The biology and treatment of EML4-ALK non-small cell lung cancer

被引：483
|
作者：
Sasaki, Takaaki [1 ,2 ]
Rodig, Scott J. [3 ]
Chirieac, Lucian R. [3 ]
Janne, Pasi A. [1 ,2 ,4 ,5 ]
机构：
[1] Dana Farber Canc Inst, Lowe Ctr Thorac Oncol, Boston, MA 02115 USA
[2] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA
[3] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
[4] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA
[5] Harvard Univ, Sch Med, Boston, MA USA
来源：
EUROPEAN JOURNAL OF CANCER | 2010年 / 46卷 / 10期
基金：
美国国家卫生研究院;
关键词：
Non-small cell lung carcinoma; Translocation; Kinase inhibitor; Clinical trial; GROWTH-FACTOR-RECEPTOR; CLINICOPATHOLOGICAL FEATURES; FUSION GENE; ANAPLASTIC LYMPHOMA; TUMOR-SUPPRESSOR; MUTATIONS; ALK; KINASE; KRAS; ADENOCARCINOMA;
D O I：
10.1016/j.ejca.2010.04.002
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The fusion between echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK),has recently been identified in a subset of non-small cell lung cancers (NSCLCs). EML4-ALK is most often detected in never smokers with lung cancer and has unique pathologic features. EML4-ALK is oncogenic both in vitro and in vivo and ALK kinase inhibitors are quite effective in pre-clinical model systems. More recently ALK inhibitors have entered clinical development and remarkably clinical efficacy has been observed in NSCLC patients harbouring EML4-ALK translocations. This review will focus on the biology, clinical characteristics, diagnosis and treatment of EML4-ALK NSCLC. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码：1773 / 1780
页数：8
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