Ying Huang, Pei Shu, Shiyuan Gu, Feng Wen, Xin Wang
Our findings suggest that the addition of savolitinib to standard chemotherapy and a VEGF inhibitor may have contributed additional antitumor activity in this patient with MET-amplified mCRC. However, the independent contribution of savolitinib cannot be determined, and this observation should be regarded as hypothesis-generating and warrants validation in prospective studies.
BACKGROUND: Metastatic colorectal cancer (mCRC) is associated with poor prognosis and low survival rates, with acquired resistance limiting the durability of standard therapies. Mesenchymal-epithelial transition factor (MET) amplification is a rare but potentially actionable molecular alteration that has been implicated in treatment resistance, while clinical evidence supporting MET-directed combination therapy in mCRC remains limited.
CASE PRESENTATION: We report a rare case of a young patient with KRAS/NRAS/BRAF wild-type descending colon cancer with liver metastases and de novo MET amplification detected in the pretreatment primary tumor. After achieving stable disease with second-line FOLFIRI plus bevacizumab, savolitinib, a highly selective MET tyrosine kinase inhibitor (TKI), was added to the ongoing regimen. The patient subsequently achieved marked radiologic and pathological regression during combination treatment, suggesting a possible additive contribution of MET inhibition.
CONCLUSION: Our findings suggest that the addition of savolitinib to standard chemotherapy and a VEGF inhibitor may have contributed additional antitumor activity in this patient with MET-amplified mCRC. However, the independent contribution of savolitinib cannot be determined, and this observation should be regarded as hypothesis-generating and warrants validation in prospective studies.