MET and colorectal carcinoma: Furthermore, c-MET activation mediates resistance to TKIs, chemotherapy, cetuximab, and radiotherapy in CRC patients.677 c-MET mediates radio-resistance by increasing cell motility and inhibiting apoptosis through autocrine and paracrine signaling.695 HGF co-amplification leads to clinical resistance in MET-amplified esophagogastric cancer.696 In conclusion, c-MET/HGF overexpression is an independent biomarker of poor prognosis and drug resistance in patients with various hematologic and solid tumors.