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10.1158/0008-5472.CAN-14-1240 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-14-1240 C4268204!4268204!25326491     free     free     free 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+Res 2014 ; 74 (24): 7285-97 Nephropedia Template TP {{tp|p=25326491|t=2014. RAGE Expression in Tumor-associated Macrophages Promotes Angiogenesis in Glioma |pdf=|usr=}}{{25326491}} gab.com Text RAGE Expression in Tumor-associated Macrophages Promotes Angiogenesis in Glioma JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25326491 #FOAvip Interaction of RAGE with its ligands can promote tumor progression, invasion and angiogenesis. Although blocking RAGE signaling has been proposed as a potential anti-cancer strategy, functional contributions of RAGE expression in the tumor microenvironment (TME) has not been investigated in detail. Here, we evaluated the effect of genetic depletion of RAGE in TME on the growth of gliomas. In both invasive and non-invasive glioma models, animal survival was prolonged in RAGE knockout (Ager?/?) mice. However, the improvement in survival in Ager?/? mice was not due to changes in tumor growth rate but rather to a reduction in tumor-associated inflammation. Furthermore, RAGE ablation in the TME abrogated angiogenesis by downregulating the expression of pro-angiogenic factors which prevented normal vessel formation, thereby generating a leaky vasculature. These alterations were most prominent in non-invasive gliomas, where the expression of VEGF and pro-inflammatory cytokines were also lower in tumor-associated macrophages (TAM) in Ager?/? mice. Interestingly, reconstitution of Ager?/? TAM with wild-type microglia or macrophages normalized tumor vascularity. Our results establish that RAGE signaling in glioma-associated microglia and TAM drives angiogenesis, underscoring the complex role of RAGE and its ligands in gliomagenesis. Twit Text FOAVip RAGE Expression in Tumor-associated Macrophages Promotes Angiogenesis in Glioma ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25326491 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25326491 #FOAvip English Wikipedia <ref>{{Cite pmid|25326491}}</ref> RAGE Expression in Tumor-associated Macrophages Promotes Angiogenesis in Glioma #MMPMID25326491 Chen X; Zhang L; Zhang IY; Liang J; Wang H; Ouyang M; Wu S; da Fonseca ACC; Weng L; Yamamoto Y; Yamamoto H; Natarajan R; Badie B Cancer Res 2014[Dec]; 74 (24): 7285-97 PMID25326491show ga Interaction of RAGE with its ligands can promote tumor progression, invasion and angiogenesis. Although blocking RAGE signaling has been proposed as a potential anti-cancer strategy, functional contributions of RAGE expression in the tumor microenvironment (TME) has not been investigated in detail. Here, we evaluated the effect of genetic depletion of RAGE in TME on the growth of gliomas. In both invasive and non-invasive glioma models, animal survival was prolonged in RAGE knockout (Ager?/?) mice. However, the improvement in survival in Ager?/? mice was not due to changes in tumor growth rate but rather to a reduction in tumor-associated inflammation. Furthermore, RAGE ablation in the TME abrogated angiogenesis by downregulating the expression of pro-angiogenic factors which prevented normal vessel formation, thereby generating a leaky vasculature. These alterations were most prominent in non-invasive gliomas, where the expression of VEGF and pro-inflammatory cytokines were also lower in tumor-associated macrophages (TAM) in Ager?/? mice. Interestingly, reconstitution of Ager?/? TAM with wild-type microglia or macrophages normalized tumor vascularity. Our results establish that RAGE signaling in glioma-associated microglia and TAM drives angiogenesis, underscoring the complex role of RAGE and its ligands in gliomagenesis. äRAGE Expression in Tumor-associated Macrophages Promotes Angiogenesis (epmc).pdf DeepDyve Pubget Overpricing