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10.1016/j.celrep.2017.02.022 http://scihub22266oqcxt.onion/10.1016/j.celrep.2017.02.022 C5374978!5374978 !28249155     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28249155 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Rep 2017 ; 18 (9 ): 2088-2095 Nephropedia Template TP {{tp|p=28249155 |t=2017. Pharmacologic Targeting of S6K1 in PTEN-Deficient Neoplasia |pdf=|usr=}}{{28249155 }} gab.com Text Pharmacologic Targeting of S6K1 in PTEN-Deficient Neoplasia JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=28249155 #FOAvip Genetic S6K1 inactivation can induce apoptosis in PTEN-deficient cells. We analyzed the therapeutic potential of S6K1 inhibitors in PTEN-deficient T cell leukemia and glioblastoma. Results revealed that the S6K1 inhibitor LY-2779964 was relatively ineffective as a single agent, while S6K1-targeting AD80 induced cytotoxicity selectively in PTEN-deficient cells. In vivo, AD80 rescued 50% of mice transplanted with PTEN-deficient leukemia cells. Cells surviving LY-2779964 treatment exhibited inhibitor-induced S6K1 phosphorylation due to increased mTOR-S6K1 co-association, which primed the rapid recovery of S6K1 signaling. In contrast, AD80 avoided S6K1 phosphorylation and mTOR co-association, resulting in durable suppression of S6K1-induced signaling and protein synthesis. Kinome analysis revealed that AD80 coordinately inhibits S6K1 together with the TAM family tyrosine kinase AXL. TAM suppression by BMS-777607 or genetic knockdown potentiated cytotoxic responses to LY-2779964 in PTEN-deficient glioblastoma cells. These results reveal that combination targeting of S6K1 and TAMs is a potential strategy for treatment of PTEN-deficient malignancy. Twit Text FOAVip Pharmacologic Targeting of S6K1 in PTEN-Deficient Neoplasia ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=28249155 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28249155 #FOAvip English Wikipedia <ref>{{Cite pmid|28249155 }}</ref> Pharmacologic Targeting of S6K1 in PTEN-Deficient Neoplasia #MMPMID28249155 Liu H ; Feng X ; Ennis KN ; Behrmann CA ; Sarma P ; Jiang TT ; Kofuji S ; Niu L ; Stratton Y ; Thomas HE ; Yoon SO ; Sasaki AT ; Plas DR Cell Rep 2017[Feb]; 18 (9 ): 2088-2095 PMID28249155 show ga Genetic S6K1 inactivation can induce apoptosis in PTEN-deficient cells. We analyzed the therapeutic potential of S6K1 inhibitors in PTEN-deficient T cell leukemia and glioblastoma. Results revealed that the S6K1 inhibitor LY-2779964 was relatively ineffective as a single agent, while S6K1-targeting AD80 induced cytotoxicity selectively in PTEN-deficient cells. In vivo, AD80 rescued 50% of mice transplanted with PTEN-deficient leukemia cells. Cells surviving LY-2779964 treatment exhibited inhibitor-induced S6K1 phosphorylation due to increased mTOR-S6K1 co-association, which primed the rapid recovery of S6K1 signaling. In contrast, AD80 avoided S6K1 phosphorylation and mTOR co-association, resulting in durable suppression of S6K1-induced signaling and protein synthesis. Kinome analysis revealed that AD80 coordinately inhibits S6K1 together with the TAM family tyrosine kinase AXL. TAM suppression by BMS-777607 or genetic knockdown potentiated cytotoxic responses to LY-2779964 in PTEN-deficient glioblastoma cells. These results reveal that combination targeting of S6K1 and TAMs is a potential strategy for treatment of PTEN-deficient malignancy. |Aminopyridines/pharmacology [MESH] |Animals [MESH] |Antineoplastic Agents/*pharmacology [MESH] |Apoptosis/drug effects [MESH] |Cell Line, Tumor [MESH] |Gene Knockdown Techniques/methods [MESH] |Glioblastoma/drug therapy/metabolism [MESH] |Heterocyclic Compounds, 4 or More Rings/pharmacology [MESH] |Humans [MESH] |Leukemia, T-Cell/drug therapy/metabolism [MESH] |Mice [MESH] |Neoplasms/*drug therapy/*metabolism [MESH] |PTEN Phosphohydrolase/*deficiency [MESH] |Phosphorylation/drug effects [MESH] |Pyridones/pharmacology [MESH] |Receptor Protein-Tyrosine Kinases/metabolism [MESH] |Ribosomal Protein S6 Kinases, 70-kDa/*metabolism [MESH] |Signal Transduction/drug effects [MESH]Pharmacologic Targeting of S6K1 in PTEN-Deficient Neoplasia (epmc).pdf DeepDyve Pubget Overpricing