Parameter
| Biomarker | c-MET (mesenchymal-epithelial transforming factor) | Full name | MET proto-oncogene, receptor tyrosine kinase | Molecular Type | Protein/nucleic acid (DNA/RNA) |
|---|---|---|---|---|---|
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, Prediction | ||
| Disease | Gastric Cancer | Disease Subtypes | / | ||
| Organ | Stomach | Test Sample / Technology Platform | Tumor tissues (IHC, FISH, NGS), circulating tumor DNA (ctDNA, NGS) | ||
| Pathobiological Mechanisms | About 5%-10% gastric cancer has MET gene amplification or protein overexpression, which promotes tumor proliferation, invasion and metastasis by activating HGF/c-MET pathway. It is an important mechanism of chemotherapy resistance and HER2-targeted therapy resistance in gastric cancer | ||||
| Clinical Availability Status | Clinical research stage: it is in phase II clinical verification (such as MET inhibitors combined with chemotherapy) and is not used as a routine test | ||||
| Notes and Dynamics | It is a potential biomarker for targeted therapy of gastric cancer, especially for patients with HER2 targeted resistance caused by MET amplification. Combined with MET inhibitors can reverse drug resistance. Dynamic monitoring of MET amplification by ctDNA can detect drug resistance at an early stage, which is a key target to overcome drug resistance in gastric cancer | ||||