Bachmann Cooley (tankmilk8)
ditions in a secondary care DM population. Although we did find a non-response bias, this cohort will be an important source to determine the prevalence and consequences of MSK conditions in a secondary care DM population. Circular RNAs (circRNAs) are implicated in the chemoresistance of human cancers. However, the functions of circRNA PR/SET domain 2 (circPRDM2) in the resistance of osteosarcoma (OS) to doxorubicin (DXR) are unknown. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was conducted to determine the levels of circPRDM2, microRNA-760 (miR-760) and enhancer of zeste homolog 2 (EZH2). RNase R assay was used to analyze the characteristics of circPRDM2. IC50 of DXR was estimated by Cell Counting Kit-8 (CCK-8) assay. Colony formation assay was performed for cell colony formation ability. Wound-healing assay and transwell assay were utilized for cell migration and invasion. Flow cytometry analysis was conducted for cell apoptosis. Western blot assay was employed for protein levels. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay were adopted to analyze the relationships among circPRDM2, miR-760 and EZH2. Murine xenograft model assay was utilized to explore DXR resistance in vivo. CircPRDM2 level was enhanced in DXR-resistant OS tissues and cells. CircPRDM2 deficiency inhibited IC50 of DXR, colony formation, migration and invasion and facilitated apoptosis in DXR-resistant OS cells in vitro. CircPRDM2 was identified as the sponge for miR-760. MiR-760 inhibition reversed the inhibitory effects of circPRDM2 knockdown on DXR resistance and cell progression in DXR-resistant OS cells. Moreover, EZH2 was identified as the target gene of miR-760 and EZH2 overexpression abolished miR-760-mediated impacts on DXR sensitivity and malignant behaviors in DXR-resistant OS cells. Also, circPRDM2 silencing improved DXR sensitivity in vivo. Our study demonstrated the role of circPRDM2/miR-760/EZH2 axis in enhancing DXR resistance. Our study demonstrated the role of circPRDM2/miR-760/EZH2 axis in enhancing DXR resistance. Circulating tumor endothelial cells (CTECs) are cells that originate from tumor endothelial cells (TECs) of blood vessels and are shed into peripheral blood. Some studies have shown that CTECs are associated with tumor angiogenesis, growth and indicate prognosis in patients with malignant solid tumor. However, the role of CTECs especially the phenotype of CTECs in pancreatic adenocarcinoma (PDAC) is still not clear. We investigated the relationship between CTECs and patients' prognosis. A total of 73 patients with resectable PDAC were enrolled in our research and underwent radical surgery. Peripheral venous blood samples were collected before surgery, on postoperative day (POD) 7 and on postoperative month (POM) 1, respectively. We used integrated subtraction enrichment and immunostaining-fluorescence in situ hybridization (SE-iFISH) platform to identify and enumerate CTECs. Immunofluorescence was used to identify CTECs expressing CD44 and vimentin. In patients with early tumor recurrence (DFS< 6 months), the preoperative CD44+ CTEC levels showed significantly higher ( = 0.023). Univariate and multivariate analysis showed that history of diabetes [HR 2.656 (1.194-5.908), = 0.017], numbers of positive lymph nodes [HR 1.871 (1.388-2.522), < 0.001], preoperative numbers of CD44+ CTECs [HR 1.216 (1.064-1.390), P = 0.004], and POM1 CA19-9 level [HR 1.002 (1.001-1.002), P < 0.001] were independent prognostic factors for DFS. The detection of CD44+CTECs in patients with resectable PDAC preoperatively could be an independent predictor of shorter DFS after radical surgery. The detection of CD44+CTECs in patients with resectable PDAC preoperatively could be an independent predictor of shorter DFS after radical surgery. Ameloblastoma is a
