Targeted Therapies in Non-Small Cell Lung Cancer—Beyond EGFR and ALK

Cancers

Sacha I. Rothschild¹ 

[1] Medical Oncology, University Hospital Basel, Petersgraben 4, 4031 Basel, Switzerland; E-Mail

关键词: lung cancer;    targeted cancer therapy;    oncogene;    ROS1;    c-MET;    RET;    BRAF;    HER2;    FGFR1;    DDR2;   

DOI  :  10.3390/cancers7020816

来源: mdpi

【 摘 要 】

Systemic therapy for non-small cell lung cancer (NSCLC) has undergone a dramatic paradigm shift over the past decade. Advances in our understanding of the underlying biology of NSCLC have revealed distinct molecular subtypes. A substantial proportion of NSCLC depends on oncogenic molecular aberrations (so-called “driver mutations”) for their malignant phenotype. Personalized therapy encompasses the strategy of matching these subtypes with effective targeted therapies. EGFR mutations and ALK translocation are the most effectively targeted oncogenes in NSCLC. EGFR mutations and ALK gene rearrangements are successfully being targeted with specific tyrosine kinase inhibitors. The number of molecular subgroups of NSCLC continues to grow. The scope of this review is to discuss recent data on novel molecular targets as ROS1, BRAF, KRAS, HER2, c-MET, RET, PIK3CA, FGFR1 and DDR2. Thereby the review will focus on therapeutic strategies targeting these aberrations. Moreover, the emerging challenge of acquired resistance to initially effective therapies will be discussed.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.