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10.1007/s10585-018-9876-z http://scihub22266oqcxt.onion/10.1007/s10585-018-9876-z C5959274!5959274!29396728     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 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\29396728.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Exp+Metastasis 2018 ; 35 (1-2): 37-51 Nephropedia Template TP {{tp|p=29396728|t=2018. Pharmacologic ascorbate (P-AscH?) suppresses hypoxia-inducible Factor-1? (HIF-1?) in pancreatic adenocarcinoma |pdf=|usr=}}{{29396728}} gab.com Text Pharmacologic ascorbate (P-AscH ) suppresses hypoxia-inducible Factor-1 (HIF-1 ) in pancreatic adenocarcinoma JO: Clin Exp Metastasis http://www.kidney.de/pget.php?&tw=1&pmid=29396728 #FOAvip HIF-1? is a transcriptional regulator that functions in the adaptation of cells to hypoxic conditions; it strongly impacts the prognosis of patients with cancer. High-dose, intravenous, pharmacological ascorbate (P-AscH?), induces cytotoxicity and oxidative stress selectively in cancer cells by acting as a pro-drug for the delivery of hydrogen peroxide (H2O2); early clinical data suggest improved survival and inhibition of metastasis in patients being actively treated with P-AscH?. Previous studies have demonstrated that activation of HIF-1? is necessary for P-AscH? sensitivity. We hypothesized that pancreatic cancer (PDAC) progression and metastasis could be be targeted by P-AscH?via H2O2-mediated inhibition of HIF-1? stabilization. Our study demonstrates an oxygen- and prolyl hydroxylase-independent regulation of HIF-1? by P-AscH?. Additionally, P-AscH? decreased VEGF secretion in a dose-dependent manner that was reversible with catalase, consistent with an H2O2-mediated mechanism. Pharmacological and genetic manipulations of HIF-1? did not alter P-AscH?-induced cytotoxicity. In vivo, P-AscH? inhibited tumor growth and VEGF expression. We conclude that P-AscH? suppresses the levels of HIF-1? protein in hypoxic conditions through a post-translational mechanism. These findings suggest potential new therapies specifically designed to inhibit the mechanisms that drive metastases as a part of PDAC treatment. Twit Text FOAVip Pharmacologic ascorbate (P-AscH ) suppresses hypoxia-inducible Factor-1 (HIF-1 ) in pancreatic adenocarcinoma ????Clin Exp Metastasis http://www.kidney.de/pget.php?&tw=1&pmid=29396728 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29396728 #FOAvip English Wikipedia <ref>{{Cite pmid|29396728}}</ref> Pharmacologic ascorbate (P-AscH?) suppresses hypoxia-inducible Factor-1? (HIF-1?) in pancreatic adenocarcinoma #MMPMID29396728 Wilkes JG; O?Leary BR; Du J; Klinger AR; Sibenaller ZA; Doskey CM; Gibson-Corley KN; Alexander MS; Tsai S; Buettner GR; Cullen JJ Clin Exp Metastasis 2018[Feb]; 35 (1-2): 37-51 PMID29396728show ga HIF-1? is a transcriptional regulator that functions in the adaptation of cells to hypoxic conditions; it strongly impacts the prognosis of patients with cancer. High-dose, intravenous, pharmacological ascorbate (P-AscH?), induces cytotoxicity and oxidative stress selectively in cancer cells by acting as a pro-drug for the delivery of hydrogen peroxide (H2O2); early clinical data suggest improved survival and inhibition of metastasis in patients being actively treated with P-AscH?. Previous studies have demonstrated that activation of HIF-1? is necessary for P-AscH? sensitivity. We hypothesized that pancreatic cancer (PDAC) progression and metastasis could be be targeted by P-AscH?via H2O2-mediated inhibition of HIF-1? stabilization. Our study demonstrates an oxygen- and prolyl hydroxylase-independent regulation of HIF-1? by P-AscH?. Additionally, P-AscH? decreased VEGF secretion in a dose-dependent manner that was reversible with catalase, consistent with an H2O2-mediated mechanism. Pharmacological and genetic manipulations of HIF-1? did not alter P-AscH?-induced cytotoxicity. In vivo, P-AscH? inhibited tumor growth and VEGF expression. We conclude that P-AscH? suppresses the levels of HIF-1? protein in hypoxic conditions through a post-translational mechanism. These findings suggest potential new therapies specifically designed to inhibit the mechanisms that drive metastases as a part of PDAC treatment. äPharmacologic ascorbate (P-AscH?) suppresses hypoxia-inducible Factor-(epmc).pdf DeepDyve Pubget Overpricing