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10.1038/nature23891 http://scihub22266oqcxt.onion/10.1038/nature23891 C5789792!5789792!28959968     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 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       Nature 2017 ; 549 (7673): 543-7 Nephropedia Template TP {{tp|p=28959968|t=2017. Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer |pdf=|usr=}}{{28959968}} gab.com Text Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=28959968 #FOAvip In mammals, the canonical somatic DNA methylation landscape is established upon specification of the embryo proper and subsequently disrupted within many cancer types1-4. However, the underlying mechanisms that direct this genome-scale transformation remain elusive, with no clear model for its systematic acquisition or potential developmental utility5,6. Here we analyzed global remethylation from the mouse preimplantation embryo into the early epiblast and extraembryonic ectoderm. We show that these two states acquire highly divergent genomic distributions with substantial disruption of bimodal, CpG density-dependent methylation in the placental progenitor7,8. The extraembryonic epigenome includes specific de novo methylation at hundreds of embryonically-protected CpG island promoters particularly those that are associated with key developmental regulators and orthologously methylated across most human cancer types9. Our data suggest that the evolutionary innovation of extraembryonic tissues may have required cooption of DNA methylation-based suppression as an alternative to the embryonically utilized Polycomb group proteins, which coordinate germlayer formation in response to extraembryonic cues10. Moreover, we establish that this decision is made deterministically downstream of promiscuously utilized, and frequently oncogenic, signaling pathways via a novel combination of epigenetic cofactors. Methylation of developmental gene promoters during tumorigenesis may therefore reflect the misappropriation of an innate trajectory and the spontaneous reacquisition of a latent, developmentally-encoded epigenetic landscape. Twit Text FOAVip Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=28959968 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28959968 #FOAvip English Wikipedia <ref>{{Cite pmid|28959968}}</ref> Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer #MMPMID28959968 Smith ZD; Shi J; Gu H; Donaghey J; Clement K; Cacciarelli D; Gnirke A; Michor F; Meissner A Nature 2017[Sep]; 549 (7673): 543-7 PMID28959968show ga In mammals, the canonical somatic DNA methylation landscape is established upon specification of the embryo proper and subsequently disrupted within many cancer types1-4. However, the underlying mechanisms that direct this genome-scale transformation remain elusive, with no clear model for its systematic acquisition or potential developmental utility5,6. Here we analyzed global remethylation from the mouse preimplantation embryo into the early epiblast and extraembryonic ectoderm. We show that these two states acquire highly divergent genomic distributions with substantial disruption of bimodal, CpG density-dependent methylation in the placental progenitor7,8. The extraembryonic epigenome includes specific de novo methylation at hundreds of embryonically-protected CpG island promoters particularly those that are associated with key developmental regulators and orthologously methylated across most human cancer types9. Our data suggest that the evolutionary innovation of extraembryonic tissues may have required cooption of DNA methylation-based suppression as an alternative to the embryonically utilized Polycomb group proteins, which coordinate germlayer formation in response to extraembryonic cues10. Moreover, we establish that this decision is made deterministically downstream of promiscuously utilized, and frequently oncogenic, signaling pathways via a novel combination of epigenetic cofactors. Methylation of developmental gene promoters during tumorigenesis may therefore reflect the misappropriation of an innate trajectory and the spontaneous reacquisition of a latent, developmentally-encoded epigenetic landscape. äEpigenetic restriction of extraembryonic lineages mirrors the somatic (epmc).pdf DeepDyve Pubget Overpricing