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10.1158/0008-5472.CAN-13-3225 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-13-3225 C4394897!4394897!24769442     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       Cancer+Res 2014 ; 74 (13): 3556-66 Nephropedia Template TP {{tp|p=24769442|t=2014. API5 confers tumoral immune escape through FGF2-dependent cell survival pathway |pdf=|usr=}}{{24769442}} gab.com Text API5 confers tumoral immune escape through FGF2-dependent cell survival pathway JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24769442 #FOAvip Identifying immune escape mechanisms used by tumors may define strategies to sensitize them to immunotherapies to which they are otherwise resistant. In this study, we show that the anti-apoptotic gene API5 acts as an immune escape gene in tumors by rendering them resistant to apoptosis triggered by tumor antigen-specific T cells. Its RNAi-mediated silencing in tumor cells expressing high levels of API5 restored antigen-specific immune sensitivity. Conversely, introducing API5 into API5low cells conferred immune resistance. Mechanistic investigations revealed that API5 mediated resistance by upregulating FGF2 signaling through a FGFR1/PKC?/ERK effector pathway that triggered degradation of the pro-apoptotic molecule BIM. Blockade of FGF2, PKC? or ERK phenocopied the effect of API5 silencing in tumor cells expressing high levels of API5, to either murine or human antigen-specific T cells. Our results identify a novel mechanism of immune escape that can be inhibited to potentiate the efficacy of targeted active immunotherapies. Twit Text FOAVip API5 confers tumoral immune escape through FGF2-dependent cell survival pathway ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24769442 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24769442 #FOAvip English Wikipedia <ref>{{Cite pmid|24769442}}</ref> API5 confers tumoral immune escape through FGF2-dependent cell survival pathway #MMPMID24769442 Noh KH; Kim SH; Kim JH; Song KH; Lee YH; Kang TH; Han HD; Sood AK; Ng J; Kim K; Sonn CH; Kumar V; Yee C; Lee KM; Kim TW Cancer Res 2014[Jul]; 74 (13): 3556-66 PMID24769442show ga Identifying immune escape mechanisms used by tumors may define strategies to sensitize them to immunotherapies to which they are otherwise resistant. In this study, we show that the anti-apoptotic gene API5 acts as an immune escape gene in tumors by rendering them resistant to apoptosis triggered by tumor antigen-specific T cells. Its RNAi-mediated silencing in tumor cells expressing high levels of API5 restored antigen-specific immune sensitivity. Conversely, introducing API5 into API5low cells conferred immune resistance. Mechanistic investigations revealed that API5 mediated resistance by upregulating FGF2 signaling through a FGFR1/PKC?/ERK effector pathway that triggered degradation of the pro-apoptotic molecule BIM. Blockade of FGF2, PKC? or ERK phenocopied the effect of API5 silencing in tumor cells expressing high levels of API5, to either murine or human antigen-specific T cells. Our results identify a novel mechanism of immune escape that can be inhibited to potentiate the efficacy of targeted active immunotherapies. äAPI5 confers tumoral immune escape through FGF2-dependent cell surviva(epmc).pdf DeepDyve Pubget Overpricing