CAJ | 학술논문

棘皮动物微管相关蛋白样4-间变性淋巴瘤激酶(echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase,EML4-ALK)作为近年来新发现的一个致癌基因,参与了非小细胞肺癌(NSCLC)的发生过程。以 EML4-ALK 为靶点的分子靶向药物成为治疗 NSCLC 的焦点,包括crizotinib 在内的多种 ALK 酪氨酸激酶抑制剂在临床前期研究及 ALK 融合基因阳性的 NSCLC 患者中疗效显著。然而,随之出现的耐药问题也引起了大家的关注。现对 EML4-ALK 酪氨酸激酶抑制剂耐药机制的研究进展和克服耐药的新策略进行综述。
극피동물미관상관단백양4-간변성림파류격매(echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase,EML4-ALK)작위근년래신발현적일개치암기인,삼여료비소세포폐암(NSCLC)적발생과정。이 EML4-ALK 위파점적분자파향약물성위치료 NSCLC 적초점,포괄crizotinib 재내적다충 ALK 락안산격매억제제재림상전기연구급 ALK 융합기인양성적 NSCLC 환자중료효현저。연이,수지출현적내약문제야인기료대가적관주。현대 EML4-ALK 락안산격매억제제내약궤제적연구진전화극복내약적신책략진행종술。
Echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase is recently identified as an oncogenic transforming fusion gene in non-small cell lung cancer (NSCLC),which participated in the process of NSCLC.ALK tyrosine kinase inhibitors,including crizotinib,are effective treatments in preclinical models and patients with ALK+ NSCLC.However,due to the high resistance rate of crizotinib,the drug resistance problem has aroused the attention of all.This review aims to discuss molecular mechanisms of resistance to crizotinib in patients with ALK+ NSCLC as well as the current strategies.