Arizona in Tucson as an assistant professor. In 1985 be became an associate professor, with joint appointments in Medicine and Biochemistry at that Institution. In 1989 he moved to UC Irvine to become the Chief of the Division of Endocrinology, Diabetes and Metabolism, and Professor of Medicine and Biological Chemistry. He was also a member of the UC Irvine Cancer Center, and a Program Leader in Growth Factor Signaling at the Cancer Center. In 1996 he also received an appointment in the Department of Pharmacology at that Institution. In 2003, Dr. Korc joined the faculty at Dartmouth as Professor and Chair of Medicine and Professor of Pharmacology and Toxicology.

Most of the work in Dr. Korc's laboratory explores aberrant signaling pathways in cancer cells. Studies include signaling by the epidermal growth factor (EGF) receptor, fibroblast growth factor (FGF) receptors, transforming growth factor beta (TGF-b) receptors and vascular endothelial cell growth factor (VEGF) receptors. The potential role of co-receptors such as glypican-1 and neuropilins are also being actively investigated. The model systems that are most often studied are cultured cell lines and genetic mouse models. The overall hypothesis guiding the studies of pancreatic cancer is that superimposed on alterations in oncogene and tumor suppressor gene functions, there is evidence for excessive mitogenic signaling, loss of negative growth constraints, and abnormal gain of function through negative signaling pathways, through suppression of differentiation, through excessive resistance to apoptosis, and through aberrant angiogenesis. Knowledge gained from these studies is being used to devise novel therapeutic strategies for this deadly disease.