Novel therapeutic targets in non-small cell lung cancer

被引:68
作者
Alamgeer, Muhammad [1 ,2 ]
Ganju, Vinod [1 ,2 ]
Watkins, D. Neil [2 ]
机构
[1] Monash Med Ctr, Dept Med Oncol, East Bentleigh, Vic 3165, Australia
[2] Monash Univ, Monash Inst Med Res, Clayton, Vic 3168, Australia
关键词
GROWTH-FACTOR RECEPTOR; TYROSINE KINASE INHIBITORS; PHASE-III TRIAL; EGFR MUTATION; OPEN-LABEL; SELECTIVE INHIBITOR; ACQUIRED-RESISTANCE; ANAPLASTIC LYMPHOMA; 1ST-LINE TREATMENT; ANTITUMOR-ACTIVITY;
D O I
10.1016/j.coph.2013.03.010
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Oncogenic driver mutations frequently occur in lung cancer and play role in carcinogenesis. These mutations are usually associated with distinct clinical and histological features and are attractive targets for anticancer therapy. Recently, several molecularly distinct phenotypes of NSCLC based on specific and mutually exclusive genetic derangements have been described. Few targets like epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma kinase (ALK) gene rearrangements have successfully been targeted with EGFR tyrosine kinase inhibitors (TKIs) and crizotinib, respectively. Many more inhibitors of specific driver mutations involving genes like ROS, c-MET, FGFR, mTOR, IGFR and RET are currently under development. However, efforts to target some mutated genes like K-RAS have been unsuccessful. Moreover, the emerging challenge of acquired resistance to initially effective therapy is becoming another major concern. In this review recent data on novel molecular targets and their future prospects are discussed.
引用
收藏
页码:394 / 401
页数:8
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