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10.1016/j.cell.2015.07.061 http://scihub22266oqcxt.onion/10.1016/j.cell.2015.07.061 C4821508!4821508!26359985     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       Cell 2015 ; 162 (6): 1271-85 Nephropedia Template TP {{tp|p=26359985|t=2015. Non-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistance |pdf=|usr=}}{{26359985}} gab.com Text Non-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistance JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=26359985 #FOAvip Clinically acquired resistance to MAPK inhibitor (MAPKi) therapies for melanoma cannot be fully explained by genomic mechanisms and may be accompanied by co-evolution of intra-tumoral immunity. We sought to discover non-genomic mechanisms of acquired resistance and dynamic immune compositions by a comparative, transcriptomic-methylomic analysis of patient-matched melanoma tumors biopsied before therapy and during disease progression. Transcriptomic alterations across resistant tumors were highly recurrent, in contrast to mutations, and were frequently correlated with differential methylation of tumor cell-intrinsic CpG sites. We identified in the tumor cell compartment supra-physiologic c-MET up-expression, infra-physiologic LEF1 down-expression, and YAP1 signature enrichment as drivers of acquired resistance. Importantly, high intra-tumoral cytolytic T-cell inflammation prior to MAPKi therapy preceded CD8 T-cell deficiency/exhaustion and loss of antigen-presentation in half of disease-progressive melanomas, suggesting cross-resistance to salvage anti-PD-1/PD-L1 immunotherapy. Thus, melanoma acquires MAPKi-resistance with highly dynamic and recurrent non-genomic alterations and co-evolving intra-tumoral immunity. Twit Text FOAVip Non-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistance ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=26359985 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26359985 #FOAvip English Wikipedia <ref>{{Cite pmid|26359985}}</ref> Non-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistance #MMPMID26359985 Hugo W; Shi H; Sun L; Piva M; Song C; Kong X; Moriceau G; Hong A; Dahlman KB; Johnson DB; Sosman JA; Ribas A; Lo RS Cell 2015[Sep]; 162 (6): 1271-85 PMID26359985show ga Clinically acquired resistance to MAPK inhibitor (MAPKi) therapies for melanoma cannot be fully explained by genomic mechanisms and may be accompanied by co-evolution of intra-tumoral immunity. We sought to discover non-genomic mechanisms of acquired resistance and dynamic immune compositions by a comparative, transcriptomic-methylomic analysis of patient-matched melanoma tumors biopsied before therapy and during disease progression. Transcriptomic alterations across resistant tumors were highly recurrent, in contrast to mutations, and were frequently correlated with differential methylation of tumor cell-intrinsic CpG sites. We identified in the tumor cell compartment supra-physiologic c-MET up-expression, infra-physiologic LEF1 down-expression, and YAP1 signature enrichment as drivers of acquired resistance. Importantly, high intra-tumoral cytolytic T-cell inflammation prior to MAPKi therapy preceded CD8 T-cell deficiency/exhaustion and loss of antigen-presentation in half of disease-progressive melanomas, suggesting cross-resistance to salvage anti-PD-1/PD-L1 immunotherapy. Thus, melanoma acquires MAPKi-resistance with highly dynamic and recurrent non-genomic alterations and co-evolving intra-tumoral immunity. äNon-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistanc(epmc).pdf DeepDyve Pubget Overpricing