ArticleOncotarget2017
An annotated list of bivalent chromatin regions in human ES cells: a new tool for cancer epigenetic research.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Cellular Biogenetic Law and Its Distortion by Protein Interactions: A Possible Unified Framework for Cancer Biology and Regenerative Medicine.International journal of molecular sciences · 2022Pooled it
- Bivalency Erosion as a Unifying Mechanism of PFAS Inter- and Transgenerational Neurotoxicity.Journal of applied toxicology : JAT · 2026Article
- Ancestral chromatin state constrains the functional landscape of bivalent domains in mammalian spermatogenesis.bioRxiv : the preprint server for biology · 2026Article
- Analysis of IDH1 and IDH2 mutations as causes of the hypermethylator phenotype in colorectal cancer.The Journal of pathology · 2025Article
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- ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency.Nature communications · 2024Article
- The pediatric leukemia oncoprotein NUP98-KDM5A induces genomic instability that may facilitate malignant transformation.Cell death & disease · 2023Article
- Inheritance of paternal lifestyles and exposures through sperm DNA methylation.Nature reviews. Urology · 2023Review
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- The Role of Mitotic Slippage in Creating a "Female Pregnancy-like System" in a Single Polyploid Giant Cancer Cell.International journal of molecular sciences · 2023Article
- Polyploidy and Myc Proto-Oncogenes Promote Stress Adaptation via Epigenetic Plasticity and Gene Regulatory Network Rewiring.International journal of molecular sciences · 2022Review
- Polycomb repressive complex 2 shields naïve human pluripotent cells from trophectoderm differentiation.Nature cell biology · 2022Article
- Polyploidy as a Fundamental Phenomenon in Evolution, Development, Adaptation and Diseases.International journal of molecular sciences · 2022Review
- m6A Topological Transition Coupled to Developmental Regulation of Gene Expression During Mammalian Tissue Development.Frontiers in cell and developmental biology · 2022Article
- Differential brain ADRA2A and ADRA2C gene expression and epigenetic regulation in schizophrenia. Effect of antipsychotic drug treatment.Translational psychiatry · 2021Article
- Growth of Biological Complexity from Prokaryotes to Hominids Reflected in the Human Genome.International journal of molecular sciences · 2021Article
- Widespread overexpression from the four DNA hypermethylated HOX clusters in aggressive (IDHwt) glioma is associated with H3K27me3 depletion and alternative promoter usage.Molecular oncology · 2021Article
- The regulatory function of tandem repeat VNTR2-1 in hTERT gene involves basic Helix-loop-helix family transcription factors.Environmental and molecular mutagenesis · 2021Article
- Stable DNMT3L overexpression in SH-SY5Y neurons recreates a facet of the genome-wide Down syndrome DNA methylation signature.Epigenetics & chromatin · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CpG islands (CGI) marked by bivalent chromatin in stem cells are believed to be more prone to aberrant DNA methylation in tumor cells. The robustness and genome-wide extent of this instructive program in different cancer types remain to be determined. To address this issue we developed a user-friendly approach to integrate the stem cell chromatin signature in customized DNA methylation analyses. We used publicly available ChIP-sequencing datasets of several human embryonic stem cell (hESC) lines to determine the extent of bivalent chromatin genome-wide. We then created annotated lists of high-confidence bivalent, H3K4me3-only and H3K27me3-only chromatin regions. The main features of bivalent regions included localization in CGI/promoters, depletion in retroelements and enrichment in specific histone modifications, including the poorly characterized H3K23me2 mark. Moreover, bivalent promoters could be classified in three clusters based on PRC2 and PolII complexes occupancy. Genes with bivalent promoters of the PRC2-defined cluster displayed the lowest expression upon differentiation. As proof-of-concept, we assessed the DNA methylation pattern of eight types of tumors and confirmed that aberrant cancer-associated DNA hypermethylation preferentially targets CGI characterized by bivalent chromatin in hESCs. We also found that such aberrant DNA hypermethylation affected particularly bivalent CGI/promoters associated with genes that tend to remain repressed upon differentiation. Strikingly, bivalent CGI were the most affected by aberrant DNA hypermethylation in both CpG Island Methylator Phenotype-positive (CIMP+) and CIMP-negative tumors, suggesting that, besides transcriptional silencing in the pre-tumorigenic cells, the bivalent chromatin signature in hESCs is a key determinant of the instructive program for aberrant DNA methylation.
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