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10.4049/jimmunol.1302895 http://scihub22266oqcxt.onion/10.4049/jimmunol.1302895 C4078793!4078793!24829407     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       J+Immunol 2014 ; 192 (12): 6111-9 Nephropedia Template TP {{tp|p=24829407|t=2014. Novel Role for Tumor-Induced Expansion of Myeloid Derived Cells in Cancer Cachexia |pdf=|usr=}}{{24829407}} gab.com Text Novel Role for Tumor-Induced Expansion of Myeloid Derived Cells in Cancer Cachexia JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24829407 #FOAvip Cancer progression is associated with inflammation, increased metabolic demand, infection, cachexia, and eventually, death. Myeloid-derived suppressor cells (MDSCs) commonly expand during cancer and are associated with adaptive immune suppression and inflammatory metabolite production. We propose that cancer-induced cachexia is driven at least in part by the expansion of MDSCs. MDSC expansion in 4T1 mammary carcinoma-bearing hosts is associated with induction of a hepatic acute phase protein response and altered host energy and fat metabolism, and eventually, reduced survival to polymicrobial sepsis and endotoxemia. Similar results are also seen in mice bearing a Lewis lung carcinoma and a C26 colon adenocarcinoma. However, a similar cachexia response is not seen with equivalent growth of the 66C4 subclone of 4T1, where MDSC expansion does not occur. Importantly, reducing MDSC numbers in 4T1-bearing animals can ameliorate some of these late responses, and reduce susceptibility to inflammation-induced organ injury and death. In addition, administering MDSCs from both tumor and nontumor-bearing mice can produce an acute phase response. Thus, we propose a previously undescribed mechanism for the development of cancer cachexia, whereby progressive MDSC expansion contributes to changes in host protein and energy metabolism, and reduced resistance to infection. Twit Text FOAVip Novel Role for Tumor-Induced Expansion of Myeloid Derived Cells in Cancer Cachexia ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24829407 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24829407 #FOAvip English Wikipedia <ref>{{Cite pmid|24829407}}</ref> Novel Role for Tumor-Induced Expansion of Myeloid Derived Cells in Cancer Cachexia #MMPMID24829407 Cuenca AG; Cuenca AL; Winfield RD; Joiner DN; Gentile L; Delano MJ; Kelly-Scumpia KM; Scumpia PO; Matheny MK; Scarpace PJ; Vila L; Efron PA; LaFace DM; Moldawer LL J Immunol 2014[Jun]; 192 (12): 6111-9 PMID24829407show ga Cancer progression is associated with inflammation, increased metabolic demand, infection, cachexia, and eventually, death. Myeloid-derived suppressor cells (MDSCs) commonly expand during cancer and are associated with adaptive immune suppression and inflammatory metabolite production. We propose that cancer-induced cachexia is driven at least in part by the expansion of MDSCs. MDSC expansion in 4T1 mammary carcinoma-bearing hosts is associated with induction of a hepatic acute phase protein response and altered host energy and fat metabolism, and eventually, reduced survival to polymicrobial sepsis and endotoxemia. Similar results are also seen in mice bearing a Lewis lung carcinoma and a C26 colon adenocarcinoma. However, a similar cachexia response is not seen with equivalent growth of the 66C4 subclone of 4T1, where MDSC expansion does not occur. Importantly, reducing MDSC numbers in 4T1-bearing animals can ameliorate some of these late responses, and reduce susceptibility to inflammation-induced organ injury and death. In addition, administering MDSCs from both tumor and nontumor-bearing mice can produce an acute phase response. Thus, we propose a previously undescribed mechanism for the development of cancer cachexia, whereby progressive MDSC expansion contributes to changes in host protein and energy metabolism, and reduced resistance to infection. äNovel Role for Tumor-Induced Expansion of Myeloid Derived Cells in Can(epmc).pdf DeepDyve Pubget Overpricing