间变性淋巴瘤激酶
碱性抑制剂
癌症研究
酪氨酸激酶
突变体
酪氨酸激酶抑制剂
激酶
肺癌
突变
靶向治疗
后天抵抗
生物
癌症
药理学
基因
遗传学
医学
信号转导
内科学
恶性胸腔积液
作者
Aya Shiba‐Ishii,Ted W. Johnson,Ibiayi Dagogo‐Jack,Mari Mino‐Kenudson,Theodore R. Johnson,Ping Wei,Scott L. Weinrich,Michele McTigue,Makeba Walcott,Linh Nguyen-Phuong,Kristin Dionne,Adam Acker,Lesli A. Kiedrowski,Andrew Do,Jennifer Peterson,Jaimie L. Barth,Beow Y. Yeap,Justin F. Gainor,W. Marston Linehan,Satoshi Yoda,Aaron N. Hata
出处
期刊:Nature cancer
[Nature Portfolio]
日期:2022-06-20
卷期号:3 (6): 710-722
被引量:45
标识
DOI:10.1038/s43018-022-00399-6
摘要
Lorlatinib is currently the most advanced, potent and selective anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor for the treatment of ALK-positive non-small cell lung cancer in the clinic; however, diverse compound ALK mutations driving therapy resistance emerge. Here, we determine the spectrum of lorlatinib-resistant compound ALK mutations in patients, following treatment with lorlatinib, the majority of which involve ALK G1202R or I1171N/S/T. We further identify structurally diverse lorlatinib analogs that harbor differential selective profiles against G1202R versus I1171N/S/T compound ALK mutations. Structural analysis revealed increased potency against compound mutations through improved inhibition of either G1202R or I1171N/S/T mutant kinases. Overall, we propose a classification of heterogenous ALK compound mutations enabling the development of distinct therapeutic strategies for precision targeting following sequential tyrosine kinase inhibitors.
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