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10.1016/j.ccell.2017.01.014 http://scihub22266oqcxt.onion/10.1016/j.ccell.2017.01.014 C5386178!5386178!28292440     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28292440&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Cell 2017 ; 31 (3): 424-35 Nephropedia Template TP {{tp|p=28292440|t=2017. A Kinase Inhibitor Targeted to mTORC1 Drives Regression in Glioblastoma |pdf=|usr=}}{{28292440}} gab.com Text A Kinase Inhibitor Targeted to mTORC1 Drives Regression in Glioblastoma JO: Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=28292440 #FOAvip Although signaling from PI3K and AKT to mTOR is prominently dysregulated in high-grade glial brain tumors, blockade of PI3K or AKT minimally affects downstream mTOR activity in glioma. Allosteric mTOR inhibitors, such as rapamycin, incompletely block mTORC1 compared to mTOR kinase inhibitors (TORKi). Here, we compared RapaLink-1, a TORKi linked to rapamycin, with earlier generation mTOR inhibitors. Compared to rapamycin and Rapalink-1, TORKi showed poor durability. RapaLink-1 associated with FKBP12, an abundant mTOR-interacting protein, enabling accumulation of RapaLink-1. RapaLink-1 showed better efficacy than rapamycin or TORKi, potently blocking cancer-derived, activating mutants of mTOR. Our study re-establishes mTOR as a central target in glioma and traces the failure of existing drugs to incomplete/nondurable inhibition of mTORC1. Twit Text FOAVip A Kinase Inhibitor Targeted to mTORC1 Drives Regression in Glioblastoma ????Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=28292440 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28292440 #FOAvip English Wikipedia <ref>{{Cite pmid|28292440}}</ref> A Kinase Inhibitor Targeted to mTORC1 Drives Regression in Glioblastoma #MMPMID28292440 Fan Q; Aksoy O; Wong RA; Ilkhanizadeh S; Novotny CJ; Gustafson WC; Truong AYQ; Cavanan G; Simonds EF; Haas-Kogan D; Phillips JJ; Nicolaides T; Okaniwa M; Shokat KM; Weiss WA Cancer Cell 2017[Mar]; 31 (3): 424-35 PMID28292440show ga Although signaling from PI3K and AKT to mTOR is prominently dysregulated in high-grade glial brain tumors, blockade of PI3K or AKT minimally affects downstream mTOR activity in glioma. Allosteric mTOR inhibitors, such as rapamycin, incompletely block mTORC1 compared to mTOR kinase inhibitors (TORKi). Here, we compared RapaLink-1, a TORKi linked to rapamycin, with earlier generation mTOR inhibitors. Compared to rapamycin and Rapalink-1, TORKi showed poor durability. RapaLink-1 associated with FKBP12, an abundant mTOR-interacting protein, enabling accumulation of RapaLink-1. RapaLink-1 showed better efficacy than rapamycin or TORKi, potently blocking cancer-derived, activating mutants of mTOR. Our study re-establishes mTOR as a central target in glioma and traces the failure of existing drugs to incomplete/nondurable inhibition of mTORC1. äA Kinase Inhibitor Targeted to mTORC1 Drives Regression in Glioblastom(epmc).pdf DeepDyve Pubget Overpricing