Evidence map›Paper›PMID 32699299›Full record

ArticleNature communications2020

Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation.

Hemalvi Patani, Michael D Rushton, Jonathan Higham, Saul A Teijeiro, David Oxley, Pedro Cutillas, Duncan Sproul, Gabriella Ficz

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. DNA Methylation Aberrant in Atherosclerosis.Frontiers in pharmacology · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Hemalvi PataniCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, EC1M 6BQ, London, UK.ORCID http://orcid.org/0000-0001-6361-9642
Michael D RushtonCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, EC1M 6BQ, London, UK.
Jonathan HighamMRC Human Genetics Unit and Edinburgh Cancer Research Centre, MRC Institute of Genetics & Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, EH4 2XU, Edinburgh, UK.
Saul A TeijeiroCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, EC1M 6BQ, London, UK.
David OxleyMass Spectrometry Facility, Babraham Institute, CB22 3AT, Cambridge, UK.
Pedro CutillasCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, EC1M 6BQ, London, UK.ORCID http://orcid.org/0000-0002-3426-2274
Duncan SproulMRC Human Genetics Unit and Edinburgh Cancer Research Centre, MRC Institute of Genetics & Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, EH4 2XU, Edinburgh, UK.ORCID http://orcid.org/0000-0001-6168-4563
Gabriella FiczCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, EC1M 6BQ, London, UK. g.ficz@qmul.ac.uk.ORCID http://orcid.org/0000-0001-9313-9578
Queen Mary University of London · GBWestern General Hospital · GBBabraham Institute · GB

Funding

Cancer Research UK 20837Cancer Research UK C47648/A20837Medical Research Council 1650326Medical Research Council MR/M01892X/1
6 · The paper itself

Abstract

Epigenetic reprogramming is a cancer hallmark, but how it unfolds during early neoplastic events and its role in carcinogenesis and cancer progression is not fully understood. Here we show that resetting from primed to naïve human pluripotency results in acquisition of a DNA methylation landscape mirroring the cancer DNA methylome, with gradual hypermethylation of bivalent developmental genes. We identify a dichotomy between bivalent genes that do and do not become hypermethylated, which is also mirrored in cancer. We find that loss of H3K4me3 at bivalent regions is associated with gain of methylation. Additionally, we observe that promoter CpG island hypermethylation is not restricted solely to emerging naïve cells, suggesting that it is a feature of a heterogeneous intermediate population during resetting. These results indicate that transition to naïve pluripotency and oncogenic transformation share common epigenetic trajectories, which implicates reprogramming and the pluripotency network as a central hub in cancer formation.

Indexed as

Cellular ReprogrammingDNA MethylationEpigenesis, GeneticAnimalsCell LineCell Transformation, NeoplasticCoculture TechniquesCpG IslandsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AFibroblastsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHEK293 CellsHistonesHuman Embryonic Stem CellsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanhistone H3 trimethyl Lys4HistonesMixed Function OxygenasesProto-Oncogene ProteinsRNA, Small InterferingTET1 protein, human

Identifiers

PMID32699299
PMCPMC7376100
OpenAlexW3043994525

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.