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Anti-N-methyl-D-aspartate receptor encephalitis: An observational as well as comparative examine within Spanish adults and children.
Based on the results of the aforementioned analysis, a multiple linear regression model named Radiation Pneumonitis Index (RPI) was built, for the assessment of Grade ≥2RP risk. Results Only previous surgery and fractional dose were discovered statistical significantly associated with grade ≥2RP. Thirty-nine effective SNPs for predicting the Grade ≥2RP risk were discovered and their coefficients of the synergistic effect were determined. The RPI score can successfully distinguish the RP≥2 population with 92.0% sensitivity and 100% specificity. Conclusions Individual radiation sensitivity can be determined with genotype information and personalized radiotherapy could be achieved based on mathematical model result. © The author(s).Introduction For pathological diagnosis of pancreatic neuroendocrine neoplasms (pNENs) the routinely used immunohistochemical markers are chromogranin A (CgA) and synaptophysin (Syn). Their ability as prognostic markers is not well established. A splice variant of actinin-4 (Actn-4sv) was recently found to be an excellent biomarker of neuroendocrine neoplasms of the lung. We aimed to investigate the expression of Actn-4sv in pNENs and evaluate its quality as a biomarker of pNENs. Methods Paraffin-embedded and frozen tissues specimens from 122 pNENs were analyzed. Western blots were performed to prove and compare the relative amount of Actn-4sv expression in pNENs tissue homogenates. For comparison pancreatic ductal adenocarcinoma (PDAC) and normal pancreatic tissues were analyzed in parallel. Immunohistochemistry (IHC) of paraffin sections of pNENs for Actn-4sv were performed and compared to the classic neuroendocrine markers CgA and Syn. Correlations were calculated between the staining intensity and distribution of Actn-4sv and staging, grading and afflicted lymph nodes respectively. Results Actn-4sv was expressed in 88.5% (108/122) of pNENs, but not in normal pancreatic tissues (0/14) or PDAC (0/14). Compared to CgA and Syn, Actn-4sv was not detectable in islet cells of the normal pancreas. Staining intensity of Actn-4sv on pNENs negatively correlated to the histological grading (Spearman r=-0.4990, p less then 0.0001) and staging (r = -0.2581, p = 0.0041) but no correlation to afflicted lymph nodes was found. A significantly better overall survival was observed for pNEN patients with higher expression of Actn-4sv (hazard ratio 2.7; log-rank test p= 0.0349). Conclusions The expression of Actn-4sv may be an important prognostic factor for patients with pNENs. Its expression correlates with the grading and staging of the tumors. © The author(s).Although baicalin, a flavonoid derived from Scutellaria baicalensis Georgi, has been reported to have anti-tumor activity in various cancers, the molecular mechanism remains imperfect. Here, we show that baicalin inhibits cell growth, migration and invasion and induces cell apoptosis by inhibiting cell cycle, viability, the epithelial-mesenchymal transition (EMT) and cellular stemness in colorectal cancer (CRC) cells. In detail, baicalin treatment in CRC cells induces cell cycle arrest in G1 phase and promotes p53-independent cell apoptosis, inhibits both endogenous and exogenous TGFβ1-induced EMT of colorectal cancer cells by inhibiting TGFβ/Smad pathway. Cell sphere-formation experiments show that baicalin has a strong inhibitory efficacy on the stemness of CRC cells by decreasing the marker proteins of cancer stem cell (CSC) and inhibits the formation of CSC-like cell spheres in CRC cells. In vivo experiments also identify that baicalin has an anti-tumor effect by down-regulating the levels of marker proteins of cell cycle, EMT and stemness in the orthotopic transplantation tumors of CRC cells in BALB/c nude mice. Collectively, our in vitro and in vivo results indicate that multiple inhibition of cell cycle, EMT and stemness is the real molecular mechanism of baicalin in effectively inducing cell growth inhibition and apoptosis in CRC cells. © The author(s).Hypoxia is a characteristic feature of the tumor microenvironment in pancreatic ductal adenocarcinoma (PDAC). We have recently explored new targeting molecules and pathways in PDAC cells under hypoxic conditions. In this study, we performed a microarray experiment to analyze the genes up-regulated in PDAC cell lines under hypoxia compared to normoxia, and identified human family with sequence similarity 115, member C (FAM115C) as a candidate gene for further study. Our data showed that FAM115C was overexpressed in PDAC cell lines under hypoxia, and FAM115C inhibition promoted PDAC cell migration and invasion in vitro. FAM115C inhibition did not affect tumor cell proliferation in PDAC. Immunohistochemically, FAM115C expression was observed ubiquitously in normal pancreas, pancreatic intraepithelial neoplasia (PanIN) and PDAC tissue, and it was located mainly in the nucleus but also in the cytoplasm of cells. In qPCR analysis, high expression of FAM115C was correlated with better prognosis in patients with PDAC. Our findings suggest that FAM115C could be a novel tumor suppressor associated with prolonged survival in patients with PDAC. © The author(s).Purpose To evaluate the value of 18F-FDG positron emission tomography (PET)/computed tomography (CT) for determining the presence of residual tumors after curettage in patients with endometrial cancer. Methods Preoperative 18F-FDG PET/CT was performed in 90 women with endometrial cancer. PET/CT parameters and clinical characteristics were compared between patients with and without residual tumors. The clinical characteristics of patients with residual tumors that showed low 18F-FDG uptake were also