Pretreatment NLR and percentages of lymphocyte and neutrophil are independent prognostic factors and may serve as clinically convenient and useful biomarkers for survival of patients with NPC.

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There was limited evidence revealing the association of Chinese maternal dietary patterns with fetal growth. We aimed to examine the relationship of maternal dietary patterns during pregnancy to neonatal birth weight and birth weight for gestational age in a Chinese population. A total of 6954 mother-child pairs were included from the Born in Guangzhou Cohort Study. Maternal diet during pregnancy was assessed using a self-administered food frequency questionnaire. Cluster analysis was used to identify dietary patterns. The following six dietary patterns were identified: “Cereals, eggs, and Cantonese soups” (n 1026, 14.8%), “Dairy” (n 1020, 14.7%), “Fruits, nuts, and Cantonese desserts” (n 799, 11.5%), “Meats” (n 1066, 15.3%), “Vegetables” (n 1383, 19.9%), and “Varied” (n 1224, 17.6%). The mean neonatal birth weight Z scores of women in the above patterns were 0.02, 0.07, 0.20, 0.01, 0.06, and 0.14, respectively. Women in the “Fruits, nuts, and Cantonese desserts” and “Varied” groups had significantly heavier infants compared with those in the “Cereals, eggs, and Cantonese soups” group. Compared with women in the “Cereals, eggs, and Cantonese soups” group, those in the “Varied” group had marginally significantly lower odds of having a small-for-gestational age (SGA) infant after adjustment for other confounders (OR 0.77, 95% CI 0.57, 1.04, p = 0.08). These findings suggest that compared to a traditional Cantonese diet high in cereals, eggs, and Cantonese soups, a diet high in fruits, nuts, and Cantonese desserts might be associated with a higher birth weight, while a varied diet might be associated with a greater birth weight and also a decreased risk of having a SGA baby.

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Objectives: The objective of this study was to evaluate the association between metformin therapy and the incidence of gastric cancer (GC) in patients with type 2 diabetes mellitus (T2DM). Methods: We systemically searched the following databases for studies published between the databases' dates of inception and Nov. 2016: PubMed, Embase, the Cochrane Library, the Web of Science, and the China National Knowledge Infrastructure (CNKI). Hazard ratios (HR) and corresponding 95% confidence intervals (CIs) for the association between metformin therapy and the incidence of GC in patients with T2DM were the outcome measures assessed in this study. STATA 12.0 (Stata Corporation, College Station, Texas, USA) was used to conduct the statistical analysis. Results: A total of seven cohort studies including 591,077 patients met all the criteria for inclusion in the analysis. Our data showed that metformin therapy was associated with a significantly lower incidence of GC in patients with T2DM than other types of therapy (HR=0.763, 95% CI: 0.642~0.905). Subgroup analysis showed that patients living in Taiwan benefitted more from metformin therapy than patients living in any other region, as metformin significantly decreased the risk of GC in patients living in Taiwan but did not significantly decrease the risk of GC in patients living in other regions (HR=0.514, 95% CI: 0.384-0.688). The results of the present analysis support the idea that metformin facilitates reductions in the risk of T2DM-related GC. Conclusions: The risk of GC among patients with T2DM is lower in patients receiving metformin therapy than in patients not receiving metformin therapy.

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Colorectal cancer (CRC) is one of the main reasons of tumor-related deaths worldwide. At present, the main treatment is surgery, but the results are unsatisfactory, and the prognosis is poor. The majority of patients die due to liver or lung metastasis or recurrence. In recent years, great progress has been made in the field of tumor gene therapy, providing a new treatment for combating CRC. As oncolytic viruses selectively replicate almost exclusively in the cytoplasm of tumor cells and do not require integration into the host genome, they are safer, more effective and more attractive as oncolytic agents. Newcastle disease virus (NDV) is a natural RNA oncolytic virus. After NDV selectively infects tumor cells, the immune response induced by NDV’s envelope protein and intracellular factors can effectively kill the tumor without affecting normal cells. Reverse genetic techniques make NDV a vector for gene therapy. Arming the virus by inserting various exogenous genes or using NDV in combination with immunotherapy can also improve the anti-CRC capacity of NDV, and good results have been achieved in animal models and clinical treatment trials. This article reviews the molecular biological characteristics and oncolytic mechanism of NDV and discusses in vitro and in vivo experiments on NDV anti-CRC capacity and clinical treatment. In conclusion, NDV is an excellent candidate for cancer treatment, but more preclinical studies and clinical trials are needed to ensure its safety and efficacy.

Neuropilins (NRP1 and NRP2) are multifunctional receptor proteins that are involved in nerve, blood vessel, and tumor development. NRP1 was first found to be expressed in neurons, but subsequent studies have demonstrated its surface expression in cells from the endothelium and lymph nodes. NRP1 has been demonstrated to be involved in the occurrence and development of a variety of cancers. NRP1 interacts with various cytokines, such as vascular endothelial growth factor family and its receptor and transforming growth factor β1 and its receptor, to affect tumor angiogenesis, tumor proliferation, and migration. In addition, NRP1 + regulatory T cells (Tregs) play an inhibitory role in tumor immunity. High numbers of NRP1 + Tregs were associated with cancer prognosis. Targeting NRP1 has shown promise, and antagonists against NRP1 have had therapeutic efficacy in preliminary clinical studies. NRP1 treatment modalities using nanomaterials, targeted drugs, oncolytic viruses, and radio-chemotherapy have gradually been developed. Hence, we reviewed the use of NRP1 in the context of tumorigenesis, progression, and treatment.