HER2 Confers Resistance to Foretinib Inhibition of MET-Amplified Esophageal Adenocarcinoma Cells

The mechanism for foretinib growth inhibition in MET-amplified EAC tumor cells is demonstrated. The interplay of dual MET/HER2 overexpression in the AKT and ERK pathways for esophageal cancer is described. Therefore, combination therapy could be a novel strategy for EAC with amplification of both MET and HER2.