Henriksen Rohde (circletank97)

Circadian rhythm pathway was demonstrated pathological functions in glioma on single-gene level. We aim to depict the multi-omics landscape of circadian rhythm pathway alteration in glioma using bioinformatic analyses. Multi-omics data were obtained from "cBioPortal" database. Comparisons were done regarding clinical parameters, differential-expressed genes and functional annotations. A pathway index was generated using the expression data from TCGA and GTEx to quantify the general alteration level of the pathway with clinical association of circadian rhythm pathway index explored. A total of 30 genes were mapped on the circadian rhythm pathway. Genomic profile ofcircadian rhythm pathway genes exhibited distinct characteristics on multiple levels between lower grade glioma (LGG) and glioblastoma multiforme (GBM) patients. LGG patients presented significantly higher frequencies of multi-omics mutations, as well as significant clinical relevance, on single-gene level. Differential-expressed genes between LGG and GBM patients revealed different functions between subtypes that related to the alteration of circadian rhythm pathway. LGG have significantly higher pathway index than normal brain tissue, while GBM significantly lower than normal tissue (P less then 0.01), indicating distinctly altered circadian pathway in LGG. Circadian rhythm pathway index correlated with the prognosis of LGG, but not GBM, patients, with higher score indicating better survival outcome (LGG HR = 0.39, 95% CI 0.26 - 0.59, P less then 0.001). In conclusion, LGG have more multi-omics alterations of circadian rhythm pathway than GBM. Quantification of circadian rhythm pathway using pathway index demonstrated hyperactivated pathway status in LGG and correlated with the prognosis of LGG patients.Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies, with poor prognosis resulting mostly from late diagnosis. Surgery remains the most effective treatment and early detection significantly increases the overall survival. Biomarkers used for diagnosis and to monitor the response to treatment, such as carbohydrate antigen 19-9 (CA19-9) and carcinoembryonic antigen (CEA), are not adequate as early detection markers of PDAC, partly due to low sensitivity/specificity. Therefore, new biomarkers for PDAC are critically needed. This review aims at recent advancements in the identification and characterization of new biomarkers, microRNAs, which might prove useful in the early detection of PDAC.Our previous study found that in nasopharyngeal carcinoma (NPC) cells, overexpression of Notch2 can inhibit epithelial-mesenchymal transition (EMT), which plays a vital role in mediating radiosensitivity. The purpose of this study was to explore the radiosensitizing efficacy of the Notch2 gene in NPC cells and its potential mechanism. We used the recombinant plasmid transfection technique to establish Notch2-overexpressing 5-8 F and CNE-2 NPC cells. Cell proliferation, radiosensitivity, apoptosis and cell cycle distribution were assessed by cell counting kit-8 (CCK-8) experiments, colony formation experiments and flow cytometry. The levels of proteins related to cell cycle, apoptosis, and the AKT/mTOR signaling pathway were evaluated by using Western blotting. click here The results suggested that Notch2 overexpression increased the radiosensitivity of NPC cells, with sensitizing enhancement ratios (SERs) of 1.24 (5-8 F cells) and 1.34 (CNE-2 cells). Flow cytometry indicated that the level of apoptosis and percentage of cells in G2/M-phase were highest in NPC cells overexpressing Notch2 and treated with radiotherapy compared to cells overexpressing Notch2 alone or administered radiotherapy alone. Western blotting showed that compared to that of cells treated with Notch2 overexpression or radiotherapy alone, the levels of γH2AX, Bax, Bcl-2, Cyclin D1 and AKT/mTOR signaling pathway-related proteins were modified in NPC cells overexpressing Notch2 and treated