已发表论文

被用于晚期非小细胞肺癌 (NSCLC) 患者早期治疗的吉非替尼 (Gefitinib) 对循环细胞因子和淋巴细胞的影响

 

Authors Sheng J, Fang W, Liu X, Xing S, Zhan J, Ma Y, Huang Y, Zhou N, Zhao H, Zhang L

Received 5 May 2016

Accepted for publication 26 August 2016

Published 21 February 2017 Volume 2017:10 Pages 1101—1110

DOI https://doi.org/10.2147/OTT.S112158

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ru Chen

Peer reviewer comments 5

Editor who approved publication: Prof. Dr. Geoffrey Pietersz

Objectives: The impact of epidermal growth factor receptor (EGFR) tyrosine-kinase inhibitors (TKIs) on the human immune system remains undefined. This study illustrates the immunomodulatory effect of gefitinib in patients with advanced non-small cell lung cancer (NSCLC) and its relevant prognostic significance.
Patients and methods: Peripheral blood samples were collected from 54 patients at baseline and after 4 weeks of gefitinib treatment. Circulating lymphocyte populations and cytokine levels were measured. Pilot investigation of the impact of gefitinib on programmed cell death ligand-1 (PD-L1) expression was conducted by immunohistochemistry (IHC).
Results and conclusion: A significant increase of peripheral natural killer cells and interferon-gamma (INF-γ) after 4 weeks of gefitinib treatment (=0.005 and 0.02, respectively). In addition, circulating interleukin (IL)-6 was significantly decreased, especially in patients sensitive to gefitinib (<0.001). Higher levels of IL-6 at baseline independently correlated with poorer progression-free survival. Experiments with NSCLC specimens illustrated that PD-L1 expression were downregulated after 4 weeks of gefitinib treatment. In summary, it was found that gefitinib treatment can alter circulating cytokines and lymphocytes. Dynamic changes of circulating lymphocytes, cytokines, and even PD-L1 IHC expression around gefitinib treatment support the specific immunomodulatory effect of this agent for advanced NSCLC.
Keywords: non-small cell lung cancer, gefitinib, PD-L1, lymphocyte, cytokine