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10.1186/s12885-017-3171-2 http://scihub22266oqcxt.onion/10.1186/s12885-017-3171-2 C5348880!5348880 !28288569     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28288569 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       BMC+Cancer 2017 ; 17 (1 ): 189 Nephropedia Template TP {{tp|p=28288569 |t=2017. Endothelial Dll4 overexpression reduces vascular response and inhibits tumor growth and metastasization in vivo |pdf=|usr=}}{{28288569 }} gab.com Text Endothelial Dll4 overexpression reduces vascular response and inhibits tumor growth and metastasization in vivo JO: BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28288569 #FOAvip BACKGROUND: The inhibition of Delta-like 4 (Dll4)/Notch signaling has been shown to result in excessive, nonfunctional vessel proliferation and significant tumor growth suppression. However, safety concerns emerged with the identification of side effects resulting from chronic Dll4/Notch blockade. Alternatively, we explored the endothelial Dll4 overexpression using different mouse tumor models. METHODS: We used a transgenic mouse model of endothelial-specific Dll4 overexpression, previously produced. Growth kinetics and vascular histopathology of several types of solid tumors was evaluated, namely Lewis Lung Carcinoma xenografts, chemically-induced skin papillomas and RIP1-Tag2 insulinomas. RESULTS: We found that increased Dll4/Notch signaling reduces tumor growth by reducing vascular endothelial growth factor (VEGF)-induced endothelial proliferation, tumor vessel density and overall tumor blood supply. In addition, Dll4 overexpression consistently improved tumor vascular maturation and functionality, as indicated by increased vessel calibers, enhanced mural cell recruitment and increased network perfusion. Importantly, the tumor vessel normalization is not more effective than restricted vessel proliferation, but was found to prevent metastasis formation and allow for increased delivery to the tumor of concomitant chemotherapy, improving its efficacy. CONCLUSIONS: By reducing endothelial sensitivity to VEGF, these results imply that Dll4/Notch stimulation in tumor microenvironment could be beneficial to solid cancer patient treatment by reducing primary tumor size, improving tumor drug delivery and reducing metastization. Endothelial specific Dll4 overexpression thus appears as a promising anti-angiogenic modality that might improve cancer control. Twit Text FOAVip Endothelial Dll4 overexpression reduces vascular response and inhibits tumor growth and metastasization in vivo ????BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28288569 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28288569 #FOAvip English Wikipedia <ref>{{Cite pmid|28288569 }}</ref> Endothelial Dll4 overexpression reduces vascular response and inhibits tumor growth and metastasization in vivo #MMPMID28288569 Trindade A ; Djokovic D ; Gigante J ; Mendonça L ; Duarte A BMC Cancer 2017[Mar]; 17 (1 ): 189 PMID28288569 show ga BACKGROUND: The inhibition of Delta-like 4 (Dll4)/Notch signaling has been shown to result in excessive, nonfunctional vessel proliferation and significant tumor growth suppression. However, safety concerns emerged with the identification of side effects resulting from chronic Dll4/Notch blockade. Alternatively, we explored the endothelial Dll4 overexpression using different mouse tumor models. METHODS: We used a transgenic mouse model of endothelial-specific Dll4 overexpression, previously produced. Growth kinetics and vascular histopathology of several types of solid tumors was evaluated, namely Lewis Lung Carcinoma xenografts, chemically-induced skin papillomas and RIP1-Tag2 insulinomas. RESULTS: We found that increased Dll4/Notch signaling reduces tumor growth by reducing vascular endothelial growth factor (VEGF)-induced endothelial proliferation, tumor vessel density and overall tumor blood supply. In addition, Dll4 overexpression consistently improved tumor vascular maturation and functionality, as indicated by increased vessel calibers, enhanced mural cell recruitment and increased network perfusion. Importantly, the tumor vessel normalization is not more effective than restricted vessel proliferation, but was found to prevent metastasis formation and allow for increased delivery to the tumor of concomitant chemotherapy, improving its efficacy. CONCLUSIONS: By reducing endothelial sensitivity to VEGF, these results imply that Dll4/Notch stimulation in tumor microenvironment could be beneficial to solid cancer patient treatment by reducing primary tumor size, improving tumor drug delivery and reducing metastization. Endothelial specific Dll4 overexpression thus appears as a promising anti-angiogenic modality that might improve cancer control. |*Gene Expression Regulation, Neoplastic [MESH] |Adaptor Proteins, Signal Transducing [MESH] |Animals [MESH] |Calcium-Binding Proteins [MESH] |Carcinoma, Lewis Lung/blood supply/genetics/pathology [MESH] |Cell Line, Tumor [MESH] |Disease Models, Animal [MESH] |Endothelium, Vascular/*metabolism [MESH] |Humans [MESH] |Insulinoma/blood supply/genetics/pathology [MESH] |Intracellular Signaling Peptides and Proteins/*genetics [MESH] |Male [MESH] |Membrane Proteins/*genetics [MESH] |Mice, Transgenic [MESH] |Neoplasm Metastasis [MESH] |Neoplasms, Experimental/blood supply/*genetics/pathology [MESH] |Neovascularization, Pathologic/*genetics [MESH]Endothelial Dll4 overexpression reduces vascular response and inhibits(epmc).pdf DeepDyve Pubget Overpricing