2026-04-17T09:46:28Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1190142025-12-05T05:45:26Zcom_2072_1057col_2072_478824col_2072_478858col_2072_478917

00925njm 22002777a 4500 dc Lee, Seung-Tae author Muench, Marcus O. author Fomin, Marina E. author Xiao, Jianqiao author Zhou, Mi author Smith, Adam de author Martín-Subero, José Ignacio author Heath, Simon C. author Houseman, E.Andres author Roy, Ritu author Wrensch, Margaret author Wiencke, John K. author Metayer, Catherine author Wiemels, Joseph L. author 2018-01-12T15:12:21Z 2018-01-12T15:12:21Z 2015-03-11 2018-01-12T15:12:21Z We investigated DNA methylomes of pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisulfite sequencing and high-definition microarrays, along with RNA expression profiles. Epigenetic alteration of B-ALLs occurred in two tracks: de novo methylation of small functional compartments and demethylation of large inter-compartmental backbones. The deviations were exaggerated in lamina-associated domains, with differences corresponding to methylation clusters and/or cytogenetic groups. Our data also suggested a pivotal role of polycomb and CTBP2 in de novo methylation, which may be traced back to bivalency status of embryonic stem cells. Driven by these potent epigenetic modulations, suppression of polycomb target genes was observed along with disruption of developmental fate and cell cycle and mismatch repair pathways and altered activities of key upstream regulators. Leucèmia Epigenètica Cèl·lules mare embrionàries Leukemia Epigenetics Embryonic stem cells Epigenetic remodeling in B-cell acute lymphoblastic leukemia occurs in two tracks and employs embryonic stem cell-like signatures.