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10.1038/nature24297 http://scihub22266oqcxt.onion/10.1038/nature24297 C5933935!5933935!29088702     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       Nature 2017 ; 551 (7679): 247-50 Nephropedia Template TP {{tp|p=29088702|t=2017. Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition |pdf=|usr=}}{{29088702}} gab.com Text Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=29088702 #FOAvip Acquired drug resistance prevents cancer therapies from achieving stable and complete responses.1 Emerging evidence implicates a key role for nonmutational drug resistance mechanisms underlying the survival of residual cancer ?persister? cells.2-4 The persister cell pool constitutes a reservoir from which drug-resistant tumours may emerge. Targeting persister cells therefore presents a therapeutic opportunity to impede tumour relapse.5 In an earlier report, we found that cancer cells in a high mesenchymal therapy-resistant cell state are dependent on the lipid hydroperoxidase GPX4 for survival.6 Here, we describe the discovery that a similar therapy-resistant cell state underlies the behavior of persister cells derived from a wide range of cancers and drug treatments. Consequently, we show that persister cells acquire a dependency on GPX4. We demonstrate that loss of GPX4 function results in selective persister cell ferroptotic death in vitro and prevents tumour relapse in vivo. These findings support targeting GPX4 as a therapeutic strategy to prevent acquired drug resistance. Twit Text FOAVip Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=29088702 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29088702 #FOAvip English Wikipedia <ref>{{Cite pmid|29088702}}</ref> Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition #MMPMID29088702 Hangauer MJ; Viswanathan VS; Ryan MJ; Bole D; Eaton JK; Matov A; Galeas J; Dhruv HD; Berens ME; Schreiber SL; McCormick F; McManus MT Nature 2017[Nov]; 551 (7679): 247-50 PMID29088702show ga Acquired drug resistance prevents cancer therapies from achieving stable and complete responses.1 Emerging evidence implicates a key role for nonmutational drug resistance mechanisms underlying the survival of residual cancer ?persister? cells.2-4 The persister cell pool constitutes a reservoir from which drug-resistant tumours may emerge. Targeting persister cells therefore presents a therapeutic opportunity to impede tumour relapse.5 In an earlier report, we found that cancer cells in a high mesenchymal therapy-resistant cell state are dependent on the lipid hydroperoxidase GPX4 for survival.6 Here, we describe the discovery that a similar therapy-resistant cell state underlies the behavior of persister cells derived from a wide range of cancers and drug treatments. Consequently, we show that persister cells acquire a dependency on GPX4. We demonstrate that loss of GPX4 function results in selective persister cell ferroptotic death in vitro and prevents tumour relapse in vivo. These findings support targeting GPX4 as a therapeutic strategy to prevent acquired drug resistance. äDrug-tolerant persister cancer cells are vulnerable to GPX4 inhibition(epmc).pdf DeepDyve Pubget Overpricing