MET and neoplasm: Data from cellular and animal tumor models suggest that the underlying biological mechanisms for tumorgenicity of c-Met are achieved in three different ways: (i) with the establishment of HGF/c-Met autocrine loops; (ii) via c-Met or HGF over-expression; and (iii) in the presence of kinase-activating mutations in the c-Met receptor coding sequence [28,30-32].