Objective: We compare the immune mechanism and clinical effects of paclitaxel/cisplatin combined with lentinan in the treatment of advanced cervical cancer.Methods: We retrospectively analyzed 46 patients with advanced cervical cancer admitted to our hospital from January 2017 to October 2018. They were divided into two groups (23 cases in each group) according to the treatment they had received. The control group was treated with paclitaxel/cisplatin combined with radiotherapy and chemotherapy; the observation group was treated with lentinan for two cycles. The changes in immune cells, short-term efficacy, and adverse reactions were analyzed and compared between the two groups.Results: After treatment, the activity of CD4, CD4/CD8, and NK cells in the observation group was significantly higher than it had been before treatment (P< 0.05). The activity of CD3, CD4, CD4/CD8, and NK cells in the control group was significantly lower than it had been before treatment (P< 0.05). The activity of CD4, CD4/CD8, and NK cells in the observation group was significantly higher than in the control group (P< 0.05). There were no significant differences in the effective rate between the observation group and the control group (P> 0.05). However, the incidence of myelosuppression, nausea, and vomiting was lower in the observation group than in the control group; the difference between the two groups was significant (P< 0.05).Conclusion: Paclitaxel/cisplatin combined with lentinan can significantly improve the immune function of patients with advanced cervical cancer. The clinical effect is positive and the side effects are minor, which improves patients' quality of life. This treatment is worthy of clinical application.

Objective Immunotherapy has emerged as another treatment modality in cancer. Appropriate combination of tumor mass reduction and neutralization of tumor-induced immunosuppression might set the right conditions for the induction of anti-tumor immune response. Besides the direct cytotoxic effect on the tumor cells, chemotherapy also decreases the immunosuppressive mechanisms induced by the tumor and allows for the priming of anti-tumor immunity. We performed an open label, single arm clinical trial in patients with metastatic castrate resistant prostate cancer (mCRPC) eligible for docetaxel treatment using autologous mature dendritic cells pulsed with killed LNCap prostate cancer cell line, DCVAC/PCa.

Both chemotherapy and epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) are widely applied for the treatment of non-small cell lung cancer (NSCLC), but the efficacy of these two treatments in combination is not yet clear. Thus, we sought to evaluate the efficacy of the intercalated combination of these two treatments in NSCLC. The PubMed database, EMBASE, Cochrane Controlled Trials Register and Chinese Biomedical Database were systematically searched by two researchers for randomized clinical trials (RCTs) that examined the intercalated combination of chemotherapy and EGFR TKIs in NSCLC. Ten studies involving 1,660 patients were included in this systematic review. The statistical results showed that the intercalated combination of chemotherapy and EGFR TKIs significantly improved overall survival (OS) (hazard ratio (HR) = 0.83, 95% confidence interval (CI): 0.70–0.98), progression-free survival (PFS) (HR = 0.65, 95% CI: 0.51–0.84) and the objective response rate (ORR) (risk ratio (RR) = 1.90, 95% CI: 1.22–2.98) compared to chemotherapy alone. Similarly, compared to EGFR TKIs monotherapy, the intercalated combination of chemotherapy and EGFR TKIs seemed superior to EGFR TKIs alone in terms of PFS, ORR and DCR (PFS: HR = 0.75, 95% CI: 0.62–0.91, ORR: RR = 1.49, 95% CI: 1.12–2.00 and DCR: RR = 1.33, 95% CI: 1.15–1.54) in advanced NSCLC therapy.

