Journal
NUCLEIC ACIDS RESEARCH
Volume 43, Issue 5, Pages 2590-2602Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkv103
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Funding
- National Institute of Environmental Health Sciences (NIEHS)
- Environmental Protection Agency (EPA) [P01ES018172]
- NIEHS [R01ES09137, P42ES04705]
- National Cancer Institute (NCI) [R01CA155461]
- Tobacco-Related Disease Research Program [18CA-0127]
- Leukemia and Lymphoma Society [6026-10]
- NIH
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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.
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