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10.1038/ncb3355 http://scihub22266oqcxt.onion/10.1038/ncb3355 C4884142!4884142!27183469     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Cell+Biol 2016 ; 18 (6): 632-44 Nephropedia Template TP {{tp|p=27183469|t=2016. Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation |pdf=|usr=}}{{27183469}} gab.com Text Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation JO: Nat Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27183469 #FOAvip Myeloid-derived suppressor cells (MDSCs) play critical roles in primary and metastatic cancer progression. While MDSC regulation is widely variable even within patients harboring the same type of malignancy, the mechanisms governing such heterogeneity are largely unknown. Here, integrating human tumor genomics and syngeneic mammary tumor models, we demonstrate that mTOR signaling in cancer cells dictates a mammary tumor?s ability to stimulate MDSC accumulation through regulating G-CSF. Inhibiting this pathway or its activators (e.g., FGFR) impairs tumor progression, which is partially rescued by restoring MDSCs or G-CSF. Tumor-initiating cells (TICs) exhibit elevated G-CSF. MDSCs reciprocally increase TIC frequency through activating Notch in tumor cells, forming a feed-forward loop. Analyses of primary breast cancers and patient-derived xenografts (PDXs) corroborate these mechanisms in patients. These findings establish a non-canonical oncogenic role of mTOR signaling in recruiting pro-tumorigenic MDSCs and show how defined cancer subsets may evolve to promote and depend upon a distinct immune microenvironment. Twit Text FOAVip Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation ????Nat Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27183469 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27183469 #FOAvip English Wikipedia <ref>{{Cite pmid|27183469}}</ref> Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation #MMPMID27183469 Welte T; Kim IS; Tian L; Gao X; Wang H; Li J; Holdman XB; Herschkowitz JI; Pond A; Xie G; Kurley S; Nguyen T; Liao L; Dobrolecki LE; Mo Q; Edwards DP; Huang S; Xin L; Xu J; Li Y; Lewis MT; Wang T; Westbrook TF; Rosen JM; Zhang XHF Nat Cell Biol 2016[Jun]; 18 (6): 632-44 PMID27183469show ga Myeloid-derived suppressor cells (MDSCs) play critical roles in primary and metastatic cancer progression. While MDSC regulation is widely variable even within patients harboring the same type of malignancy, the mechanisms governing such heterogeneity are largely unknown. Here, integrating human tumor genomics and syngeneic mammary tumor models, we demonstrate that mTOR signaling in cancer cells dictates a mammary tumor?s ability to stimulate MDSC accumulation through regulating G-CSF. Inhibiting this pathway or its activators (e.g., FGFR) impairs tumor progression, which is partially rescued by restoring MDSCs or G-CSF. Tumor-initiating cells (TICs) exhibit elevated G-CSF. MDSCs reciprocally increase TIC frequency through activating Notch in tumor cells, forming a feed-forward loop. Analyses of primary breast cancers and patient-derived xenografts (PDXs) corroborate these mechanisms in patients. These findings establish a non-canonical oncogenic role of mTOR signaling in recruiting pro-tumorigenic MDSCs and show how defined cancer subsets may evolve to promote and depend upon a distinct immune microenvironment. äOncogenic mTOR signaling recruits myeloid-derived suppressor cells to (epmc).pdf DeepDyve Pubget Overpricing