Background The combination of chemotherapy and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) currently has become the hotspot issue in the treatment of non-small lung cancer (NSCLC). This systematic review was conducted to compare the efficacy and safety of the synchronous combination of these two treatments with EGFR TKIs or chemotherapy alone in advanced NSCLC. Methods EMBASE, PubMed, the Central Registry of Controlled Trials in the Cochrane Library (CENTRAL), Chinese biomedical literature database (CNKI) and meeting summaries were searched. The Phase II/III randomized controlled trials were selected by which patients with advanced NSCLC were randomized to receive a combination of EGFR TKIs and chemotherapy by synchronous mode vs. EGFR TKIs or chemotherapy alone. Results A total of six randomized controlled trials (RCTs) including 4675 patients were enrolled in the systematic review. The meta-analysis demonstrated that the synchronous combination group of chemotherapy and EGFR TKIs did not reach satisfactory results; there was no significant difference in overall survival (OS), time to progression (TTP) and objective response rate (ORR), compared with monotherapy (OS: HR = 1.05, 95%CI = 0.98–1.12; TTP: HR = 0.94, 95%CI = 0.89–1.00; ORR: RR = 1.07, 95%CI = 0.98–1.17), and no significant difference in OS and progression-free survival (PFS), compared with EGFR TKIs alone (OS: HR = 1.10, 95% CI = 0.83–1.46; PFS: HR = 0.86, 95% CI = 0.67–1.10). The patients who received synchronous combined therapy presented with increased incidences of grade 3/4 anemia (RR = 1.40, 95% CI = 1.10–1.79) and rash (RR = 7.43, 95% CI = 4.56–12.09), compared with chemotherapy, grade 3/4 anemia (RR = 6.71, 95% CI = 1.25–35.93) and fatigue (RR = 9.60, 95% CI = 2.28–40.86) compared with EGFR TKI monotherapy. Conclusions The synchronous combination of chemotherapy and TKIs is not superior to chemotherapy or EGFR TKIs alone for the first-line treatment of NSCLC.

Abstract Passive immunotherapy with monoclonal antibodies represents a cornerstone of human anticancer therapies, but has not been established in veterinary medicine yet. As the tumor-associated antigen EGFR (ErbB-1) is highly conserved between humans and dogs, and considering the effectiveness of the anti-EGFR antibody cetuximab in human clinical oncology, we present here a “caninized” version of this antibody, can225IgG, for comparative oncology studies. Variable region genes of 225, the murine precursor of cetuximab, were fused with canine constant heavy gamma and kappa chain genes, respectively, and transfected into Chinese hamster ovary (CHO) DUKX-B11 cells. Of note, 480 clones were screened and the best clones were selected according to productivity and highest specificity in EGFR-coated ELISA. Upon purification with Protein G, the recombinant cetuximab-like canine IgG was tested for integrity, correct assembly, and functionality. Specific binding to the surface of EGFR-overexpressing cells was assessed by flow cytometry and immunofluorescence; moreover, binding to canine mammary tissue was demonstrated by immunohistochemistry. In cell viability and proliferation assays, incubation with can225IgG led to significant tumor cell growth inhibition. Moreover, this antibody mediated significant tumor cell killing via phagocytosis in vitro. We thus present here, for the first time, the generation of a canine IgG antibody and its hypothetical structure. On the basis of its cetuximab-like binding site, on the one hand, and the expression of a 91% homologous EGFR molecule in canine cancer, on the other hand, this antibody may be a promising research compound to establish passive immunotherapy in dog patients with cancer. Mol Cancer Ther; 13(7); 1777–90. ©2014 AACR.

In this study we evaluated the frequency of fusion between TMPRSS2 and ETS family members (ERG, ETV1, ETV4) in prostate cancers in patients from northern China in order to explore differences in fusion rates among regions in northern and southern China, other parts of Asia, Europe, and North America. We examined 100 prostate cancer patients, diagnosed by means of prostate biopsy; fluorescence in situ hybridization (FISH) was used to detect the expression of TMPRSS2, ERG, ETV1 and ETV4 in cancer tissue. Differences in gene fusion rates among different ethnics groups were also analyzed. Of the 100 prostate cancer patients, 55 (55%) had the fusion gene. Among the patients with the fusion gene, 46 (83.6%) patients had the TMPRSS2:ERG fusion product, 8 (14.8%) patients had TMPRSS2:ETV1 fusion, 1 (1.6%) patient had TMPRSS2:ETV4.