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Current Molecular-Targeted Therapies in NSCLC and Their Mechanism of Resistance

机译:非小细胞肺癌的分子靶向治疗及其耐药机制

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摘要

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.
机译:肺癌可以通过许多常规疗法进行治疗,例如手术,放疗和化疗。但是,这些疗法具有多种不良副作用。为了绕开这些常规疗法引起的副作用,目前正在使用或正在开发分子靶向疗法。当前的分子靶向疗法有效地靶向了特定的生物标志物,这些标志物通常在肺癌中过表达,并可能导致致癌性增加。不幸的是,几种分子靶向疗法与最初的剧烈反应有关,随后由于自发突变或信号通路的激活而获得了耐药性。获得的对分子靶向疗法的抗性在肺癌的治疗中提出了主要的临床挑战。因此,为了应对这一临床挑战并改善肺癌患者的预后,我们需要了解对当前疗法获得性耐药的机制,并开发其他新颖疗法。这篇综述着重于各种肺癌生物标志物,包括EGFR,ALK和BRAF,以及它们潜在的耐药性机制。

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