Although patients with ALK-positive non-small cell lung cancer (NSCLC) are initially effective on treatment with ALK tyrosine kinase inhibitors (TKIs), resistance will inevitably develop. Of these patients, 2/3 will develop ALK-independent resistance and little is known about the mechanisms of ALK-independent resistance. In pre-clinical studies, the activation of several bypass signaling pathways has been implicated in the development of resistance, including the MET, EGFR, SRC and IGF1R pathways. Among these, the MET pathway is one of the signaling pathways that has recently been extensively studied, and activation of this pathway is one of the mechanisms of ALK-independent drug resistance. Here, we report a successful case of an advanced NSCLC patient who was resistant to treatment with ALK TKIs and developed MET amplification, who achieved 23 months of progression-free survival after post-line treatment with ensartinib.

中文翻译：

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Ensartinib 可有效治疗多线 ALK-TKI 耐药后伴有 MET 扩增的晚期非小细胞肺癌：病例报告。

尽管 ALK 阳性非小细胞肺癌 (NSCLC) 患者最初使用 ALK 酪氨酸激酶抑制剂 (TKI) 治疗有效，但不可避免地会产生耐药性。这些患者中，2/3 会出现 ALK 独立耐药性，但人们对 ALK 独立耐药性的机制知之甚少。在临床前研究中，多个旁路信号通路的激活与耐药性的发展有关，包括 MET、EGFR、SRC 和 IGF1R 通路。其中，MET通路是最近被广泛研究的信号通路之一，该通路的激活是ALK非依赖性耐药的机制之一。在这里，我们报告了一名晚期 NSCLC 患者的成功病例，该患者对 ALK TKI 治疗耐药并出现 MET 扩增，在恩沙替尼线后治疗后实现了 23 个月的无进展生存期。