ALK-positive lung cancer: a moving target

被引：107

作者：

Schneider, Jaime L. ^{[1
,2
,3
]}

Lin, Jessica J. ^{[1
,2
,3
]}

Shaw, Alice T. ^{[1
,2
,4
]}

机构：

[1] Massachusetts Gen Hosp, Canc Ctr, Boston, MA 02114 USA

[2] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA

[3] Harvard Med Sch, Boston, MA USA

[4] Novartis Inst Biomed Res, Cambridge, MA 02139 USA

来源：

NATURE CANCER | 2023年 / 4卷 / 03期

关键词：

PREFERRED 1ST-LINE OPTION; OPEN-LABEL; HISTOLOGICAL TRANSFORMATION; REARRANGED ADENOCARCINOMA; ACQUIRED-RESISTANCE; CONFER RESISTANCE; TYROSINE KINASE; TUMOR-ANTIGEN; MOUSE MODEL; CRIZOTINIB;

D O I：

10.1038/s43018-023-00515-0

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Shaw and colleagues discuss the oncogenic roles of ALK in lung cancer, targeting approaches and the mechanisms underlying acquired resistance to ALK-directed therapy. Anaplastic lymphoma kinase (ALK) is a potent oncogenic driver in lung cancer. ALK tyrosine kinase inhibitors yield significant benefit in patients with ALK fusion-positive (ALK(+)) lung cancers; yet the durability of response is limited by drug resistance. Elucidation of on-target resistance mechanisms has facilitated the development of next-generation ALK inhibitors, but overcoming ALK-independent resistance mechanisms remains a challenge. In this Review, we discuss the molecular underpinnings of acquired resistance to ALK-directed therapy and highlight new treatment approaches aimed at inducing long-term remission in ALK(+) disease.

引用

页码：330 / 343

页数：14

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