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Of note, over-activation of the HGF/MET pathway through germline MET and sporadic MET mutations or even protein over-expression increases tumorigenesis and tumor progressions in numerous cancer forms, such as renal cell carcinoma, metaplasia-dysplasia-adenocarcinoma evolution in esophageal cancer, osteosarcomas, and melanomas, as well as brain, gastric, gliomas, breast, and head and neck cancers [1, 4,5,6]

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