Targeting EGFR and ALK in NSCLC: current evidence and future perspective.

Pub Date : 2016-06-01 Epub Date: 2016-06-23 DOI:10.2217/lmt-2016-0005
Chiara Bennati, Luca Paglialunga, Biagio Ricciuti, Giulio Metro, Luca Marcomigni, Alessio Gili, Lucio Crinò
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Abstract

The advent of molecular therapy targeting specific driver oncogenes has dramatically changed the prognosis of a subset of NSCLC, dilating survival and improving the quality of life of patients with advanced disease. Two of the major targets for treatment with receptor TKIs are the activated mutated forms of the EGFR and the ALK gene fusions. In advanced NSCLC patients harboring EGFR mutations or ALK rearrangements, the use of TKIs in the first-line setting, have provided unexpected large progression-free survival and overall survival benefits, compared with cytotoxic chemotherapy. However, despite initial responses and durable remissions, the development of resistance inevitably leads to treatment failure. The aim of this review is to discuss the treatment strategy currently used for tumors harboring these two genetic targets and to focus on what will be available in clinical practice in the near future.

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靶向EGFR和ALK在NSCLC中的作用:当前证据和未来展望。
靶向特定驱动致癌基因的分子疗法的出现极大地改变了一部分NSCLC的预后,扩大了晚期疾病患者的生存率,提高了患者的生活质量。受体TKIs治疗的两个主要靶点是EGFR和ALK基因融合的活化突变形式。在携带EGFR突变或ALK重排的晚期NSCLC患者中,与细胞毒性化疗相比,在一线环境中使用TKIs提供了意想不到的大的无进展生存率和总体生存益处。然而,尽管有最初的反应和持久的缓解,耐药性的发展不可避免地会导致治疗失败。这篇综述的目的是讨论目前用于携带这两个基因靶点的肿瘤的治疗策略,并关注在不久的将来临床实践中可用的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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