analyzed. Results Among the 90 patients, 86 had residual tumors. ROC analysis identified a lesion SUVmax value of 5.0 as the optimal cut-off value for predicting whether or not patients had a residual tumor. With the SUVmax cut-off of 5, the sensitivity, specificity, positive predictive value, and negative predictive values for residual tumor prediction were 87.2%, 100%, 100%, and 26.7%, respectively. Univariate analysis showed significant associations between the high PET group (SUVmax > 5) and low PET group (SUVmax ≤ 5), and histologic type (P = 0.043) and tumor size (P less then 0.001) in patients with residual tumors. In patients with low-grade and clear cell carcinomas and a tumor size less then 1.35 cm, the probability of being in the low-PET group was 47.6%. In such patients, major parts of the residual tumors showed low 18F-FDG uptake, similar to that in patients with no residual tumors. Conclusion SUVmax was the lone predictive value for the presence of residual tumors after curettage in patients with endometrial cancer. Lesion SUVmax greater than 5 suggested a high possibility of residual tumors. In patients with low-grade and clear cell carcinomas with tumor size less then 1.35 cm, residual tumors may present low 18F-FDG uptake, mimicking the metabolic phenotypes of patients without residual tumors. © The author(s).Background With the anti-cancer efficacies of cold atmospheric plasma being increasingly recognized in vitro, a demand on creating an effective tool feasible for in vivo animal treatment has emerged. Methods Through the use of co-axial needles with different calibers in diameter, we designed a novel in situ ejection source of cold atmospheric plasma, namely invivoPen, for animal experiments. It punches just a single pinhole that could considerably ease the complexity of operating with small animals such as mouse. Results We showed that invivoPen could deliver similar efficacies as plasma activated medium with reduced cost in suppressing cell proliferation and migration as well as potentially boosting the viabilities of mice receiving invivoPen treatment. find more Blood test, renal and liver functionalities tests all suggest that physical plasma could effectively return tumor-carrying mice to the healthy state without harm to body conditions, and invivoPen slightly outweighs PAM in boosting animal immunity and reducing inflammation. Conclusion Our study contributes to the community in providing a minimal invasive in situ plasma source, having partly explained the efficacies of cold atmospheric plasma in treating triple negative breast cancers, and proposing the potential synergies between physical plasma and conventional drugs for cancer treatment. © The author(s).Objectives Lung adenocarcinomas with or without epidermal growth factor receptor (EGFR) mutations have shown different drug effects against EGFR inhibitors. But it is not very clear if EGFR mutation status affects the biological behavior of lung adenocarcinoma, because tumor gene regulation is very complicated and can be affected by many factors. We aimed to explore if EGFR mutation status is related with tumor malignant degree by investigating the relevance of EGFR mutation status with DNA content and aneuploid peaks of lung adenocarcinoma cells in pleural fluids without using EGFR-TKIs. Materials and Methods 591 cases of lung adenocarcinoma patients in Hebei Tumor Hospital who had undergone EGFR gene detection and DNA quantitative analysis were collected from January 2012 to August 2018.They were divided into two groups EGFR mutant group and non-mutant group. EGFR mutations were detected by Amplification Refractory Mutation System (ARMS) and ABI 7500 Fluorescence quantitative PCR with pleural effusions. DNA content and aneuploid peaks were detected by LD DNA image cytometry (DNA-ICM). Rank-sum test of SPSS 16 was used for statistical analysis. Results The maximum DI, the mean DI of the first 20 cells greater than 5C, the percentage of cells greater than 5C and the number of cells greater than 9C of the first 20 cells in the mutant group were all higher than those in the non-mutant group, having statistical significance (p less then 0.001); the peaks of aneuploid cells in the mutant group occurred more often than those in the non-mutant group, having statistical significance (p less then 0.001). Conclusions Our study has shown that advanced lung adenocarcinomas with EGFR-mutations had higher DI values, more aneuploid cells and more frequent aneuploid peaks compared with those without EGFR-mutations, suggesting that advanced lung adenocarcinomas with EGFR mutations are more aggressive than those without EGFR mutations. © The author(s).YWHAZ (also named 14-3-3ζ) is a central hub protein for many signal transduction pathways and plays a significant role in tumor progression. Accumulating evidences have demonstrated that YWHAZ is frequently up-regulated in multiple types of cancers and acts as an oncogene in a wide range of cell activities including cell growth, cell cycle, apoptosis, migration, and invasion. Moreover, YWHAZ was reported to be regulated by microRNAs (miRNAs) or long non-coding RNAs and exerted its malignant functions by targeting downstream molecules like protein kinase, apoptosis proteins, and metastasis-related molecules. Additionally, YWHAZ may be a potential biomarker of diagnosis, prognosis and chemoresistance in several cancers. Targeting YWHAZ by siRNA, shRNA or miRNA was reported to have great help in suppressing malignant properties of cancer cells. In this review, we perform literature and bioinformatics analysis to reveal the oncogenic role and molecular mechanism of YWHAZ in cancer, and discuss the potential clinical applications of YWHAZ concerning diagnosis, prognosis, and therapy in malignant tumors.
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