随着下一代测序（NGS）在实体瘤中的广泛使用，间充质到上皮转化因子（MET）重排/融合已在多种癌症类型中得到证实。 MET 扩增和 MET 外显子 14 跳跃突变诱导蛋白质自磷酸化；然而，MET融合的致病机制和药物敏感性仍不清楚。以下报告描述了一名被诊断为携带 TFG-MET 基因融合的鳞状肺癌患者的临床病例。体外试验表明，由于 TFG-MET 重排，MET 磷酸化和致癌能力均被克唑替尼治疗抑制。该患者接受克唑替尼治疗，获得持续部分缓解超过 17 个月。总的来说，细胞分析和我们的病例报告强调了 MET 融合作为实体瘤个性化靶向治疗的预测生物标志物的潜力。© 作者 2024。由牛津大学出版社出版。

With the widespread use of next-generation sequencing (NGS) for solid tumors, mesenchymal-to-epithelial transition factor (MET) rearrangement/fusion has been confirmed in multiple cancer types. MET amplification and MET exon 14 skipping mutations induce protein autophosphorylation; however, the pathogenic mechanism and drug sensitivity of MET fusion remain unclear. The following report describes the clinical case of a patient diagnosed with squamous lung cancer bearing a TFG-MET gene fusion. In vitro assays demonstrated MET phosphorylation and oncogenic capacity due to the TFG-MET rearrangement, both of which were inhibited by crizotinib treatment. The patient was treated with crizotinib, which resulted in sustained partial remission for more than 17 months. Collectively, cellular analyses and our case report emphasize the potential of MET fusion as a predictive biomarker for personalized target therapy for solid tumors.© The Author(s) 2024. Published by Oxford University Press.