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Targeting the c-MET/HGF signaling pathway in pancreatic ductal adenocarcinoma

Author(s):

Sadaf Ghanaatgar-Kasbi, Shadi Khorrami, Amir Avan, Seyed Amir Aledavoud and Gordon A. Ferns*  

Abstract:


The c-mesenchymal-epithelial transition factor (c-MET) is involved in the tumorigenesis of various cancers. HGF/Met inhibitors are now attracting considerable interest due to their anti-tumor activity in multiple malignancies such as pancreatic cancer. It is likely that within the next few years, HGF/Met inhibitors will become a crucial component for cancer management. In this review, we summarize the role of HGF/Met pathway in the pathogenesis of pancreatic cancer, with particular emphasize on HGF/Met inhibitors in the clinical setting, including Cabozantinib (XL184, BMS-907351), Crizotinib (PF-02341066), MK-2461, Merestinib (LY2801653), Tivantinib (ARQ197), SU11274, Onartuzumab (MetMab), Emibetuzumab (LY2875358), Ficlatuzumab (AV-299), Rilotumumab (AMG 102), NK4 in pancreatic cancer.

Keywords:

c-mesenchymal-epithelial transition factor, HGF/Met inhibitors, pancreatic cancer

Affiliation:

Metabolic syndrome Research center, and Cancer Research Center Mashhad University of Medical Sciences, Mashhad, Metabolic syndrome Research center, and Cancer Research Center Mashhad University of Medical Sciences, Mashhad, Metabolic syndrome Research center, and Cancer Research Center Mashhad University of Medical Sciences, Mashhad, Metabolic syndrome Research center, and Cancer Research Center Mashhad University of Medical Sciences, Mashhad, Brighton & Sussex Medical School, Division of Medical Education, Falmer, Brighton, Sussex BN1 9PH



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