New Targetable Oncogenes in Non-Small-Cell Lung Cancer

被引：262

作者：

Oxnard, Geoffrey R. ^{[1
,2
]}

Binder, Adam ^{[3
]}

Jaenne, Pasi A. ^{[1
,2
]}

机构：

[1] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Boston, MA USA

[3] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA

来源：

JOURNAL OF CLINICAL ONCOLOGY | 2013年 / 31卷 / 08期

基金：

美国国家卫生研究院;

关键词：

GROWTH-FACTOR RECEPTOR; ANAPLASTIC LYMPHOMA KINASE; PHASE-II TRIAL; SIGNALING PATHWAY; THYROID-CANCER; BRAF MUTATIONS; GENE; INHIBITOR; PIK3CA; TRASTUZUMAB;

D O I：

10.1200/JCO.2012.42.9829

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The identification of oncogenic driver mutations underlying sensitivity to epidermal growth factor receptor and anaplastic lymphoma kinase tyrosine kinase inhibitors has led to a surge of interest in identifying additional targetable oncogenes in non-small-cell lung cancer. A number of new potentially oncogenic gene alterations have been characterized in recent years, including BRAF mutations, HER2 insertions, PIK3CA mutations, FGFR1 amplifications, DDR2 mutations, ROS1 rearrangements, and RET rearrangements. In this review, we will discuss the techniques used to discover each of these candidate oncogenes, the prevalence of each in non-small-cell lung cancer, the preclinical data supporting their role in lung cancer, and data on small molecular inhibitors in development. J Clin Oncol 31:1097-1104. (C) 2013 by American Society of Clinical Oncology

引用

页码：1097 / 1104

页数：8

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