MET is associated with the progression of pancreatic cancer; therefore, we evaluated the effect of a MET inhibitor, crizotinib, on peritoneal dissemination of pancreatic cancer.
The expression levels of h-TERT, CK20, CEA, and C-MET were detected in a model of circulating micrometastasis in pancreatic cancer that were enriched using immune-magnetic separation of the circulating cancer cells.
Hepatocyte growth factor (HGF) is a stromal-derived cytokine that plays a crucial role in invasion and metastasis of tumor cells through the interaction with HGF receptor, c-Met, which is frequently overexpressed in pancreatic cancer.
We have established a clinically relevant animal model for pancreatic cancer by developing a double transgenic mouse model (called MET) that expresses human MUC1 as self molecule and develops spontaneous tumors of the pancreas.
These data suggest that the Met/HGF receptor may be involved in the growth and behavior of pancreatic cancer and may contribute to the ductal phenotype of these tumors.