Clinical benefit from EGFR-TKI plus ginsenoside Rg3 in patients with advanced non-small cell lung cancer harboring EGFR active mutation

• Published in: Oncotarget Vol. 7; no. 43; pp. 70535 - 70545
• Main Authors: Li, Yan, Wang, Yanmei, Niu, Kai, Chen, Xiewan, Xia, Liqin, Lu, Dingxi, Kong, Rui, Chen, Zhengtang, Duan, Yuzhong, Sun, Jianguo
• Format: Journal Article
• Language: English
• Published: United States Impact Journals LLC 25-10-2016
• Subjects: Adult; Aged; Aged, 80 and over; Anorexia - chemically induced; Antineoplastic Combined Chemotherapy Protocols - therapeutic use; Carcinoma, Non-Small-Cell Lung - drug therapy; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - pathology; Disease-Free Survival; Exanthema - chemically induced; Female; Ginsenosides - administration & dosage; Ginsenosides - adverse effects; Humans; Lung Neoplasms - drug therapy; Lung Neoplasms - genetics; Lung Neoplasms - pathology; Male; Middle Aged; Mutation; Protein Kinase Inhibitors - administration & dosage; Protein Kinase Inhibitors - adverse effects; Receptor, Epidermal Growth Factor - genetics; Research Paper; Retrospective Studies; Vascular Endothelial Growth Factor A - genetics; targeted molecular therapy; ginsenoside Rg3; advanced NSCLC; EGFR active mutation; angiogenesis
• ISSN: 1949-2553; 1949-2553
• 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.