癌症研究
肺癌
克里唑蒂尼
信号转导
间变性淋巴瘤激酶
酪氨酸激酶
后天抵抗
医学
抗药性
癌症
肿瘤科
生物
内科学
细胞生物学
遗传学
恶性胸腔积液
作者
Yanping Yang,Xincheng He,Wenxuan Xiao,Jun Bai,Yi Liu
出处
期刊:Anti-Cancer Drugs
[Ovid Technologies (Wolters Kluwer)]
日期:2023-12-13
卷期号:35 (3): 292-297
标识
DOI:10.1097/cad.0000000000001559
摘要
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.
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