Hebei Province Chest Hospital

Shijiazhuang, China

Hebei Province Chest Hospital

Shijiazhuang, China
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Li D.-R.,Hebei Province Chest Hospital | Yang Y.-H.,Hebei Province Chest Hospital | Li H.,Hebei Province Chest Hospital
Journal of Practical Oncology | Year: 2015

To evaluate the clinical efficacy of haploidentical allogeneic cytokine induced killer cell (CIK) therapy for advanced non-small-cell lung cancer (NSCLC). Twenty-five patients with advanced NSCLC received CIK therapy. The peripheral blood mononuclear cells (PBMCs) from offspring of patients were collected. PBMCs were co-cultured with interferon γ (IFN-γ), interleukin-1α (IL-1α) and IL-2 in flasks coated with CD3 McAb and RetroNectin for 14 d. CIK cell surface markers were analyzed by flow cytometry (FCM). The condition of patients was evaluated with WHO general curative effect evaluation criteria. CIK cells were expanded to 10.7×109 after 2 weeks of culture. The viability of CIK cells remained (98.2±1.0)%. The ratio of CD56+CD16+CD3+ cells was (30.2±1.5)% after co-culture as shown by FCM. The level of CIK cells in peripheral blood of patients increased 10 d and 20 d after CIK therapy (P<0.05). Among 25 cases, there were 10 patients with CR, 8 patients with PR, 5 patients with NC, 2 patients with PD with an overall effective rate (CR + PR) of 72.0%. The median remission time was 10.1 months, the median survival time was 12.0 months, and the 1 year survival rate was 64.0% (16/25). No bone marrow inhibition, hair loss, phlebitis or gastrointestinal reaction was observed. Haploidentical allogeneic CIK therapy is effective for advanced NSCLC and it may prolong survival and improve the quality of life, with little side effects. © 2015, Editorial Board of Journal of Practical Oncology. All right reserved.


Li D.,Hebei Province Chest Hospital | Yang Y.,Hebei Province Chest Hospital | Gao L.,Hebei Normal University | Guo S.,Hebei Province Chest Hospital | And 4 more authors.
Open Medicine (Poland) | Year: 2016

Cytokine-induced killer (CIK) cells were isolated and proliferation from human peripheral blood and cultured in appropriate growth medium. The biological characteristics of CIK cells were further determined by the characterization of surface markers by flow cytometry. CIK cells inhibited the proliferation of human lung adenocarcinoma NCL-H157 cells. Vascular endothelial growth factor (VEGF) expression was down-regulated in CIK cells co-cultured with NCL-H157 cells by western blotting analysis. Furthermore, in comparison with cells untreated by CIK, the NCL-H157 had a lower proliferation capacity. We proposed that the pharmacological mechanisms of NCL-H157 promoted by CIK can be estimated possibly with different biological significance that can be ascribed to down-regulated VEGF expression in vitro. The results suggest that the VEGF pathway guides developmental inhibiting of NCL-H157, and we speculate that the function of VEGF pathways is to guide NCL-H157 to inhibition by abundant CIK. © 2016 Dengrui Li et al.


Gao L.,Hebei Normal University | Zhang J.,Hebei Medical University | Liu X.,Hebei Province Chest Hospital | Zhao M.,Hebei Province Chest Hospital | And 3 more authors.
Thoracic Cancer | Year: 2013

Background: The aim of this study was to evaluate the cytotoxic and antitumor activity of spider venom (SV). Methods: Cell proliferation and cytotoxicity were determined by 3H-methyl thymidine incorporation ([3H]-TDR) assay. DNA fragmentation and cell cycle kinetics were analyzed by FACS. In vivo inhibition of tumor size of nude mice by SV (5.0, 10.0, 20.0mg/kg mice) was constructed. Results: SV exhibited significant anti-cancer effects on human squamous esophageal carcinoma cells TE13, mainly as a result of cell apoptosis induced by SV. The anti-cancer effects were likely achieved through decreasing [3H]-TdR. TE13 cells treated with SV (25, 50, 100μg/mL), which were arrested in the G0/G1 phase. SV treatment leads to anti-proliferation effects, and significant apoptosis in TE13 cells with reactive oxygen species (ROS) levels can increase dramatically and decrease cellular mitochondrial membrane potential (MMP). In addition, Western blotting analysis showed that one of the pharmacological mechanisms of SV was to activate the expression of P21. In vivo testing revealed that tumor size was significantly decreased after 21 days of treatment with the venom (P < 0.01). Conclusions: Our data showed that SVs could inhibit TE13 cell proliferation in vitro and in vivo. © 2012 Tianjin Lung Cancer Institute and Wiley Publishing Asia Pty Ltd.


PubMed | Hebei Province Chest Hospital and Hebei Normal University
Type: Journal Article | Journal: Thoracic cancer | Year: 2015

Adenocarcinoma, the most common form of lung cancer, is one of main human malignant tumors. In this paper, we focus on the effect of antitumor activity of cytokine-induced killer (CIK) cells on human lung adenocarcinoma cell line A549.CIK cells were obtained by inducing peripheral blood mononuclear cells with recombinant human (rh) interferon-gamma, monoclonal anti-CD3 antibody, rh interleukin (IL)-1alpha, and rhIL-2, which were added into the culture. A549 cell viability of CIK cells was determined using MTS assay. Flow cytometry (FCM) experiments were performed to detect cell cycle changes. The expression of P27 in A549 cells treated by CIK cells was evaluated by Western blot.The percentage of CD3+CD16+CD56+ T cells in a representative peripheral blood mononucleated cell sample was 33.7 1.3%. CIK cells, in dose and time dependent manners, inhibited the proliferation of A549. FCM demonstrated that A549 cells were accumulated in G2/M and G0/G1 phases when treated with CIK cells. FCM was used to analyze whether A549 cells treated with CIK cells induced apotosis or necrosis at 10:1 or 20:1. Compared to the control group, P27 was prominently upregulated in the CIK treated group.We propose that the pharmacological mechanisms of A549 cells inhibited by CIK cells can be estimated to possibly elicit different biological significance, which, in part, can be ascribed to a different mass transport rate in vitro.

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