PT -期刊文章AU - Lu,君非盟-钟,华盟——楚,专业非盟-张,竟在非盟-李,荣盟——太阳,世纪佳缘盟——钟,Runbo AU -杨,Yuqin AU -阿拉姆,默罕默德·沙阿非盟-卢,余庆盟——徐,王健林盟——张艘Yanwei盟——吴,君非盟-李,晓伟盟,赵小东盟-李,凯盟- Lu,李明AU -汉,宝会TI -角色anlotinib-induced CCL2减少抗血管生成和响应预测nonsmall细胞肺癌治疗援助- 10.1183/13993003.01562 -2018 DP - 2019年3月01 TA -欧洲呼吸杂志》第六PG - 1801562 - 53年IP - 3 4099 - //www.qdcxjkg.com/content/53/3/1801562.short 4100//www.qdcxjkg.com/content/53/3/1801562.full SO - Eur Respir J2019 3月1日;Anlotinib已在临床试验中证实能够有效延长难治性晚期非小细胞肺癌(NSCLC)患者的无进展生存期(PFS)和总生存期(OS)。然而，安洛替尼潜在的分子机制和预测生物标志物仍不清楚。方法回顾性分析294例NSCLC患者使用安洛替尼的情况，筛选安洛替尼应答患者的潜在生物标志物。通过转录组和功能分析来了解安洛替尼的抗肿瘤分子机制。分析血清CCL2水平的变化，以检验有反应者和无反应者对安诺替尼反应的相关性。结果安洛替尼治疗对驱动基因突变阳性的NSCLC患者，特别是上皮生长因子受体(EGFR)T790M突变的患者，有利于延长OS。此外，安洛替尼通过抑制CCL2抑制nci - h1975来源的异种移植模型中的血管生成。 Finally, anlotinib-induced serum CCL2 level decreases were associated with the benefits of PFS and OS in refractory advanced NSCLC patients.Conclusions Our study reports a novel anti-angiogenesis mechanism of anlotinib via inhibiting CCL2 in an NCI-H1975-derived xenograft model and suggests that changes in serum CCL2 levels may be used to monitor and predict clinical outcomes in anlotinib-administered refractory advanced NSCLC patients using third-line therapy or beyond.The underlying molecular mechanisms and predictive biomarkers of anlotinib benefitting NSCLC patients are still unclear. In this study, anlotinib-induced CCL2 decrease contributes to a novel insight for its anti-angiogenesis mechanism and responsive prediction. http://ow.ly/YZL930mXlfV