The objective of this study was to evaluate the effects of dendritic cell and cytokine-induced killer (DC-CIK) cell-based immunotherapy combined with chemotherapy on the treatment of patients with advanced colorectal cancer. We prospectively included patients with advanced colorectal cancer and assessed the efficacy of DC-CIK cell-based immunotherapy combined with chemotherapy compared to treatment with chemotherapy alone. T cell subtypes, progression-free survival (PFS), overall survival (OS), and adverse events were evaluated in each group. In total, 134 patients were included in the DC-CIK group and 121 patients were included in the control group. No significant differences were observed in the percentages of CD3(+), CD3(+)CD4(+), CD3(+)CD8(+), and NK cells after DC-CIK cell-based immunotherapy compared to before chemotherapy in the DC-CIK group. The median PFS and OS in the DC-CIK treatment group were 8.8 months (95 % CI 8.4-9.1) and 14.7 months (95 % CI 13.9-15.5), respectively, which were significantly improved compared to the PFS and OS in the control group. The frequencies of grade III and IV leukopenia (8.2 vs. 19.0 %, P = 0.011), grade III and IV anemia (3.0 vs. 9.1 %, P = 0.039), and grade III and IV thrombocytopenia (3.7 vs. 10.7 %, P = 0.029) were significantly lower in the DC-CIK group compared to the control group. DC-CIK cell-based immunotherapy could induce an immune response against colorectal cancer and prolong PFS and OS. DC-CIK cell-based immunotherapy combined with chemotherapy had a significant benefit in terms of survival in patients with colorectal cancer compared to chemotherapy alone.
Background: Rectal cancer (RC) has been documented to be a highly invasive malignant neoplasm worldwide. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine involved in cell-mediated immunity, immunoregulation, inflammation. In vitro and in vivo studies have identified that MIF was involved in the carcinogenesis and progression of RC. Patients and Methods: This case-control study evaluated associations of genetic variants of the MIF gene and serum level of MIF with susceptibility of RC. Results: We found MIF level was associated with an increased risk of RC (OR for per unit: 1.38, 95% CI:1.32-1.44; P < 0.001). Both MIF rs2012133 (OR = 1.30; 95% CIs = 1.08-1.58; P = 0.007) and rs755622 (OR = 1.45; 95% CIs = 1.15-1.82; P = 0.002) were significantly associated with increased risk of RC. Besides, we also found MIF rs5844572 was significantly associated with increased susceptibility of RC, with OR for per CATT repeat of 1.28 (95% CIs: 1.16-1.41; P < 0.001). Further, we found all three variants of the MIF gene, rs5844572, rs2012133 and rs755622, could increase serum level of MIF. Conclusion: This study suggests that MIF plays an important role in the carcinogenesis of RC and could be used as a biomarker for early detection and prediction of RC.
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