Cellular immunotherapy has appeared to be a promising modality for the treatment of malignant tumor. The objective of this study was to evaluate the efficacy of cellular immunotherapy combined with minimally invasive therapy. We searched PubMed, Web of Science and The Cochrane Library through March 2016 for relevant studies. Short-term efficacy (the disease control rate, the control rate of quality life and the AFP descent rate) and long-term efficacy (overall survival (OS) and progression-free survival (PFS) rate) were compared as the major outcome measures. The meta-analysis was performed using Review Manager 5.3. A total of 1174 references in 3 databases were found of which 19 individual studies with 1774 HCC patients enrolled in this meta-analysis. Meta-analysis results showed that cellular immunotherapy combined with minimally-invasive treatment significantly improved the measures of short-term response (the disease control rate (OR = 5.91, P = 0.007), the control rate of quality lift (OR = 3.38, P = 0.003) and the AFP descent rate (OR = 4.48, P = 0.02)). Also higher 6-month PFS (OR = 2.78, P = 0.05), ≥12-month PFS (OR = 3.56, P<0.00001) rate and 6-month OS (OR = 2.81, P = 0.0009), 12-month OS (OR = 3.05, P<0.00001) and 24-month OS (OR = 3.52, P<0.0001) rate were observed in patients undergoing cellular immunotherapy. This meta-analysis suggested that cellular immunotherapy is a feasible adjuvant treatment that could be beneficial for the improvement of the clinical outcomes for hepatocellular carcinoma (HCC) patients after minimally invasive treatment, including short-term response and long-term survival.

Significance: NontypeableHaemophilus influenzae(NTHi) is a major cause of community acquired pneumonia and exacerbation of chronic obstructive pulmonary disease. Current effort in NTHi vaccine development has focused on generating antibody responses to surface antigens and has had limited success, largely because of antigenic diversity among the numerous circulating NTHi strains. In this study, we have uncovered Th17 responses as the immune mechanism of cross-protection and identified Th17 antigens that are conserved and induce protection against NTHi lung infection, thus making a critical first step toward development of a broadly protective “universal” vaccine—the Holy Grail of vaccine development against respiratory pathogens.

Purpose: Serum bilirubin plays an important role in antioxidant and anticancer processes. The inverse association between serum bilirubin and cancer risk have been widely reported in multiple cancers. The aim of this retrospective study was to investigate the prognostic impact of serum bilirubin in colorectal cancer patients undergoing surgical resection. Methods: The value of serum bilirubin including total bilirubin, direct bilirubin, and indirect bilirubin were tested at pre-operatively in 330 colorectal cancer patients. The optimal cut-off values for these three biomarkers were determined by X-tile program. The relationship between serum bilirubin and outcomes were examined using Kaplan–Meier curves log-rank test, univariate and multivariate cox regression. Moreover, a number of risk factors were used to form a nomogram for evaluating risk of survival. Results: The optimal cut-off points of serum total bilirubin, direct bilirubin, and indirect bilirubin were 19.5 μmol/L, 5.0 μmol/L and 8.1 μmol/L, respectively. Elevated total bilirubin and direct bilirubin were significantly associated with overall survival in surgical colorectal cancer patients. Additionally, predictive nomogram including total bilirubin and direct bilirubin for overall survival was established for predicting overall survival in surgical colorectal cancer patients. Conclusions: These findings indicated that preoperative elevated total bilirubin and direct bilirubin could be considered as independent prognostic biomarkers for poor overall survival of colorectal cancer patients.

The clinical trials using immunotherapy have been performed for the treatment of variety of malignant tumors. However, large-scale meta-analysis of combined DC-CTL/CIK therapy on immune and clinical response in patients has not been well studied yet. The purpose of this study is to investigate the role of DC-CTL/CIK therapy and evaluate the changes of immune indicators and tumor serological markers both at an individual level and at a system level, which is an important basis for immunotherapy as well as prognosis estimation. Three cohorts were designed to estimate therapeutic effects on patients with malignant tumors. Tumor serological markers were detected pre- and post-treatment by immunoradiometric methods using commercially available diagnostic kits. Lymphocyte subsets were identified by flow cytometry. The quality of life was assessed by EORTC QLQ-C30 questionnaire. In this study, we found out that Tregs was significantly reduced after transfusion of DC-CTL/CIK cells companied by decreasing serological tumor markers including AFP, CA199 and CA242 in primary liver cancer and CA724 in gastric cancer. A system-level analysis showed that lower percentages of Tregs were detected in patients with long-lasting courses of immunotherapy. Strikingly, a tumor progression indicator, myeloid-derived suppressor cells (MDSC), was dramatically decreased in patients after DC-CTL/CIK treatment. These results suggested that DC-CTL/CIK therapy improves immune functions and the quality of life post-treatment versus pre-therapy, indicating that DC-CTL/CIK therapy might block the deterioration of invasive cancers in these patients. This study demonstrated that DC-CTL/CIK therapy could reduce Tregs, MDSCs, and several crucial serological tumor markers in particular tumors, and improve the function of T cells immune systems and the quality of life in patients with malignant tumor.

With recent advances in microarray technology, there has been a flourish in genome-scale identification of molecular signatures for cancer. However, the differentially expressed genes obtained by different laboratories are highly divergent. The present discrepancy at gene level indicates a need for a novel strategy to obtain more robust signatures for cancer. In this paper we hypothesize that (1) the expression signatures of different cancer microarray datasets are more similar at pathway level than at gene level; (2) the comparability of the cancer molecular mechanisms of different individuals is related to their genetic similarities. In support of the hypotheses, we summarized theoretical and experimental evidences, and conducted case studies on colorectal and prostate cancer microarray datasets. Based on the above assumption, we propose that reliable cancer signatures should be investigated in the context of biological pathways, within a cohort of genetically homogeneous population. It is hoped that the hypotheses can guide future research in cancer mechanism and signature discovery.