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10.1038/cgt.2015.21 http://scihub22266oqcxt.onion/10.1038/cgt.2015.21 C4470814!4470814!25908451     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25908451&cmd=llinks): Failed to open stream: HTTP request failed! 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The Receptor for Advanced Glycation End Products (RAGE) Enhances Autophagy and Neutrophil Extracellular Traps in Pancreatic Cancer |pdf=|usr=}}{{25908451}} gab.com Text The Receptor for Advanced Glycation End Products (RAGE) Enhances Autophagy and Neutrophil Extracellular Traps in Pancreatic Cancer JO: Cancer Gene Ther http://www.kidney.de/pget.php?&tw=1&pmid=25908451 #FOAvip Neutrophil extracellular traps (NETs) are formed when neutrophils expel their DNA, histones and intracellular proteins into the extracellular space or circulation. NET formation is dependent on autophagy and is mediated by citrullination of histones to allow for unwinding and subsequent expulsion of DNA. NETs play an important role in the pathogenesis of several sterile inflammatory diseases, including malignancy, therefore we investigated the role of NETs in the setting of pancreatic ductal adenocarcinoma (PDA). Neutrophils isolated from two distinct animal models of PDA had an increased propensity to form NETs following stimulation with platelet activating factor (PAF). Serum DNA, a marker of circulating NET formation, was elevated in tumor bearing animals as well as in patients with PDA. Citrullinated histone H3 expression, a marker of NET formation, was observed in pancreatic tumors obtained from murine models and patients with PDA. Inhibition of autophagy with chloroquine or genetic ablation of RAGE resulted in decreased propensity for NET formation, decreased serum DNA, and decreased citrullinated histone H3 expression in the pancreatic tumor microenvironment. We conclude that NETs are upregulated in pancreatic cancer through RAGE dependent/autophagy pathways. Twit Text FOAVip The Receptor for Advanced Glycation End Products (RAGE) Enhances Autophagy and Neutrophil Extracellular Traps in Pancreatic Cancer ????Cancer Gene Ther http://www.kidney.de/pget.php?&tw=1&pmid=25908451 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25908451 #FOAvip English Wikipedia <ref>{{Cite pmid|25908451}}</ref> The Receptor for Advanced Glycation End Products (RAGE) Enhances Autophagy and Neutrophil Extracellular Traps in Pancreatic Cancer #MMPMID25908451 Boone BA; Orlichenko L; Schapiro NE; Loughran P; Gianfrate GC; Ellis JT; Singhi AD; Kang R; Tang D; Lotze MT; Zeh HJ Cancer Gene Ther 2015[Jun]; 22 (6): 326-34 PMID25908451show ga Neutrophil extracellular traps (NETs) are formed when neutrophils expel their DNA, histones and intracellular proteins into the extracellular space or circulation. NET formation is dependent on autophagy and is mediated by citrullination of histones to allow for unwinding and subsequent expulsion of DNA. NETs play an important role in the pathogenesis of several sterile inflammatory diseases, including malignancy, therefore we investigated the role of NETs in the setting of pancreatic ductal adenocarcinoma (PDA). Neutrophils isolated from two distinct animal models of PDA had an increased propensity to form NETs following stimulation with platelet activating factor (PAF). Serum DNA, a marker of circulating NET formation, was elevated in tumor bearing animals as well as in patients with PDA. Citrullinated histone H3 expression, a marker of NET formation, was observed in pancreatic tumors obtained from murine models and patients with PDA. Inhibition of autophagy with chloroquine or genetic ablation of RAGE resulted in decreased propensity for NET formation, decreased serum DNA, and decreased citrullinated histone H3 expression in the pancreatic tumor microenvironment. We conclude that NETs are upregulated in pancreatic cancer through RAGE dependent/autophagy pathways. äThe Receptor for Advanced Glycation End Products (RAGE) Enhances Autop(epmc).pdf DeepDyve Pubget Overpricing