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10.1158/2159-8290.CD-15-1439 http://scihub22266oqcxt.onion/10.1158/2159-8290.CD-15-1439 C5096974!5096974!27630126     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       Cancer+Discov 2016 ; 6 (11): 1237-47 Nephropedia Template TP {{tp|p=27630126|t=2016. Chronic myelogenous leukemia initiating cells require Polycomb group protein EZH2 |pdf=|usr=}}{{27630126}} gab.com Text Chronic myelogenous leukemia initiating cells require Polycomb group protein EZH2 JO: Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=27630126 #FOAvip Tyrosine kinase inhibitors (TKIs) have revolutionized chronic myelogenous leukemia (CML) management. Disease eradication, however, is hampered by innate resistance of leukemia initiating cells (LICs) to TKI-induced killing, which also provides the basis for subsequent emergence of TKI-resistant mutants. We report that EZH2, the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), is overexpressed in CML LICs, required for colony formation, and survival and cell cycle progression of CML cell lines. A critical role for Ezh2 is supported by genetic studies in a mouse CML model. Inactivation of Ezh2 in conventional conditional mice and through CRISPR/Cas9-mediated gene editing prevents initiation and maintenance of disease and survival of LICs, irrespective of BCR-ABL1 mutational status, and extends survival. Expression of the Ezh2 homolog Ezh1 is reduced in Ezh2-deficient CML LICs, creating a scenario resembling complete loss of PRC2. EZH2-dependence of CML LICs raises prospects for improved therapy of TKI-resistant CML and/or eradication of disease by addition of EZH2 inhibitors. Twit Text FOAVip Chronic myelogenous leukemia initiating cells require Polycomb group protein EZH2 ????Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=27630126 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27630126 #FOAvip English Wikipedia <ref>{{Cite pmid|27630126}}</ref> Chronic myelogenous leukemia initiating cells require Polycomb group protein EZH2 #MMPMID27630126 Xie H; Peng C; Huang J; Li BE; Kim W; Smith EC; Fujiwara Y; Qi J; Cheloni G; Das PP; Nguyen M; Li S; Bradner JE; Orkin SH Cancer Discov 2016[Nov]; 6 (11): 1237-47 PMID27630126show ga Tyrosine kinase inhibitors (TKIs) have revolutionized chronic myelogenous leukemia (CML) management. Disease eradication, however, is hampered by innate resistance of leukemia initiating cells (LICs) to TKI-induced killing, which also provides the basis for subsequent emergence of TKI-resistant mutants. We report that EZH2, the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), is overexpressed in CML LICs, required for colony formation, and survival and cell cycle progression of CML cell lines. A critical role for Ezh2 is supported by genetic studies in a mouse CML model. Inactivation of Ezh2 in conventional conditional mice and through CRISPR/Cas9-mediated gene editing prevents initiation and maintenance of disease and survival of LICs, irrespective of BCR-ABL1 mutational status, and extends survival. Expression of the Ezh2 homolog Ezh1 is reduced in Ezh2-deficient CML LICs, creating a scenario resembling complete loss of PRC2. EZH2-dependence of CML LICs raises prospects for improved therapy of TKI-resistant CML and/or eradication of disease by addition of EZH2 inhibitors. äChronic myelogenous leukemia initiating cells require Polycomb group p(epmc).pdf DeepDyve Pubget Overpricing