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©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 14, 2014; 20(26): 8458-8470
Published online Jul 14, 2014. doi: 10.3748/wjg.v20.i26.8458
Published online Jul 14, 2014. doi: 10.3748/wjg.v20.i26.8458
c-Met signaling in the development of tumorigenesis and chemoresistance: Potential applications in pancreatic cancer
Daniel Delitto, Steven J Hughes, Kevin E Behrns, Jose G Trevino, Department of Surgery, University of Florida-Gainesville, Gainesville, FL 32610, United States
Eva Vertes-George, Department of Pathology, University of Florida-Gainesville, Gainesville, FL 32610, United States
Author contributions: All the authors contributed to this manuscript.
Correspondence to: Jose G Trevino, MD, Department of Surgery, University of Florida-Gainesville, 1600 SW Archer Rd, Rm 6175, PO Box 100109, Gainesville, FL 32610, United States. jose.trevino@surgery.ufl.edu
Telephone: +1-352-2737967 Fax: +1-352-2650761
Received: September 23, 2013
Revised: December 18, 2013
Accepted: April 1, 2014
Published online: July 14, 2014
Processing time: 294 Days and 7.8 Hours
Revised: December 18, 2013
Accepted: April 1, 2014
Published online: July 14, 2014
Processing time: 294 Days and 7.8 Hours
Core Tip
Core tip: As one of the leading causes of cancer-related deaths, pancreatic cancer remains elusive to our current therapeutic options. These modest advances in current therapies for pancreatic cancer have led to the recognition and development of targeted therapies toward tyrosine kinase receptors such as the c-Met receptor. In this review, we characterize the role of c-Met in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of c-Met as a therapeutic target in pancreatic cancer.