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10.1158/2159-8290.CD-15-0822 http://scihub22266oqcxt.onion/10.1158/2159-8290.CD-15-0822 C4783189!4783189!26715642     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26715642&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Discov 2016 ; 6 (3): 256-69 Nephropedia Template TP {{tp|p=26715642|t=2016. Hif1? deletion reveals pro-neoplastic function of B cells in pancreatic neoplasia |pdf=|usr=}}{{26715642}} gab.com Text Hif1 deletion reveals pro-neoplastic function of B cells in pancreatic neoplasia JO: Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=26715642 #FOAvip Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related deaths worldwide, with an exceedingly low 5-year survival rate. PDAC tumors are characterized by an extensive desmoplastic stromal response and hypovascularity, suggesting that tumor hypoxia could regulate PDAC initiation and/or progression. Using a well-defined, autochthonous KrasG12D-driven murine model, as well as human tumors, we demonstrate that hypoxia and stabilization of hypoxia-inducible factor 1? (HIF1?), a principal mediator of hypoxic adaptation, emerge early during preinvasive stages of PDAC. Surprisingly, pancreas-specific Hif1? deletion drastically accelerated KrasG12D-driven pancreatic neoplasia, and was accompanied by significant increases in intrapancreatic B lymphocytes, featuring prominent influx of a rare ?B1b? B cell subtype. Finally, treatment of HIF1?-deficient mice with B cell-depleting ?CD20 monoclonal antibodies inhibited progression of pancreatic intraepithelial neoplasia (PanIN). Our data reveal a previously unrecognized role for B cells in promoting pancreatic tumorigenesis, and implicate HIF1? as a critical regulator of PDAC development. Twit Text FOAVip Hif1 deletion reveals pro-neoplastic function of B cells in pancreatic neoplasia ????Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=26715642 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26715642 #FOAvip English Wikipedia <ref>{{Cite pmid|26715642}}</ref> Hif1? deletion reveals pro-neoplastic function of B cells in pancreatic neoplasia #MMPMID26715642 Lee K; Spata M; Bayne LJ; Buza EL; Durham AC; Allman D; Vonderheide RH; Simon MC Cancer Discov 2016[Mar]; 6 (3): 256-69 PMID26715642show ga Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related deaths worldwide, with an exceedingly low 5-year survival rate. PDAC tumors are characterized by an extensive desmoplastic stromal response and hypovascularity, suggesting that tumor hypoxia could regulate PDAC initiation and/or progression. Using a well-defined, autochthonous KrasG12D-driven murine model, as well as human tumors, we demonstrate that hypoxia and stabilization of hypoxia-inducible factor 1? (HIF1?), a principal mediator of hypoxic adaptation, emerge early during preinvasive stages of PDAC. Surprisingly, pancreas-specific Hif1? deletion drastically accelerated KrasG12D-driven pancreatic neoplasia, and was accompanied by significant increases in intrapancreatic B lymphocytes, featuring prominent influx of a rare ?B1b? B cell subtype. Finally, treatment of HIF1?-deficient mice with B cell-depleting ?CD20 monoclonal antibodies inhibited progression of pancreatic intraepithelial neoplasia (PanIN). Our data reveal a previously unrecognized role for B cells in promoting pancreatic tumorigenesis, and implicate HIF1? as a critical regulator of PDAC development. äHif1? deletion reveals pro-neoplastic function of B cells in pancreati(epmc).pdf DeepDyve Pubget Overpricing