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10.1080/15548627.2015.1053680 http://scihub22266oqcxt.onion/10.1080/15548627.2015.1053680 C4590661!4590661 !26054373     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26054373 &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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26054373 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Autophagy 2015 ; 11 (8 ): 1198-208 Nephropedia Template TP {{tp|p=26054373 |t=2015. Glutaminolysis and autophagy in cancer |pdf=|usr=}}{{26054373 }} gab.com Text Glutaminolysis and autophagy in cancer JO: Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=26054373 #FOAvip The remarkable metabolic differences between cancer cells and normal cells result in the potential for targeted cancer therapy. The upregulation of glutaminolysis provides energetic advantages to cancer cells. The recently described link between glutaminolysis and autophagy, mediated by MTORC1, may constitute an attractive target for therapeutic strategies. A combination of therapies targeting simultane-ously cell signaling, cancer metabolism, and autophagy can solve therapy resistance and tumor relapse problems, commonly observed in patients treated with most of the current targeted therapies. In this review we summarize the mechanistic link between glutaminolysis and autophagy, and discuss the impacts of these processes on cancer progression and the potential for therapeutic intervention. Twit Text FOAVip Glutaminolysis and autophagy in cancer ????Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=26054373 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26054373 #FOAvip English Wikipedia <ref>{{Cite pmid|26054373 }}</ref> Glutaminolysis and autophagy in cancer #MMPMID26054373 Villar VH ; Merhi F ; Djavaheri-Mergny M ; Durán RV Autophagy 2015[]; 11 (8 ): 1198-208 PMID26054373 show ga The remarkable metabolic differences between cancer cells and normal cells result in the potential for targeted cancer therapy. The upregulation of glutaminolysis provides energetic advantages to cancer cells. The recently described link between glutaminolysis and autophagy, mediated by MTORC1, may constitute an attractive target for therapeutic strategies. A combination of therapies targeting simultane-ously cell signaling, cancer metabolism, and autophagy can solve therapy resistance and tumor relapse problems, commonly observed in patients treated with most of the current targeted therapies. In this review we summarize the mechanistic link between glutaminolysis and autophagy, and discuss the impacts of these processes on cancer progression and the potential for therapeutic intervention. |*Autophagy [MESH] |*Gene Expression Regulation, Neoplastic [MESH] |Animals [MESH] |Cell Proliferation [MESH] |Cell Transformation, Neoplastic [MESH] |Drug Resistance, Neoplasm [MESH] |Glutamine/*metabolism [MESH] |Humans [MESH] |Ketoglutaric Acids/chemistry [MESH] |Mechanistic Target of Rapamycin Complex 1 [MESH] |Multiprotein Complexes/metabolism [MESH] |Neoplasm Recurrence, Local [MESH] |Neoplasms/metabolism/*pathology [MESH] |Reactive Oxygen Species/metabolism [MESH] |Signal Transduction [MESH]Glutaminolysis and autophagy in cancer (epmc).pdf DeepDyve Pubget Overpricing