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10.1158/1078-0432.CCR-14-2425 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-14-2425 C4400826!4400826!25878364     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25878364&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\25878364.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Cancer+Res 2015 ; 21 (8): 1828-34 Nephropedia Template TP {{tp|p=25878364|t=2015. Metabolic Dependencies in RAS-Driven Cancers |pdf=|usr=}}{{25878364}} gab.com Text Metabolic Dependencies in RAS-Driven Cancers JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25878364 #FOAvip The ability to inhibit the RAS oncogene has been the holy grail of oncology because of the critical role of this gene in a multitude of tumor types. Additionally, RAS mutant tumors are amongst the most aggressive and refractory to treatment. While directly targeting the RAS oncogene has proven challenging, an alternative approach for treating RAS-driven cancers is to inhibit critical downstream events that are required for tumor maintenance. Indeed, much focus has been put on inhibiting signaling cascades downstream of RAS. Recent studies have shown that oncogenic RAS promotes a metabolic reprogramming of tumor cells, shifting them towards an anabolic metabolism necessary to produce biomass to support unconstrained proliferation. These cancers also use a diverse set of fuel sources to meet their metabolic needs and have even developed a variety of mechanisms to act as metabolic scavengers to obtain necessary metabolic substrates from both extracellular and intracellular sources. Collectively, these adaptations can create ?metabolic bottlenecks? whereby tumor cells rely on particular pathways or rate-limiting metabolites. In this regard, inhibiting individual or combinations of these metabolic pathways can attenuate growth in preclinical models. Because these dependencies are tumor selective and downstream of oncogenic RAS, there is the opportunity for therapeutic intervention. While targeting tumor metabolism is still in the early days of translation to patients, our continued advances in understanding critical metabolic adaptations in RAS-driven cancers as well as the ability to study this altered metabolism in relevant tumor models, will accelerate the development of new therapeutic approaches. Twit Text FOAVip Metabolic Dependencies in RAS-Driven Cancers ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25878364 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25878364 #FOAvip English Wikipedia <ref>{{Cite pmid|25878364}}</ref> Metabolic Dependencies in RAS-Driven Cancers #MMPMID25878364 Kimmelman AC Clin Cancer Res 2015[Apr]; 21 (8): 1828-34 PMID25878364show ga The ability to inhibit the RAS oncogene has been the holy grail of oncology because of the critical role of this gene in a multitude of tumor types. Additionally, RAS mutant tumors are amongst the most aggressive and refractory to treatment. While directly targeting the RAS oncogene has proven challenging, an alternative approach for treating RAS-driven cancers is to inhibit critical downstream events that are required for tumor maintenance. Indeed, much focus has been put on inhibiting signaling cascades downstream of RAS. Recent studies have shown that oncogenic RAS promotes a metabolic reprogramming of tumor cells, shifting them towards an anabolic metabolism necessary to produce biomass to support unconstrained proliferation. These cancers also use a diverse set of fuel sources to meet their metabolic needs and have even developed a variety of mechanisms to act as metabolic scavengers to obtain necessary metabolic substrates from both extracellular and intracellular sources. Collectively, these adaptations can create ?metabolic bottlenecks? whereby tumor cells rely on particular pathways or rate-limiting metabolites. In this regard, inhibiting individual or combinations of these metabolic pathways can attenuate growth in preclinical models. Because these dependencies are tumor selective and downstream of oncogenic RAS, there is the opportunity for therapeutic intervention. While targeting tumor metabolism is still in the early days of translation to patients, our continued advances in understanding critical metabolic adaptations in RAS-driven cancers as well as the ability to study this altered metabolism in relevant tumor models, will accelerate the development of new therapeutic approaches. �Metabolic Dependencies in RAS-Driven Cancers (epmc).pdf DeepDyve Pubget Overpricing