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10.1158/2159-8290.CD-15-0843

http://scihub22266oqcxt.onion/10.1158/2159-8290.CD-15-0843
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C5709038!5709038!26715643
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suck abstract from ncbi


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pmid26715643      Cancer+Discov 2016 ; 6 (3): 247-55
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  • IL-35 producing B cells promote the development of pancreatic neoplasia #MMPMID26715643
  • Pylayeva-Gupta Y; Das S; Handler JS; Hajdu CH; Coffre M; Koralov SB; Bar-Sagi D
  • Cancer Discov 2016[Mar]; 6 (3): 247-55 PMID26715643show ga
  • A salient feature of pancreatic ductal adenocarcinoma (PDA) is an abundant fibroinflammatory response characterized by the recruitment of immune and mesenchymal cells and the consequent establishment of a pro-tumorigenic microenvironment. Here we report the prominent presence of B cells in human pancreatic intraepithelial neoplasia (PanIN) and PDA lesions as well as in oncogenic K-Ras-driven pancreatic neoplasms in the mouse. The growth of orthotopic pancreatic neoplasms harboring oncogenic K-Ras was significantly compromised in B cell-deficient mice (?MT), and this growth deficiency could be rescued by the reconstitution of a CD1dhighCD5+ B cell subset. The pro-tumorigenic effect of B cells was mediated by their expression of IL-35 through a mechanism involving IL-35-mediated stimulation of tumor cell proliferation. Our results identify a previously unrecognized role for IL-35-producing CD1dhighCD5+ B cells in the pathogenesis of pancreatic cancer and underscore the potential significance of a B cell/IL-35 axis as a therapeutic target.
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