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10.1038/cddis.2017.455 http://scihub22266oqcxt.onion/10.1038/cddis.2017.455 C5680577!5680577!28981109     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (10): e3064- Nephropedia Template TP {{tp|p=28981109|t=2017. Dexamethasone mediates pancreatic cancer progression by glucocorticoid receptor, TGF? and JNK/AP-1 |pdf=|usr=}}{{28981109}} gab.com Text Dexamethasone mediates pancreatic cancer progression by glucocorticoid receptor, TGF and JNK/AP-1 JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28981109 #FOAvip Glucocorticoids such as dexamethasone are widely co-prescribed with cytotoxic therapy because of their proapoptotic effects in lymphoid cancer, reduction of inflammation and edema and additional benefits. Concerns about glucocorticoid-induced therapy resistance, enhanced metastasis and reduced survival of patients are largely not considered. We analyzed dexamethasone-induced tumor progression in three established and one primary human pancreatic ductal adenocarcinoma (PDA) cell lines and in PDA tissue from patients and xenografts by FACS and western blot analysis, immunohistochemistry, MTT and wound assay, colony and spheroid formation, EMSA and in vivo tumor growth and metastasis of tumor xenografts on chicken eggs and mice. Dexamethasone in concentrations observed in plasma of patients favored epithelial?mesenchymal transition, self-renewal potential and cancer progression. Ras/JNK signaling, enhanced expression of TGF?, vimentin, Notch-1 and SOX-2 and the inhibition of E-cadherin occurred. This was confirmed in patient and xenograft tissue, where dexamethasone induced tumor proliferation, gemcitabine resistance and metastasis. Inhibition of each TGF? receptor-I, glucocorticoid receptor or JNK signaling partially reversed the dexamethasone-mediated effects, suggesting a complex signaling network. These data reveal that dexamethasone mediates progression by membrane effects and binding to glucocorticoid receptor. Twit Text FOAVip Dexamethasone mediates pancreatic cancer progression by glucocorticoid receptor, TGF and JNK/AP-1 ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28981109 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28981109 #FOAvip English Wikipedia <ref>{{Cite pmid|28981109}}</ref> Dexamethasone mediates pancreatic cancer progression by glucocorticoid receptor, TGF? and JNK/AP-1 #MMPMID28981109 Liu L; Aleksandrowicz E; Schönsiegel F; Gröner D; Bauer N; Nwaeburu CC; Zhao Z; Gladkich J; Hoppe-Tichy T; Yefenof E; Hackert T; Strobel O; Herr I Cell Death Dis 2017[Oct]; 8 (10): e3064- PMID28981109show ga Glucocorticoids such as dexamethasone are widely co-prescribed with cytotoxic therapy because of their proapoptotic effects in lymphoid cancer, reduction of inflammation and edema and additional benefits. Concerns about glucocorticoid-induced therapy resistance, enhanced metastasis and reduced survival of patients are largely not considered. We analyzed dexamethasone-induced tumor progression in three established and one primary human pancreatic ductal adenocarcinoma (PDA) cell lines and in PDA tissue from patients and xenografts by FACS and western blot analysis, immunohistochemistry, MTT and wound assay, colony and spheroid formation, EMSA and in vivo tumor growth and metastasis of tumor xenografts on chicken eggs and mice. Dexamethasone in concentrations observed in plasma of patients favored epithelial?mesenchymal transition, self-renewal potential and cancer progression. Ras/JNK signaling, enhanced expression of TGF?, vimentin, Notch-1 and SOX-2 and the inhibition of E-cadherin occurred. This was confirmed in patient and xenograft tissue, where dexamethasone induced tumor proliferation, gemcitabine resistance and metastasis. Inhibition of each TGF? receptor-I, glucocorticoid receptor or JNK signaling partially reversed the dexamethasone-mediated effects, suggesting a complex signaling network. These data reveal that dexamethasone mediates progression by membrane effects and binding to glucocorticoid receptor. äDexamethasone mediates pancreatic cancer progression by glucocorticoid(epmc).pdf DeepDyve Pubget Overpricing