CAJ | 학술논문

随着分子生物学的发展，晚期非小细胞肺癌的治疗由传统的化疗转向以基因分型为指导的分子靶向治疗。其中应用较多的是表皮生长因子受体酪氨酸激酶抑制剂（EGFR-TKI）类药物。然而EGFR-TKI 的耐药问题近年来受到越来越多的关注，其机制主要有 EGFR 基因二次突变，c-MET、人类表皮生长因子受体2（Her2）等靶基因的扩增，组织表型的改变，旁路途径的激活，p53基因的缺失，细胞信号通路负反馈的减弱以及多重机制叠加等。
수착분자생물학적발전，만기비소세포폐암적치료유전통적화료전향이기인분형위지도적분자파향치료。기중응용교다적시표피생장인자수체락안산격매억제제（EGFR-TKI）류약물。연이EGFR-TKI 적내약문제근년래수도월래월다적관주，기궤제주요유 EGFR 기인이차돌변，c-MET、인류표피생장인자수체2（Her2）등파기인적확증，조직표형적개변，방로도경적격활，p53기인적결실，세포신호통로부반궤적감약이급다중궤제첩가등。
Since the development of molecular biology,the treatment of advanced non-small cell cancer is shifting from traditional chemotherapy into molecular targeted therapy with genotyping as a guide′s help.The most widely used is epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs).With the appli-cation of EGFR-TKIs,the resistances to EGFR inhibitors are paid more and more attention,in recent years. The main mechanisms of acquired resistances are as follows:secondary mutation of the EGFR gene,amplifica-tion of c-MET,Her2 and other target genes,histological transformation,activation of the bypass mechanisms, loss of p53,the relief of negative feedback loops,overlap of mechanisms,etc.