Li Yan, Wang Yanmei, Niu Kai, Chen Xiewan, Xia Liqin, Lu Dingxi, Kong Rui, Chen Zhengtang, Duan Yuzhong, Sun Jianguo
Department of Oncology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Medical English Department, College of Basic Medicine, Third Military Medical University, Chongqing, 400038, China.
Oncotarget. 2016 Oct 25;7(43):70535-70545. doi: 10.18632/oncotarget.12059.
Acquired resistance is a bottleneck that restricts the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) for lung cancer. Ginsenoside Rg3 is an antiangiogenic agent which can down-regulate the expressions of vascular endothelial growth factor (VEGF) and EGFR. Combination of EGFR-TKI and ginsenoside Rg3 may be a promising strategy to delay acquired resistance. This retrospective study explored the efficacy and safety of this combined regimen in patients with EGFR mutation and advanced non-small cell lung cancer (NSCLC).
By the deadline of March 31th 2016, the median follow-up period reached 22.9 months. The median PFS was significantly longer in group A than in group B (12.4 months vs 9.9 months, P = 0.017). In addition, ORR was significantly higher in group A than in group B (59.6% vs 41.7%, P = 0.049). The median OS in group A showed no extended tendency compared with that in group B (25.4 months vs 21.4 months, P = 0.258). No significant difference in side effects was found between the two groups.
A total of 124 patients with advanced NSCLC and EGFR active mutation were collected and analyzed. All of them were treated with first-line EGFR-TKI and divided into two groups. In group A (n=52), patients were administered EGFR-TKI plus ginsenoside Rg3 at standard doses. In group B (n=72), patients received EGFR-TKI alone. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR) and side effects were analyzed.
Ginsenoside Rg3 improves median PFS and ORR of first-line EGFR-TKI treatment in EGFR-mutant advanced NSCLC patients, thus providing a new regimen to delay acquired resistance of EGFR-TKI.
获得性耐药是限制表皮生长因子受体酪氨酸激酶抑制剂（EGFR-TKI）治疗肺癌疗效的瓶颈。人参皂苷Rg3是一种抗血管生成剂，可下调血管内皮生长因子（VEGF）和EGFR的表达。EGFR-TKI与人参皂苷Rg3联合使用可能是延缓获得性耐药的一种有前景的策略。本回顾性研究探讨了这种联合方案在EGFR突变的晚期非小细胞肺癌（NSCLC）患者中的疗效和安全性。
截至2016年3月31日，中位随访期达22.9个月。A组的中位无进展生存期显著长于B组（12.4个月对9.9个月，P = 0.017）。此外，A组的客观缓解率显著高于B组（59.6%对41.7%，P = 0.049）。A组的中位总生存期与B组相比无延长趋势（25.4个月对21.4个月，P = 0.258）。两组间副作用无显著差异。
收集并分析124例晚期NSCLC且EGFR激活突变的患者。所有患者均接受一线EGFR-TKI治疗并分为两组。A组（n = 52）患者接受标准剂量的EGFR-TKI加人参皂苷Rg3治疗。B组（n = 72）患者仅接受EGFR-TKI治疗。分析无进展生存期（PFS）、总生存期（OS）、客观缓解率（ORR）和副作用。
人参皂苷Rg3可改善EGFR突变的晚期NSCLC患者一线EGFR-TKI治疗的中位PFS和ORR，从而提供一种延缓EGFR-TKI获得性耐药的新方案。
