Abstract
BACKGROUND: Gastric cancer (GC) is one of the leading contributors to global malignancies incidence and mortality worldwide. Advanced GC had a relatively poor prognosis. The emerging of targeted therapy improved the survival and prognosis of GC patients. In the treatment of GC, crizotinib, although an unapproved drug, has shown satisfactory treatment benefits in some cases. CASE DESCRIPTION: A GC hepatocyte growth factor receptor (MET) amplification patient with extensive abdominal cavity metastasis who was diagnosed as intermediate-low differentiated adenocarcinoma. After 34 months of treatment with crizotinib, the patient's MET gene amplification mutation disappeared and gained high-quality life during this period. However, based on new testing evidence, the patient's tumor lesion did not disappear and there were Class II mutations such as tumor protein p53 (TP53) mutations and kirsten rat sarcoma viral oncogene homologue (KRAS) amplification, Class III mutations such as caspase recruitment domain family member 11 (CARD11), lysine methyltransferase 2D (MLL2), and kinetochore localized astrin binding protein (C15orf23) mutations. Based on genetic testing results, a mini patient-derived xenograft (miniPDX) mouse model was used for drug sensitivity testing to screen effective targeted drugs for this patient. The time window since the miniPDXs model establishment and drug sensitivity results came out took about 2 weeks. The final analysis showed that trametinib exhibited a strong inhibition of tumor cell growth in this sample. CONCLUSIONS: This report describes a GC MET amplification patient who treated with crizotinib for 34 months. During the period, the patient's MET amplification mutation disappeared and gained high-quality life. After drug resistance developed, trametinib was used according to the new mutation sites. Until now. The patient got a good quality of life for three years, which is relatively rare among the reported cases.