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10.1016/j.semcdb.2015.08.003 http://scihub22266oqcxt.onion/10.1016/j.semcdb.2015.08.003 C4818970!4818970 !26277543     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26277543 &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\26277543 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Semin+Cell+Dev+Biol 2015 ; 43 (ä): 11-21 Nephropedia Template TP {{tp|p=26277543 |t=2015. MYC and metabolism on the path to cancer |pdf=|usr=}}{{26277543 }} gab.com Text MYC and metabolism on the path to cancer JO: Semin Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=26277543 #FOAvip The MYC proto-oncogene is frequently deregulated in human cancers, activating genetic programs that orchestrate biological processes to promote growth and proliferation. Altered metabolism characterized by heightened nutrients uptake, enhanced glycolysis and glutaminolysis and elevated fatty acid and nucleotide synthesis is the hallmark of MYC-driven cancer. Recent evidence strongly suggests that Myc-dependent metabolic reprogramming is critical for tumorigenesis, which could be attenuated by targeting specific metabolic pathways using small drug-like molecules. Understanding the complexity of MYC-mediated metabolic re-wiring in cancers as well as how MYC cooperates with other metabolic drivers such as mammalian target of rapamycin (mTOR) will provide translational opportunities for cancer therapy. Twit Text FOAVip MYC and metabolism on the path to cancer ????Semin Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=26277543 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26277543 #FOAvip English Wikipedia <ref>{{Cite pmid|26277543 }}</ref> MYC and metabolism on the path to cancer #MMPMID26277543 Hsieh AL ; Walton ZE ; Altman BJ ; Stine ZE ; Dang CV Semin Cell Dev Biol 2015[Jul]; 43 (ä): 11-21 PMID26277543 show ga The MYC proto-oncogene is frequently deregulated in human cancers, activating genetic programs that orchestrate biological processes to promote growth and proliferation. Altered metabolism characterized by heightened nutrients uptake, enhanced glycolysis and glutaminolysis and elevated fatty acid and nucleotide synthesis is the hallmark of MYC-driven cancer. Recent evidence strongly suggests that Myc-dependent metabolic reprogramming is critical for tumorigenesis, which could be attenuated by targeting specific metabolic pathways using small drug-like molecules. Understanding the complexity of MYC-mediated metabolic re-wiring in cancers as well as how MYC cooperates with other metabolic drivers such as mammalian target of rapamycin (mTOR) will provide translational opportunities for cancer therapy. |Cell Proliferation/physiology [MESH] |Cell Transformation, Neoplastic/*pathology [MESH] |Glucose/*metabolism [MESH] |Glycolysis/*physiology [MESH] |Homeostasis/*physiology [MESH] |Humans [MESH] |Neoplasms/*pathology [MESH] |Proto-Oncogene Mas [MESH] |Proto-Oncogene Proteins c-myc/genetics/*metabolism [MESH] |TOR Serine-Threonine Kinases/metabolism [MESH]MYC and metabolism on the path to cancer (epmc).pdf DeepDyve Pubget Overpricing