Effect of Combined Therapy Inhibiting EGFR and VEGFR Pathways in Non Small-cell Lung Cancer on Progression-free and Overall Survival
Effect of Combined Therapy Inhibiting EGFR and VEGFR Pathways in Non Small-cell Lung Cancer on Progression-free and Overall Survival
复制标题
抑制 EGFR 和 VEGFR 通路的联合疗法对非小细胞肺癌无进展生存期和总生存期的影响
DOI：
10.1016/j.cllc.2016.12.012
复制
发表时间：
2017-07-01
影响因子：
3.6
通讯作者：
Zhou, Caicun
中科院分区：
文献类型：
--
作者：
Jiang, Tao;Qiao, Meng;Zhou, Caicun
The effect of combined epidermal growth factor receptor and vascular endothelial growth factor (VEGF) receptor pathway inhibitors on progression-free survival and overall survival in patients with non small-cell lung cancer remains controversial. Our analysis showed that epidermal growth factor receptor tyrosine kinase inhibitors plus anti-VEGFNEGF receptor therapy significantly prolonged progression-free survival in the second-line treatment of non small-cell lung cancer. Epidermal growth factor receptor mutation is a promising indication for this combination treatment.Background: To investigate the effect of combined epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) receptor (VEGFR) pathway inhibitors on progression-free survival (PFS) and overall survival (OS) in patients with non small-cell lung cancer (NSCLC). Materials and Methods: We included 15 randomized clinical trials that had compared the combination of EGFR tyrosine kinase inhibitors and anti-VEGFNEGFR therapy with different control groups. Pooled estimates of treatment efficacy were calculated, and subgroup analyses were conducted according to treatment line and EGFR status. Results: Ten of 15 trials involving 3317 NSCLC patients were included. For all settings, the combined regimen demonstrated no PFS (hazard ratio [HR], 0.82; P = .10) or OS (HR, 0.97; P = .54) benefit compared with the control groups. In the first-line setting, combined therapy showed similar PFS (HR, 1.01; P = .99) but poor OS (HR, 1.36; P = .03) compared with the control groups. In the second-line or subsequent settings, combined therapy resulted in significantly longer PFS (HR, 0.75; P < .01) but similar OS (HR, 0.93; P = .16) compared with the control groups. A subgroup analysis stratified by EGFR status suggested that combined treatment substantially improved PFS (HR, 0.57; P = .04) and OS (HR, 0.45; P < .01) in patients with EGFR mutations rather than EGFR wild type. Conclusion: EGFR-tyrosine kinase inhibitors plus anti-VEGFNEGFR therapy significantly prolonged PFS in the second-line treatment of NSCLC patients. An EGFR mutation is a promising indication for this combination treatment. More data are required to confirm this strategy in first-line therapy.
