K. Fukahi, M. Fukasawa, G. Neufeld, J. Itakura, and M. Korc. Expression of neuropilins in pancreatic cancer. Clinical Cancer Res., 10: 581-590, 2004.
M. Fukasawa, and M. Korc. Vascular Endothelial Growth Factor-Trap Suppresses Tumorigenicity in Pancreatic Cancer Cell Lines. Clinical Cancer Res., 10:3327-3332, 2004.
N.B. Arnold, K. Ketterer, J. Kleeff, H. Friess, M. W. Büchler, and M. Korc. Thioredoxin is downstream of Smad7 in a pathway that promotes growth and suppresses cisplatin-induced apoptosis in pancreatic cancer. Cancer Res., 64:3599-3606, 2004.
K. Matsuda, T. Idezawa, X.J. You, N.H. Kothari, H. Fan, and M. Korc Multiple mitogenic pathways in pancreatic cancer cells are blocked by a truncated EGF receptor. Cancer Res., 62: 5611-5617, 2002.
M. Korc Pathways for aberrant angiogenesis in pancreatic cancer. Molecular Cancer, 2: 1-8, 2003.
Research / Lab Interests
Molecular biology of pancreatic cancer; mechanisms of action of peptide hormones and growth factors; abnormal gain of function through negative pathways; resistance of cancer cells to apoptosis; tumor angiogenesis.
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 system that is most often studied is pancreatic cancer. 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.
Grants, Honors, Invited Lectures
Dysregulation of TGF-beta Actions in Pancreatic Cancer, NCI, RO1 CA-75059, 09/30/97 - 02/28/07.
The overall goals of this project are to assess the role of TGF-betas and their receptors in pancreatic cancer.
EGF Receptors and Pancreatic Cancer, NCI, RO1 CA-40162, 04/01/89-11/30/05.
The overall goals of this project are to study the role of the EGF receptor family in pancreatic cancer, compare the signaling pathways activated by these receptors, and evaluate the effectiveness of dominant-negative EGF receptor constructs and chemical inhibitors that target the EGFR tyrosine kinase to suppress pancreatic cancer cell growth.
Role of Neuropilins in Pancreatic Cancer, NCI, R01 CA-102687, 09/30/03-08/31/08.
The overall goal of this project is to find out whether neuropilins contribute to VEGFR-dependent signaling pathways.
Role of Glypican-1 in Pancreatic Cancer, NCI, R01 CA101306, 04/01/03-03/31/08.
The overall goals of this project is to determine the clinical significance of glypican-1 expression in pancreatic cancer cells in vivo; determine the biological significance of glypican-1 expression in pancreatic cancer cells; investigate the basis for the unique role of glypican-1 in cell growth control.
