107例KRAS突变阳性非小细胞肺癌患者临床分析  

Clinical Analysis of 107 NSCLC Patients Harboring KRAS Mutation

作　　者：张权[1] 王敬慧[1] 李曦[1] 张卉[1] 农靖颖[1] 秦娜[1] 张新勇[1] 吴羽华[1] 杨新杰[1] 吕嘉林[1] 张树才[1] 

机构地区：[1]首都医科大学附属北京胸科医院/北京市结核病胸部肿瘤研究所肿瘤内科,北京101149

出　　处：《结核病与胸部肿瘤》2016年第3期173-178,共6页Tuberculosis and Thoracic Tumor

摘　　要：背景与目的鼠类肉瘤病毒癌基因（Kirsten rat sarcoma viral oncogene, KRAS ）是非小细胞肺癌（non-small cell lung cancer,NSCLC）的重要驱动基因之一，研究显示KRAS是表皮生长因子受体酪氨酸激酶抑制剂（epidermal growth factor receptor tyrosine kinase inhibitors, EGFR-TKIs）药物的耐药标志，但其对于化疗敏感性及预后方面的意义存在争议。本研究旨在积累KRAS突变阳性的NSCLC患者治疗经验。方法我们回顾性分析了107例KRAS突变阳性的NSCLC患者的临床资料，分析KRAS突变阳性的NSCLC患者一线化疗疗效以及靶向治疗疗效。结果52例接受一线化疗的晚期KRAS突变阳性NSCLC患者客观缓解率（objective response rate，ORR）为9．6％，疾病控制率（disease control rate，DCR）为53．8％，中位疾病无进展生存期（progression-free survival，PFS）为3个月；21例接受EGFR-TKIs药物治疗的KRAS突变阳性NSCLC患者ORR为9．5％，DCR为23．8％，PFS为1个月，其中EGFR／KRAS共突变患者接受EGFR-TKIs治疗的ORR及DCR均要显著高于单纯KRAS突变人群（50％vs0，P=0．029；75％vs11．8％，P=0．043），EGFR／KRAS共突变患者接受EGFR—TKIs治疗的PFS较单纯KRAS突变患者延长，可见统计学差异（3个月vs1个月，P=0．004）。结论KRAS突变阳性NSCLC患者化疗有效率低，缓解时间短，EGFR—TKIs治疗效果差，亟需研发新的药物；EGFR／KRAS共突变现象客观存在，EGFR-TKIs药物可作为这类患者有效的治疗选择之一。Background and objective Kirsten rat sarcoma viral oncogene （K/L/S） mutation is one of the major driver genes of non-small cell lung cancer （NSCLC）. KRAS is a resistant predictor of epidermal growth factor receptor tyrosine kinase inhibitors （EGFR-TKIs）, which raises controversy because of its role in chemotherapy sensitivity and prognosis. The aim of this study is to accumulate clinical experience in treating NSCLC patients harboring KRAS mutation. Methods A total of 107 NSCLC patients harboring KRAS mutation were analyzed retrospectively. The efficacy was analyzed in terms of first-line chemotherapy or EGFR-TKIs therapy. Results The objective response rate （ORR） to first-line chemotherapy of 52 patients with advanced disease harboring KRAS mutation was 9.6%. The disease control rate （DCR） was 53.8%, and the median progression-free survival （PFS） was 3 months, The ORR to EGFR-TKIs therapy in 21 patients harboring KRAS mutation and EGFR/KRAS co-mutation was 9.5%; the DCR was 23.8%, and the median PFS was 1 month. The ORR and DCR to EGFRTKIs therapy of patients with EGFR/KRAS co-mutatiun were significantly higher than those of patients with KRAS mutation （50% vs 0, P=0.029; 75% vs 11.8%, P=0.043）; the median PFS was also significantly longer （3 months vs 1 month, P=0.004）. Conclusion The efficacy to first-line chemotherapy and EGFR-TKIs therapy in NSCLC patients harboring KRAS mutation was poor; thus, new drugs should be developed. Furthermore, the existence of EGFR/KRAS co-mutation was confirmed. Hence, EGFR-TKIs therapy should be administered to patients with EGFR/KRAS co-mutation.

关 键 词：KRAS突变 肺肿瘤 一线化疗 靶向治疗 

分 类 号：R734.2[医药卫生—肿瘤]