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10.1038/nm.4055 http://scihub22266oqcxt.onion/10.1038/nm.4055 C4892846!4892846!26950360     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       Nat+Med 2016 ; 22 (4): 427-32 Nephropedia Template TP {{tp|p=26950360|t=2016. Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer |pdf=|usr=}}{{26950360}} gab.com Text Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer JO: Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=26950360 #FOAvip Expression of the oncogenic transcription factor MYC is disproportionately elevated in triple-negative breast cancer (TNBC) compared to estrogen, progesterone and human epidermal growth factor 2 receptor-positive (RP) breast tumors1,2. We and others have shown that MYC alters metabolism during tumorigenesis3,4. However, the role of MYC in TNBC metabolism remains largely unexplored. We hypothesized that MYC-dependent metabolic dysregulation is essential for MYC-overexpressing (MO) TNBC and may thus identify novel therapeutic targets for this clinically challenging subset of breast cancer. Using a targeted metabolomics approach, we identified fatty acid oxidation (FAO) intermediates as being dramatically upregulated in a MYC-driven model of TNBC. A lipid metabolism gene signature was identified in patients with TNBC from The Cancer Genome Atlas (TCGA) database and multiple other clinical datasets, implicating FAO as a dysregulated pathway critical for TNBC metabolism. We find that MO-TNBC displays increased bioenergetic reliance upon fatty acid oxidation (FAO), and that pharmacologic inhibition of FAO catastrophically decreases energy metabolism of MO-TNBC, blocks growth of a MYC-driven transgenic TNBC model and that of MO-TNBC patient-derived xenografts. Our results demonstrate that inhibition of FAO is a novel therapeutic strategy against MO-TNBC. Twit Text FOAVip Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer ????Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=26950360 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26950360 #FOAvip English Wikipedia <ref>{{Cite pmid|26950360}}</ref> Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer #MMPMID26950360 Camarda R; Zhou Z; Kohnz RA; Balakrishnan S; Mahieu C; Anderton B; Eyob H; Kajimura S; Tward A; Krings G; Nomura DK; Goga A Nat Med 2016[Apr]; 22 (4): 427-32 PMID26950360show ga Expression of the oncogenic transcription factor MYC is disproportionately elevated in triple-negative breast cancer (TNBC) compared to estrogen, progesterone and human epidermal growth factor 2 receptor-positive (RP) breast tumors1,2. We and others have shown that MYC alters metabolism during tumorigenesis3,4. However, the role of MYC in TNBC metabolism remains largely unexplored. We hypothesized that MYC-dependent metabolic dysregulation is essential for MYC-overexpressing (MO) TNBC and may thus identify novel therapeutic targets for this clinically challenging subset of breast cancer. Using a targeted metabolomics approach, we identified fatty acid oxidation (FAO) intermediates as being dramatically upregulated in a MYC-driven model of TNBC. A lipid metabolism gene signature was identified in patients with TNBC from The Cancer Genome Atlas (TCGA) database and multiple other clinical datasets, implicating FAO as a dysregulated pathway critical for TNBC metabolism. We find that MO-TNBC displays increased bioenergetic reliance upon fatty acid oxidation (FAO), and that pharmacologic inhibition of FAO catastrophically decreases energy metabolism of MO-TNBC, blocks growth of a MYC-driven transgenic TNBC model and that of MO-TNBC patient-derived xenografts. Our results demonstrate that inhibition of FAO is a novel therapeutic strategy against MO-TNBC. äInhibition of fatty acid oxidation as a therapy for MYC-overexpressing(epmc).pdf DeepDyve Pubget Overpricing