Schrank Zachary, Chhabra Gagan, Lin Leo, Iderzorig Tsatsral, Osude Chike, Khan Nabiha, Kuckovic Adijan, Singh Sanjana, Miller Rachel J, Puri Neelu
Department of Biomedical Sciences, University of Illinois College of Medicine at Rockford, Rockford, IL 61107, USA.
Cancers (Basel). 2018 Jul 4;10(7):224. doi: 10.3390/cancers10070224.
Lung cancer is treated with many conventional therapies, such as surgery, radiation, and chemotherapy. However, these therapies have multiple undesirable side effects. To bypass the side effects elicited by these conventional treatments, molecularly-targeted therapies are currently in use or under development. Current molecularly-targeted therapies effectively target specific biomarkers, which are commonly overexpressed in lung cancers and can cause increased tumorigenicity. Unfortunately, several molecularly-targeted therapies are associated with initial dramatic responses followed by acquired resistance due to spontaneous mutations or activation of signaling pathways. Acquired resistance to molecularly targeted therapies presents a major clinical challenge in the treatment of lung cancer. Therefore, to address this clinical challenge and to improve lung cancer patient prognosis, we need to understand the mechanism of acquired resistance to current therapies and develop additional novel therapies. This review concentrates on various lung cancer biomarkers, including EGFR, ALK, and BRAF, as well as their potential mechanisms of drug resistance.
肺癌采用多种传统疗法进行治疗，如手术、放疗和化疗。然而，这些疗法有多种不良副作用。为了规避这些传统治疗引发的副作用，目前正在使用或研发分子靶向疗法。当前的分子靶向疗法有效地靶向特定生物标志物，这些生物标志物在肺癌中通常过度表达，并可导致肿瘤发生性增加。不幸的是，几种分子靶向疗法会出现初始显著反应，随后由于自发突变或信号通路激活而产生获得性耐药。分子靶向疗法的获得性耐药是肺癌治疗中的一个主要临床挑战。因此，为应对这一临床挑战并改善肺癌患者的预后，我们需要了解当前疗法获得性耐药的机制，并开发更多新型疗法。本综述集中讨论各种肺癌生物标志物，包括表皮生长因子受体（EGFR）、间变性淋巴瘤激酶（ALK）和B-Raf原癌基因丝氨酸/苏氨酸激酶（BRAF），以及它们潜在的耐药机制。
