Department of Medicine, Vanderbilt-Ingram Cancer Center, Nashville, TN 37232–6307, USA.
Lancet Oncol. 2011 Feb;12(2):175-80. doi: 10.1016/S1470-2045(10)70087-5.
Treatment decisions for patients with lung cancer have historically been based on tumour histology. Some understanding of the molecular composition of tumours has led to the development of targeted agents, for which initial findings are promising. Clearer understanding of mutations in relevant genes and their effects on cancer cell proliferation and survival, is, therefore, of substantial interest. We review current knowledge about molecular subsets in non-small-cell lung cancer that have been identified as potentially having clinical relevance to targeted therapies. Since mutations in EGFR and KRAS have been extensively reviewed elsewhere, here, we discuss subsets defined by so-called driver mutations in ALK, HER2 (also known as ERBB2), BRAF, PIK3CA, AKT1, MAP2K1, and MET. The adoption of treatment tailored according to the genetic make-up of individual tumours would involve a paradigm shift, but might lead to substantial therapeutic improvements.
治疗决策肺癌患者历来基于肿瘤组织学。对肿瘤分子成分的某些了解导致了靶向药物的开发，初步发现这些药物很有前景。因此，对相关基因的突变及其对癌细胞增殖和存活的影响有更清晰的认识具有重要意义。我们回顾了目前关于非小细胞肺癌中已被确定为可能对靶向治疗具有临床意义的分子亚群的知识。由于 EGFR 和 KRAS 的突变已在其他地方进行了广泛的综述，因此，在这里，我们讨论了所谓的 ALK、HER2（也称为 ERBB2）、BRAF、PIK3CA、AKT1、MAP2K1 和 MET 驱动突变定义的亚群。根据个体肿瘤的遗传构成进行治疗的采用将涉及范式转变，但可能会带来实质性的治疗改善。
