Lin Luping, Bivona Trever G
Division of Hematology/Oncology, Department of Medicine, USCF Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158, USA.
Chemother Res Pract. 2012;2012:817297. doi: 10.1155/2012/817297. Epub 2012 Aug 29.
The epidermal growth factor receptor (EGFR) is a well-characterized oncogene that is frequently activated by somatic kinase domain mutations in non-small cell lung cancer (NSCLC). EGFR TKIs are effective therapies for NSCLC patients whose tumors harbor an EGFR activating mutation. However, EGFR TKI treatment is not curative in patients because of both primary and secondary treatment resistance. Studies over the last decade have identified mechanisms that drive primary and secondary resistance to EGFR TKI treatment. The elucidation of mechanisms of resistance to EGFR TKI treatment provides a basis for the development of therapeutic strategies to overcome resistance and enhance outcomes in NSCLC patients. In this paper, we summarize the mechanisms of resistance to EGFR TKIs that have been identified to date and discusses potential therapeutic strategies to overcome EGFR TKI resistance in NSCLC patients.
表皮生长因子受体（EGFR）是一种特征明确的癌基因，在非小细胞肺癌（NSCLC）中常因体细胞激酶结构域突变而被激活。EGFR酪氨酸激酶抑制剂（EGFR TKIs）是治疗肿瘤携带EGFR激活突变的NSCLC患者的有效疗法。然而，由于原发性和继发性治疗耐药性，EGFR TKI治疗对患者并非治愈性的。过去十年的研究已经确定了导致对EGFR TKI治疗原发性和继发性耐药的机制。对EGFR TKI治疗耐药机制的阐明为开发克服耐药性并改善NSCLC患者预后的治疗策略提供了基础。在本文中，我们总结了迄今为止已确定的对EGFR TKIs耐药的机制，并讨论了克服NSCLC患者EGFR TKI耐药性的潜在治疗策略。
