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10.1016/j.tem.2014.04.002 http://scihub22266oqcxt.onion/10.1016/j.tem.2014.04.002 C4077930!4077930 !24856037     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24856037 &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 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 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\24856037 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Trends+Endocrinol+Metab 2014 ; 25 (7 ): 364-73 Nephropedia Template TP {{tp|p=24856037 |t=2014. mTORC2 in the center of cancer metabolic reprogramming |pdf=|usr=}}{{24856037 }} gab.com Text mTORC2 in the center of cancer metabolic reprogramming JO: Trends Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=24856037 #FOAvip Metabolic reprogramming is a central hallmark of cancer, enabling tumor cells to obtain the macromolecular precursors and energy needed for rapid tumor growth. Understanding how oncogenes coordinate altered signaling with metabolic reprogramming and global transcription may yield new insights into tumor pathogenesis, and provide a new landscape of promising drug targets, while yielding important clues into mechanisms of resistance to the signal transduction inhibitors currently in use. We review here the recently identified central regulatory role for mechanistic target of rapamycin complex 2 (mTORC2), a downstream effector of many cancer-causing mutations, in metabolic reprogramming and cancer drug resistance. We consider the impact of mTORC2-related metabolism on epigenetics and therapeutics, with a particular focus on the intractable malignant brain tumor, glioblastoma multiforme (GBM). Twit Text FOAVip mTORC2 in the center of cancer metabolic reprogramming ????Trends Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=24856037 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24856037 #FOAvip English Wikipedia <ref>{{Cite pmid|24856037 }}</ref> mTORC2 in the center of cancer metabolic reprogramming #MMPMID24856037 Masui K ; Cavenee WK ; Mischel PS Trends Endocrinol Metab 2014[Jul]; 25 (7 ): 364-73 PMID24856037 show ga Metabolic reprogramming is a central hallmark of cancer, enabling tumor cells to obtain the macromolecular precursors and energy needed for rapid tumor growth. Understanding how oncogenes coordinate altered signaling with metabolic reprogramming and global transcription may yield new insights into tumor pathogenesis, and provide a new landscape of promising drug targets, while yielding important clues into mechanisms of resistance to the signal transduction inhibitors currently in use. We review here the recently identified central regulatory role for mechanistic target of rapamycin complex 2 (mTORC2), a downstream effector of many cancer-causing mutations, in metabolic reprogramming and cancer drug resistance. We consider the impact of mTORC2-related metabolism on epigenetics and therapeutics, with a particular focus on the intractable malignant brain tumor, glioblastoma multiforme (GBM). |Animals [MESH] |Epigenomics [MESH] |Glioblastoma/metabolism [MESH] |Humans [MESH] |Mechanistic Target of Rapamycin Complex 2 [MESH] |Multiprotein Complexes/*metabolism [MESH] |Mutation [MESH] |Neoplasms/genetics/*metabolism [MESH] |Signal Transduction/genetics/physiology [MESH]mTORC2 in the center of cancer metabolic reprogramming (epmc).pdf DeepDyve Pubget Overpricing