Resistance to molecularly targeted therapy in non-small-cell lung cancer

被引：43
|
作者：
Asao, Tetsuhiko [1 ]
Takahashi, Fumiyuki [1 ]
Takahashi, Kazuhisa [1 ]
机构：
[1] Juntendo Univ, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan
来源：
RESPIRATORY INVESTIGATION | 2019年 / 57卷 / 01期
关键词：
Lung cancer; Molecularly targeted therapy; Acquired resistance; EGFR; ALK; TYROSINE KINASE INHIBITORS; BIM DELETION POLYMORPHISM; ACQUIRED-RESISTANCE; EGFR MUTATIONS; OPEN-LABEL; 1ST-LINE TREATMENT; RESPONSE DURATION; MET AMPLIFICATION; CLINICAL ACTIVITY; T790M MUTATION;
D O I：
10.1016/j.resinv.2018.09.001
中图分类号：
R56 [呼吸系及胸部疾病];
学科分类号：
摘要：
The discovery of oncogenic driver gene mutations, including epidermal growth factor receptor (EGFR) mutation, anaplastic lymphoma kinase (ALK) fusion, ROS proto-oncogene 1 (ROS1) fusion, and ret proto-oncogene (RET) fusion, has led to the development of molecularly targeted therapy for non-small-cell lung cancer (NSCLC). This therapy has changed the standard of care for NSCLC. Despite the dramatic response to molecularly targeted therapy, almost all patients ultimately develop resistance to the drugs. To understand the mechanisms of resistance to molecularly targeted agents, it is essential to understand the molecular pathways of NSCLC. Here, we review the mechanisms of resistance to molecularly targeted therapy and discuss strategies to overcome drug resistance. (C) 2018 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.
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页码：20 / 26
页数：7
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