EML4-ALK融合介导EGFR-TKI耐药晚期肺腺癌个案报告  

EML4-ALK fusion-mediated EGFR-TKI resistant in advanced lung adenocarcinoma:a case report

作　　者：赵妍妍 张以若 吕遐智 刘萍萍[2] 笪洁[2] 杜瀛瀛[2] ZHAO Yanyan;ZHANG Yiruo;LÜXiazhi;LIU Pingping;DA Jie;DU Yingying(Department of Oncology,the Second Affiliated Hospital of Bengbu Medical Colledge,Bengbu,233000,Anhui,China;Department of Oncology,the First Affiliated Hospital of Anhui Medical University,Hefei,230000,Anhui,China;Department of Oncology,Lu’an Hospital of Anhui Medical University,Lu’an,237000,Anhui,China)

机构地区：[1]蚌埠医学院第二附属医院肿瘤内科,安徽蚌埠233000 [2]安徽医科大学第一附属医院肿瘤内科,安徽合肥230000 [3]安徽医科大学附属六安医院肿瘤科,安徽六安237000

出　　处：《肿瘤药学》2023年第4期424-426,共3页Anti-Tumor Pharmacy

摘　　要：表皮生长因子受体(EGFR)基因突变和间变性淋巴瘤激酶(ALK)基因融合的发现显著改变了非小细胞肺癌的治疗模式,并使患者生存显著获益。ALK融合突变是EGFR酪氨酸激酶抑制剂(TKI)耐药的机制之一。我们报告了1例64岁晚期肺腺癌女性患者,其存在EGFR突变,并在EGFR-TKI耐药后发生了ALK融合,通过先后使用EGFR-TKI或ALK-TKI获得了长期生存,为ALK融合介导的EGFR-TKI耐药患者的靶向治疗药物选择提供参考。The identification of genetic modifications in the epidermal growth factor receptor(EGFR)and anaplastic lymphoma kinase(ALK)in non-small cell lung cancers has resulted in notable shifts in the approach to treatment,and has shown considerable improvements in patient survival rates.Research indicates that the fusion mutation of the ALK gene is one of the mechanisms responsible for resistance to EGFR-tyrosine kinase inhibitors(TKI).In this case report,we present the case of a 64-year-old female patient with advanced lung adenocarcinoma,who initially harbored an EGFR mutation but subsequently developed ALK fusion following treatment with EGFR-TKIs.Through sequential using EGFR-TKIs or ALK-TKIs,a long survival was achieved,hoping to guide the choosing of target therapy drugs for patients with ALK fusionmediated EGFR-TKIs resistance.

关 键 词：EGFR-TKI耐药 ALK融合 非小细胞肺癌 靶向治疗 

分 类 号：R734.2[医药卫生—肿瘤]