Medical Oncology Department, Hospital de Mataró, Carretera de la Cirera, s/n, 08304 Mataró, Barcelona, Spain.
Cancer Treat Rev. 2014 Feb;40(1):93-101. doi: 10.1016/j.ctrv.2013.06.002. Epub 2013 Jul 3.
The discovery of mutated oncogenes has opened up a new era for the development of more effective treatments for non-small cell lung cancer patients (NSCLC) harbouring EGFR mutations. However, patients with EGFR-activating mutation ultimately develop acquired resistance (AR). Several studies have identified some of the mechanisms involved in the development of AR to EGFR tyrosine kinase inhibitors (TKI) that can be potential therapeutic strategies, although in up to 30% of cases, the underlying mechanism of AR are still unexplained. In this review we aim to summarize the main mechanisms of AR to EGFR TKI and some clinical strategies that can be used in the daily clinical practice to overcome this resistance and try to prolong the outcomes in this subgroup of patients.
突变致癌基因的发现为开发更有效的治疗方法开辟了新纪元,适用于携带 EGFR 突变的非小细胞肺癌 (NSCLC) 患者。然而,携带 EGFR 激活突变的患者最终会产生获得性耐药 (AR)。有几项研究已经确定了一些与 EGFR 酪氨酸激酶抑制剂 (TKI) 耐药相关的机制,这些机制可能成为潜在的治疗策略,尽管在多达 30%的情况下,耐药的潜在机制仍未得到解释。在这篇综述中,我们旨在总结 EGFR TKI 耐药的主要机制,以及一些可以在日常临床实践中用于克服这种耐药的临床策略,试图延长这部分患者的预后。