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分子靶向药物的出现使癌症的治疗步入了新的阶段,与传统的化疗药物相比,具有瞄准特定的分子靶点、不良反应小和特异性强等。继EGFR-TKI后,针对EML4-ALK融合基因为靶点的crizotinib(PF-02341066)成为NSCLC靶向药物中的耀眼新星。EML4-ALK融合基因的发生率约为4%～7%,ALK+的患者在多程治疗后接受crizotinib治疗1年生存率可达到77%,2年生存率为64%。此外,临床病理学研究提示,EML4-ALK融合基因更倾向于发生在青年、男性、不吸烟或少吸烟的腺癌患者中,并且EML4-ALK融合基因与EGFR突变和K-ras突变存在互斥性。因此crizotinib将来可能作为TKI治疗失败的腺癌患者的新选择。
The emergence of molecular targeted drugs to cancer treatment entered a new phase, compared with the traditional chemotherapy drugs, targeting a specific molecular target, adverse reactions and specificity and so on. Following the EGFR-TKI, crizotinib (PF-02341066) targeting the EML4-ALK fusion gene becomes a dazzling new star in NSCLC-targeted drugs. The incidence of EML4-ALK fusion gene was about 4% to 7%. The ALK + patients receiving crizotinib after multiprocessing had a 1-year survival rate of 77% and a 2-year survival rate of 64%. In addition, clinicopathological studies suggest that the EML4-ALK fusion gene is more likely to occur in young, males, non-smokers or less-smokers with adenocarcinoma, and the EML4-ALK fusion gene is mutually exclusive with EGFR and K-ras mutations Sex. Therefore, crizotinib may serve as a new option for patients with adenocarcinoma who fail the treatment of TKI in the future.