Crizotinib in the management of advanced-stage non-small-cell lung cancer

被引：1
|
作者：
Loong, Herbert H. [1 ,2 ]
Mok, Kevin [3 ]
Leung, Linda K. S. [1 ,2 ]
Mok, Tony S. K. [1 ,2 ]
机构：
[1] Chinese Univ Hong Kong, Fac Med, State Key Lab Oncol South China, Dept Clin Oncol, Shatin, Hong Kong, Peoples R China
[2] Prince Wales Hosp, Shatin, Hong Kong, Peoples R China
[3] Chinese Univ Hong Kong, Fac Med, Shatin, Hong Kong, Peoples R China
来源：
FUTURE ONCOLOGY | 2015年 / 11卷 / 05期
关键词：
acquired resistance; brain metastases; c-Met; crizotinib; EML4-ALK fusion; non-small-cell lung cancer; ROS1; ANAPLASTIC LYMPHOMA KINASE; RECEPTOR TYROSINE KINASE; 1ST-LINE TREATMENT; ALK INHIBITOR; OPEN-LABEL; ANTITUMOR EFFICACY; C-MET; CHEMOTHERAPY; GENE; ROS1;
D O I：
10.2217/FON.14.314
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Rearrangement of ALK gene has been identified as exerting a potent transforming effect as driver oncogene in patients with non-small-cell lung cancer (NSCLC). Crizotinib is a small-molecule oral inhibitor of ALK, c-Met/HGF receptor and ROS1 receptor kinases. Its efficacy in ALK-rearranged NSCLC has been established. Crizotinib's effect on ROS1 receptor kinases and c-Met with relevance to NSCLC is also actively being explored. Resistance mechanisms such as secondary gatekeeper mutations in ALK gene and activation of other oncogenes have been identified to confer acquired resistance to crizotinib. This article reviews the pharmacological properties of crizotinib, preclinical and clinical results that led to its approval in ALK-positive NSCLC and current directions of clinical research in overcoming crizotinib resistance.
引用
收藏
页码：735 / 745
页数：11
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