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10.15252/emmm.201404396 http://scihub22266oqcxt.onion/10.15252/emmm.201404396 C4459821!4459821!25872941     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2015 ; 7 (6): 831-47 Nephropedia Template TP {{tp|p=25872941|t=2015. ZEB1-associated drug resistance in cancer cells is reversed by the class I HDAC inhibitor mocetinostat |pdf=|usr=}}{{25872941}} gab.com Text ZEB1-associated drug resistance in cancer cells is reversed by the class I HDAC inhibitor mocetinostat JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25872941 #FOAvip Therapy resistance is a major clinical problem in cancer medicine and crucial for disease relapse and progression. Therefore, the clinical need to overcome it, particularly for aggressive tumors such as pancreatic cancer, is very high. Aberrant activation of an epithelial?mesenchymal transition (EMT) and an associated cancer stem cell phenotype are considered a major cause of therapy resistance. Particularly, the EMT-activator ZEB1 was shown to confer stemness and resistance. We applied a systematic, stepwise strategy to interfere with ZEB1 function, aiming to overcome drug resistance. This led to the identification of both its target gene miR-203 as a major drug sensitizer and subsequently the class I HDAC inhibitor mocetinostat as epigenetic drug to interfere with ZEB1 function, restore miR-203 expression, repress stemness properties, and induce sensitivity against chemotherapy. Thereby, mocetinostat turned out to be more effective than other HDAC inhibitors, such as SAHA, indicating the relevance of the screening strategy. Our data encourage the application of mechanism-based combinations of selected epigenetic drugs with standard chemotherapy for the rational treatment of aggressive solid tumors, such as pancreatic cancer. Twit Text FOAVip ZEB1-associated drug resistance in cancer cells is reversed by the class I HDAC inhibitor mocetinostat ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25872941 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25872941 #FOAvip English Wikipedia <ref>{{Cite pmid|25872941}}</ref> ZEB1-associated drug resistance in cancer cells is reversed by the class I HDAC inhibitor mocetinostat #MMPMID25872941 Meidhof S; Brabletz S; Lehmann W; Preca BT; Mock K; Ruh M; Schüler J; Berthold M; Weber A; Burk U; Lübbert M; Puhr M; Culig Z; Wellner U; Keck T; Bronsert P; Küsters S; Hopt UT; Stemmler MP; Brabletz T EMBO Mol Med 2015[Jun]; 7 (6): 831-47 PMID25872941show ga Therapy resistance is a major clinical problem in cancer medicine and crucial for disease relapse and progression. Therefore, the clinical need to overcome it, particularly for aggressive tumors such as pancreatic cancer, is very high. Aberrant activation of an epithelial?mesenchymal transition (EMT) and an associated cancer stem cell phenotype are considered a major cause of therapy resistance. Particularly, the EMT-activator ZEB1 was shown to confer stemness and resistance. We applied a systematic, stepwise strategy to interfere with ZEB1 function, aiming to overcome drug resistance. This led to the identification of both its target gene miR-203 as a major drug sensitizer and subsequently the class I HDAC inhibitor mocetinostat as epigenetic drug to interfere with ZEB1 function, restore miR-203 expression, repress stemness properties, and induce sensitivity against chemotherapy. Thereby, mocetinostat turned out to be more effective than other HDAC inhibitors, such as SAHA, indicating the relevance of the screening strategy. Our data encourage the application of mechanism-based combinations of selected epigenetic drugs with standard chemotherapy for the rational treatment of aggressive solid tumors, such as pancreatic cancer. äZEB1-associated drug resistance in cancer cells is reversed by the cla(epmc).pdf DeepDyve Pubget Overpricing