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10.1158/0008-5472.CAN-14-2946 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-14-2946 C4470771!4470771!25908586     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2015 ; 75 (12): 2566-79 Nephropedia Template TP {{tp|p=25908586|t=2015. G-CSF promotes neuroblastoma tumorigenicity and metastasis via STAT3-dependent cancer stem cell activation |pdf=|usr=}}{{25908586}} gab.com Text G-CSF promotes neuroblastoma tumorigenicity and metastasis via STAT3-dependent cancer stem cell activation JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25908586 #FOAvip Increasing evidence suggests that inflammatory cytokines play a critical role in tumor initiation and progression. We previously isolated a Cancer Stem Cell-like (CSC) subpopulation in neuroblastoma based on differential expression of the receptor for G-CSF (Granulocyte-Colony Stimulating Factor). Here we demonstrate that G-CSF selectively activates signal transducer and activator of transcription 3 (STAT3) within neuroblastoma CSC subpopulations, promoting their expansion in vitro and in vivo. Exogenous G-CSF enhances tumor growth and metastasis in human xenograft and murine neuroblastoma tumor models. In response to G-CSF, STAT3 transcriptionally activates the G-CSF receptor (encoded by CSF3R), creating a CSC sustaining positive-feedback loop. Blockade of G-CSF/STAT3 signaling loop with either anti-G-CSF antibody or STAT3 inhibitor depletes the CSC subpopulation within tumors, driving correlated tumor regression, blocking metastasis and increasing chemosensitivity. Taken together, these data define G-CSF as a tumorigenic growth factor for neuroblastoma and suggest a comprehensive re-evaluation of the clinical use of G-CSF in these patients. Our data also demonstrate that direct targeting of the G-CSF/STAT3 signaling represents a novel therapeutic approach for neuroblastoma. Twit Text FOAVip G-CSF promotes neuroblastoma tumorigenicity and metastasis via STAT3-dependent cancer stem cell activation ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25908586 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25908586 #FOAvip English Wikipedia <ref>{{Cite pmid|25908586}}</ref> G-CSF promotes neuroblastoma tumorigenicity and metastasis via STAT3-dependent cancer stem cell activation #MMPMID25908586 Agarwal S; Lakoma A; Chen Z; Hicks J; Metelitsa LS; Kim ES; Shohet JM Cancer Res 2015[Jun]; 75 (12): 2566-79 PMID25908586show ga Increasing evidence suggests that inflammatory cytokines play a critical role in tumor initiation and progression. We previously isolated a Cancer Stem Cell-like (CSC) subpopulation in neuroblastoma based on differential expression of the receptor for G-CSF (Granulocyte-Colony Stimulating Factor). Here we demonstrate that G-CSF selectively activates signal transducer and activator of transcription 3 (STAT3) within neuroblastoma CSC subpopulations, promoting their expansion in vitro and in vivo. Exogenous G-CSF enhances tumor growth and metastasis in human xenograft and murine neuroblastoma tumor models. In response to G-CSF, STAT3 transcriptionally activates the G-CSF receptor (encoded by CSF3R), creating a CSC sustaining positive-feedback loop. Blockade of G-CSF/STAT3 signaling loop with either anti-G-CSF antibody or STAT3 inhibitor depletes the CSC subpopulation within tumors, driving correlated tumor regression, blocking metastasis and increasing chemosensitivity. Taken together, these data define G-CSF as a tumorigenic growth factor for neuroblastoma and suggest a comprehensive re-evaluation of the clinical use of G-CSF in these patients. Our data also demonstrate that direct targeting of the G-CSF/STAT3 signaling represents a novel therapeutic approach for neuroblastoma. äG-CSF promotes neuroblastoma tumorigenicity and metastasis via STAT3-d(epmc).pdf DeepDyve Pubget Overpricing