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10.1016/j.leukres.2017.05.004 http://scihub22266oqcxt.onion/10.1016/j.leukres.2017.05.004 C5507334!5507334!28505595     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28505595&cmd=llinks): Failed to open stream: HTTP request failed! 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Epigenetic drug combination induces remission in mouse xenograft models of pediatric acute myeloid leukemia |pdf=|usr=}}{{28505595}} gab.com Text Epigenetic drug combination induces remission in mouse xenograft models of pediatric acute myeloid leukemia JO: Leuk Res http://www.kidney.de/pget.php?&tw=1&pmid=28505595 #FOAvip Aberrations in epigenetic modifications contribute to leukemogenesis in childhood acute myeloid leukemia (AML). We combined DNA hypomethylating agent azacitidine with histone deacetylase inhibitor panobinostat in preclinical models of childhood AML. Synergistic cytotoxic effect upon treatment with azacitidine and panobinostat with combination indices < 1.0 was observed. Azacitidine and panobinostat increased median survival by 26 and 6 days respectively in MV4;11 xenografted mice. Mice treated with both drugs showed a drastic reduction in leukemic burden leading to complete remission sustained for the duration of the experimental period lasting more than 519 days. Reduced leukemic burden and prolonged survival was also observed in AML-193 xenografted mice treated with azacitidine-panobinostat combination. Differential gene expression profiling was performed on AML cells treated with azacitidine, panobinostat or azacitidine-panobinostat combination. Functional mapping of transcripts uniquely regulated by the azacitidine-panobinostat combination in MV4;11 cells identified p53 as an upstream regulator. A comparison of the uniquely modulated transcripts by azacitidine-panobinostat combination in MV4;11 cells versus AML-193 and THP-1 cells, bearing mutated p53, also revealed p53 as the topmost upstream regulator. Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML. Twit Text FOAVip Epigenetic drug combination induces remission in mouse xenograft models of pediatric acute myeloid leukemia ????Leuk Res http://www.kidney.de/pget.php?&tw=1&pmid=28505595 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28505595 #FOAvip English Wikipedia <ref>{{Cite pmid|28505595}}</ref> Epigenetic drug combination induces remission in mouse xenograft models of pediatric acute myeloid leukemia #MMPMID28505595 Gopalakrishnapillai A; Kolb EA; McCahan SM; Barwe SP Leuk Res 2017[Jul]; 58 (ä): 91-7 PMID28505595show ga Aberrations in epigenetic modifications contribute to leukemogenesis in childhood acute myeloid leukemia (AML). We combined DNA hypomethylating agent azacitidine with histone deacetylase inhibitor panobinostat in preclinical models of childhood AML. Synergistic cytotoxic effect upon treatment with azacitidine and panobinostat with combination indices < 1.0 was observed. Azacitidine and panobinostat increased median survival by 26 and 6 days respectively in MV4;11 xenografted mice. Mice treated with both drugs showed a drastic reduction in leukemic burden leading to complete remission sustained for the duration of the experimental period lasting more than 519 days. Reduced leukemic burden and prolonged survival was also observed in AML-193 xenografted mice treated with azacitidine-panobinostat combination. Differential gene expression profiling was performed on AML cells treated with azacitidine, panobinostat or azacitidine-panobinostat combination. Functional mapping of transcripts uniquely regulated by the azacitidine-panobinostat combination in MV4;11 cells identified p53 as an upstream regulator. A comparison of the uniquely modulated transcripts by azacitidine-panobinostat combination in MV4;11 cells versus AML-193 and THP-1 cells, bearing mutated p53, also revealed p53 as the topmost upstream regulator. Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML. äEpigenetic drug combination induces remission in mouse xenograft model(epmc).pdf DeepDyve Pubget Overpricing