The aim of this study was to identify new protein markers of the intestinal and diffuse type gastric adenocarcinoma and to determine their relation to local relapses and distant metastasis. Using two-dimensional gel electrophoresis, we searched for proteins that are overexpressed in the intestinal and/or diffuse type gastric adenocarcinoma, as compared to matched normal mucosa samples with further change confirmation by Western blot. Expression of the selected proteins was further assessed by immunohistocemistry in a large panel of gastric adenocarcinoma with various clinicopathological features. Expression level of cyclophilin A measured with western blot appeared to be increased on average ten times in 63 % of gastric adenocarcinoma vs. paired samples of normal mucosa. The frequency of immunihistochemistry detected cyclophilin A protein expression was found to be equal in tumor of both histotypes, but staining intensity was higher in intestinal versus diffuse types of gastric adenocarcinoma. cyclophilin A protein expression appeared to be lower in deeply invading glandular and cribriform structures of intestinal tumors, as well as in discretely placed groups of the intestinal tumor cells. Local relapses as well as distant metastases registered within 3 year follow up were observed to occur much less frequently in patients with positive cyclophilin A immunostaining in gastric tumors. Analysis of cyclophilin A expression has a potential value for prognosis of gastric adenocarcinoma recurrence and distant metastasis.
It is known that angiogenesis plays a critical role in the growth and progression of brain gliomas. Inducing factor in neoangiogenesis are changes primarily occur within the intra-tumoral events: changing the structure of the microvasculature of tumor tissue, increased hypoxia adaptation of tumor cells and the synthesis of angiogenic factors, cell growth. Due to the location of abnormal blood vessels in the tumor tissue generated chaotic flow of blood, which leads to severe hypoxia - as a key factor in inducing the angiogenesis process. Hypoxia-inducible factor 1 (HIF-1) is the main molecule that regulates the growth and progression of glial tumors. Glioma cells, with their inherent properties of stem cells actively synthesized HIF-1. This population of cells called - “glioma stem cells” inducing synthesis of vascular endothelial growth factor (VEGF). It VEGF is central to the process of angiogenesis. A promising area of targeted therapy of brain gliomas is the anti-angiogenic therapy. Applications, both direct and indirect angiogenesis inhibitors, significantly improved the prognosis of patients with glial brain tumors. Undoubtedly an integrated approach to the study of microvascular disturbances, hypoxia, biology and cell behavior of “glioma stem cells” and the role of various factors of cell growth in the tumorigenesis of brain gliomas of the brain allows us to develop new and effective methods of diagnosis and treatment of this disease in the near future.
The purpose - was to perform a meta-analysis based on the results of randomized controlled trials that examined the efficacy and safety of using anti-VEGF (vascular endothelial growth factor (vascular endothelial growth factor, VEGF)) drugs as an auxiliary treatment for patients with glioblastoma (GBM). Material and methods. A search for randomized controlled trials was conducted in the Pubmed, EMBASE, eLibrary and Cohrane Library databases published from January 2008 to March 2019, which examined the efficacy and safety of using anti-VEGF agents as an auxiliary method of treating GBM patients. The odds ratio (OR) and 95% confidence interval (CI) were used to calculate the overall survival and progression-free survival values. Results. According to the eligibility criteria, 9 randomized controlled trials included in this meta-analysis that examine the results of using anti-VEGF drugs in 3189 patients with GBM. The overall survival rates of patients with GBM using anti-VEGF therapy exceed those in the group of patients with standard therapy without statistically significant differences (OR=0.89, 95% CI: 0.76, 1.04, p=0.13). Significant differences in progression-free survival were noted in favor of anti-VEGF agents (OR=0.70, 95% CI: 0.60, 0.82, p<0.00001). The performed subgroup analysis showed the absence of a statistically significant effect of bevacizumab on the overall survival rates of patients with GBM (OR=0.89, 95% CI: 0.75, 1.06, p=0.20). Using a combination of bevacizumab and standard therapy can significantly improve the progression-free survival rates in patients with GBM (OR=0.63, 95% CI: 0.51, 0.78, p<0.0001). Conclusion. The performed meta-analysis clearly demonstrated that the combination of anti-VEGF agents and standard therapy does not significantly increase the overall survival rate of patients with GBM. However, the use of anti-VEGF drugs statistically significantly improves the values of progression-free survival in patients with GBM.
The aim of our study was to compare the features of macrophage (mf) composition of the kidneys in patients with fatal myocardial infarction (MI) and in patients without cardiovascular diseases (CVD). We used kidney fragments taken during autopsy. Macrophage infiltration was assessed by immunohistochemistry: antibodies CD68 were used as a common mf marker, CD80—M1 type mf marker, CD163, CD206, and stabilin-1—M2 type. Macrophage composition of the kidneys in patients with fatal MI was characterized by the predominance of CD163+ cells among studied cells, and the control group was characterized by the predominance of CD163+, CD206+, and CD68+. In patients with MI, biphasic response from kidney cells was characterized for CD80+ and CD206+: their number decreased by the long-term period of MI; other cells did not show any dynamics. The exact number of CD80+ cells in kidneys of individuals without CVD was slightly higher than in patients with MI, and the number of CD206+—strikingly predominant. Subsequent analysis of CD80+ and CD206+ cells in a larger sample, as well as comparison of data with results obtained from survivors of MI, may bring us closer to understanding whether the influence on these cells can serve as a new target in personalized therapy in postinfarction complications.
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