Abstract
Gastric cancer is a common and lethal malignancy worldwide. It lacks specific clinical symptoms during the early stages, and when detected, the optimal surgical opportunity is lost. Chemotherapy alone offers limited benefits in advanced inoperable disease or postoperative recurrence. Gastric cancer is a heterogeneous tumor involving multiple gene regulations; thus, multi-target combination therapy is the trend in research. The c-MET protein is a tyrosine kinase receptor belonging to the MET family, encoded by the MET proto-oncogene. After binding with its ligand, the hepatocyte growth factor, MET activates cellular signaling pathways in proliferation, motility, migration, and invasion. In addition, it may be abnormally activated in cancers via mutation, amplification, and protein overexpression. We report a 35-year-old male with advanced gastric cancer and bone metastasis who was intolerant to chemotherapy. He was in poor general condition, with thrombocytopenia and anemia. Next-generation sequencing (NGS) suggested MET gene amplification in the tumor. After savolitinib treatment, the condition improved significantly without noticeable adverse reactions and maintained a progression-free status for 14 weeks. This case report provides evidence for MET tyrosine kinase inhibitors in treating gastric cancer patients with MET gene amplification. It also shows that MET detection is a target in gastric cancer.
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