[Latest Research Findings on the Role of Non-Tumor Cells in Glioma Microenvironment].

As the tumor cell-centered treatment strategies cannot curb the malignant progression of glioblastoma effectively, the therapeutic effect of glioblastoma is still not satisfactory. In addition to glioma cells, glioma microenvironment (GME) comprises massive numbers of non-tumor cells and soluble cytokines. The non-tumor cells include endothelial cells, pericytes, microglia/macrophages, mesenchymal cells, astrocytes, neurons, etc. These non-tumor cell components, together with glioma cells, form one organism which regulates the progression of glioma. Considerable progress has been been in research on GME, which will be conducive to the development of non-tumor cell targeted therapies and and improvements in the prognosis of glioma patients. Herein, we summarized the interaction of glioma cells with endothelial cells, pericytes, microglia/macrophages, astrocytes, neurons and mesenchymal cells, a topic that has been extensively researched, as well as the corresponding translational studies. We also discussed the potential challenges and opportunities of developing glioma treatments based on tumor microenvironment.

The significance of preoperative hematological inflammatory markers in patients with meningiomas.

OBJECTIVE: This study was designed to evaluate whether preoperative hematological inflammatory markers would be useful in predicting the pathological grade of meningiomas. PATIENTS AND METHODS: A retrospective study of 944 patients with newly diagnosed meningioma was conducted. Preoperative blood results were obtained, including platelet, leukocyte, neutrophil, lymphocyte, and monocyte counts, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), albumin level, globulin level, and albumin-to-globulin ratio (AGR). Logistic regression analysis was performed to identify the independent predictive factors for high-grade meningiomas. RESULTS: Univariate logistic regression analysis indicated that the hematological inflammatory markers associated with tumor grade were leukocyte, neutrophil, and monocyte counts and the LMR (P < 0.05 for all). Multivariate logistic regression analysis showed that high leukocyte count (P = 0.007) and low LMR (P = 0.041) were independent predictive factors for high-grade meningiomas. CONCLUSIONS: Preoperative high leukocyte count and low LMR were independent predictive factors of high-grade meningiomas, suggesting that leukocyte count and LMR could be useful in the assessment of the grade of meningiomas.

[The Research on the Anti-glioma Effect and Mechanism of Cinobufagin].

OBJECTIVE: To study the effect of cinobufagin (CB) on the proliferation inhibition and induction of apoptosis in glioblastoma cell lines U87 and its molecular mechanism. METHODS: A gradient concentration (0-20 µmol/L) of CB was used to treat the U87 glioma cells for 6 h,12 h,24 h and 48 h,respectively. Cell viabilities were determined by CCK-8 assay to discover the effects of different concentrations of CB on the proliferation of glioma cells. Different concentrations (1-20 µmol/L) of CB were used to treat the U87 glioma cells for 12 h and 24 h,hochest33342 staining assay was used to assess the apoptosis levels. Immunofluorescence staining was used to determine the expression of growth related proteins phospho-protein kinase B(T308)[ p-AKT(T308)] in U87 glioma cells after being treated with CB for 24 h. Western blot was used to determine the apoptotic related proteins (BAX,cleaved-caspase 3,cleaved-caspase 9) and growth related proteins [phospho-inositide 3-kinase (p-PI3K),p-AKT(T308),p-AKT(S473),phospho-ribosomal protein S6 kinase (PS6),phospho-4E-binding protein 1 (p-4EBP1)]. RESULTS: A significant effect of CB on the proliferation inhibition and induction of apoptosis in U87 glioma cells in a time- and dose-dependent manner was observed. Treatment with CB induced the expression levels of apoptosis-related protein,cleaved-caspase 3 and BAX,and the PI3K-AKT-4EBP1 signaling pathway related proteins p-AKT(T308) and p-4EBP1 were decreased. CONCLUSION: CB can inhibit U87 glioma cells growth and induce apoptosis,which may involve the PI3K-AKT-4EBP1 and BAX-caspase signaling pathways.