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10.1158/0008-5472.CAN-16-0810 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-16-0810 C5135633!5135633!27758884     free     free     free 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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2016 ; 76 (23): 6911-23 Nephropedia Template TP {{tp|p=27758884|t=2016. mTORC2 signaling drives the development and progression of pancreatic cancer |pdf=|usr=}}{{27758884}} gab.com Text mTORC2 signaling drives the development and progression of pancreatic cancer JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27758884 #FOAvip mTOR signaling controls several critical cellular functions and is deregulated in many cancers, including pancreatic cancer. To date, most efforts have focused on inhibiting the mTORC1 complex. However, clinical trials of mTORC1 inhibitors in pancreatic cancer have failed, raising questions about this therapeutic approach. We employed a genetic approach to delete the obligate mTORC2 subunit Rictor and identified the critical times during which tumorigenesis requires mTORC2 signaling. Rictor deletion resulted in profoundly delayed tumorigenesis. Whereas previous studies showed most pancreatic tumors were insensitive to rapamycin, treatment with a dual mTORC1/2 inhibitor strongly suppressed tumorigenesis. In late-stage tumor-bearing mice, combined mTORC1/2 and PI3K inhibition significantly increased survival. Thus, targeting mTOR may be a potential therapeutic strategy in pancreatic cancer. Twit Text FOAVip mTORC2 signaling drives the development and progression of pancreatic cancer ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27758884 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27758884 #FOAvip English Wikipedia <ref>{{Cite pmid|27758884}}</ref> mTORC2 signaling drives the development and progression of pancreatic cancer #MMPMID27758884 Driscoll DR; Karim SA; Sano M; Gay DM; Jacob W; Yu J; Mizukami Y; Gopinathan A; Jodrell DI; Evans TJ; Bardeesy N; Hall MN; Quattrochi BJ; Klimstra DS; Barry ST; Sansom OJ; Lewis BC; Morton JP Cancer Res 2016[Dec]; 76 (23): 6911-23 PMID27758884show ga mTOR signaling controls several critical cellular functions and is deregulated in many cancers, including pancreatic cancer. To date, most efforts have focused on inhibiting the mTORC1 complex. However, clinical trials of mTORC1 inhibitors in pancreatic cancer have failed, raising questions about this therapeutic approach. We employed a genetic approach to delete the obligate mTORC2 subunit Rictor and identified the critical times during which tumorigenesis requires mTORC2 signaling. Rictor deletion resulted in profoundly delayed tumorigenesis. Whereas previous studies showed most pancreatic tumors were insensitive to rapamycin, treatment with a dual mTORC1/2 inhibitor strongly suppressed tumorigenesis. In late-stage tumor-bearing mice, combined mTORC1/2 and PI3K inhibition significantly increased survival. Thus, targeting mTOR may be a potential therapeutic strategy in pancreatic cancer. ämTORC2 signaling drives the development and progression of pancreatic (epmc).pdf DeepDyve Pubget Overpricing