Clinical benefit from EGFR-TKI plus ginsenoside Rg3 in patients with advanced non-small cell lung cancer harboring EGFR active mutation
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Yan Li1,*, Yanmei Wang1,*, Kai Niu1, Xiewan Chen2, Liqin Xia1, Dingxi Lu2, Rui Kong1, Zhengtang Chen1, Yuzhong Duan1, Jianguo Sun1
1Department of Oncology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China
2Medical English Department, College of Basic Medicine, Third Military Medical University, Chongqing, 400038, China
*These authors have contributed equally to this work
Yuzhong Duan, email: firstname.lastname@example.org
Jianguo Sun, email: email@example.com
Keywords: advanced NSCLC, EGFR active mutation, targeted molecular therapy, ginsenoside Rg3, angiogenesis
Received: April 11, 2016 Accepted: August 25, 2016 Published: September 16, 2016
Purpose: 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).
Results: 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.
Methods: 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.
Conclusions: 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.
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