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10.1038/ncomms7170 http://scihub22266oqcxt.onion/10.1038/ncomms7170 C4313575!4313575!25636082     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+Commun 2015 ; 6 (ä): 6170 Nephropedia Template TP {{tp|p=25636082|t=2015. NR2F1 controls tumor cell dormancy via SOX9 and RAR? driven quiescence programs |pdf=|usr=}}{{25636082}} gab.com Text NR2F1 controls tumor cell dormancy via SOX9 and RAR driven quiescence programs JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25636082 #FOAvip Metastases can originate from disseminated tumor cells (DTCs), which may be dormant for years before reactivation. Here we find that the orphan nuclear receptor NR2F1 is epigenetically upregulated in experimental HNSCC dormancy models and in DTCs from prostate cancer patients carrying dormant disease for 7?18 years. NR2F1-dependent dormancy is recapitulated by a co-treatment with the DNA demethylating agent 5-Aza-C and retinoic acid across various cancer types. NR2F1-induced quiescence is dependent on SOX9, RAR? and CDK inhibitors. Intriguingly, NR2F1 induces global chromatin repression and the pluripotency gene NANOG, which contributes to dormancy of DTCs in the bone marrow. When NR2F1 is blocked in vivo, growth arrest or survival of dormant DTCs is interrupted in different organs. We conclude that NR2F1 is a critical node in dormancy induction and maintenance by integrating epigenetic programs of quiescence and survival in DTCs. Twit Text FOAVip NR2F1 controls tumor cell dormancy via SOX9 and RAR driven quiescence programs ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25636082 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25636082 #FOAvip English Wikipedia <ref>{{Cite pmid|25636082}}</ref> NR2F1 controls tumor cell dormancy via SOX9 and RAR? driven quiescence programs #MMPMID25636082 Sosa MS; Parikh F; Maia AG; Estrada Y; Bosch A; Bragado P; Ekpin E; George A; Zheng Y; Lam HM; Morrissey C; Chung CY; Farias EF; Bernstein E; Aguirre-Ghiso JA Nat Commun 2015[]; 6 (ä): 6170 PMID25636082show ga Metastases can originate from disseminated tumor cells (DTCs), which may be dormant for years before reactivation. Here we find that the orphan nuclear receptor NR2F1 is epigenetically upregulated in experimental HNSCC dormancy models and in DTCs from prostate cancer patients carrying dormant disease for 7?18 years. NR2F1-dependent dormancy is recapitulated by a co-treatment with the DNA demethylating agent 5-Aza-C and retinoic acid across various cancer types. NR2F1-induced quiescence is dependent on SOX9, RAR? and CDK inhibitors. Intriguingly, NR2F1 induces global chromatin repression and the pluripotency gene NANOG, which contributes to dormancy of DTCs in the bone marrow. When NR2F1 is blocked in vivo, growth arrest or survival of dormant DTCs is interrupted in different organs. We conclude that NR2F1 is a critical node in dormancy induction and maintenance by integrating epigenetic programs of quiescence and survival in DTCs. äNR2F1 controls tumor cell dormancy via SOX9 and RAR? driven quiescence(epmc).pdf DeepDyve Pubget Overpricing