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表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)在肺癌治疗领域的应用备受关注,其优势人群是有EGFR突变的患者。然而大多数起始有效的患者经过约6～12个月治疗后会产生获得性耐药现象,其主要的耐药机制包括EGFR二次突变和“激酶转换”机制。EGFRT790M突变占所有耐药的50%,c-Met扩增占获得性耐药的20%左右。其他一些“激酶转换”机制如IGFR-1和mTOR均逐渐进入临床前研究。联合应用多种信号通路抑制剂可能是克服EGFR-TKI获得性耐药的有效方法。全文主要对以上进行综述。
The application of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) in the treatment of lung cancer has attracted much attention, and the predominant population is EGFR mutation patients. However, most of the initial effective patients develop acquired drug resistance after about 6 to 12 months of treatment, and their major mechanisms of resistance include the EGFR secondary mutation and the “kinase conversion” mechanism. EGFRT790M mutation accounts for 50% of all resistance, c-Met amplification accounts for about 20% of acquired resistance. Other “kinase converting” mechanisms such as IGFR-1 and mTOR have gradually entered preclinical studies. Combined use of multiple signal pathway inhibitors may be an effective way to overcome acquired resistance to EGFR-TKI. The full text mainly summarizes the above.