Evidence map›Paper›PMID 32665538›Full record

ArticleNature communications2020

Endogenous retroviruses are a source of enhancers with oncogenic potential in acute myeloid leukaemia.

Özgen Deniz, Mamataz Ahmed, Christopher D Todd, Ana Rio-Machin, Mark A Dawson, Miguel R Branco

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 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
18.5field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 145 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. How Oncovirus Affects Drug Resistance in Cancer Cells.Recent patents on anti-cancer drug discovery · 2026
    Review
  9. Review
  10. HERV-K TM Subunit Elicits CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Revisiting Clonal Evolution Through the Light of Retrotransposons.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

36 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Özgen DenizBlizard Institute, Barts and The London School of Medicine and Dentistry, QMUL, London, E1 2AT, UK. o.deniz@qmul.ac.uk.ORCID http://orcid.org/0000-0001-7268-1923
Mamataz AhmedBlizard Institute, Barts and The London School of Medicine and Dentistry, QMUL, London, E1 2AT, UK.
Christopher D ToddBlizard Institute, Barts and The London School of Medicine and Dentistry, QMUL, London, E1 2AT, UK.ORCID http://orcid.org/0000-0003-2663-6173
Ana Rio-MachinCentre for Genomic Health, Life Sciences Institute, QMUL, London, E1 2AB, UK.ORCID http://orcid.org/0000-0001-6733-9752
Mark A DawsonCancer Research Division, Peter MacCallum Cancer Center, Melbourne, Victoria, 3002, Australia.ORCID http://orcid.org/0000-0002-5464-5029
Miguel R BrancoBlizard Institute, Barts and The London School of Medicine and Dentistry, QMUL, London, E1 2AT, UK. m.branco@qmul.ac.uk.ORCID http://orcid.org/0000-0001-9447-1548
Queen Mary University of London · GBBabraham Institute · GBPeter MacCallum Cancer Centre · AU

Funding

Wellcome Trust 101225/Z/13/Z
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is characterised by a series of genetic and epigenetic alterations that result in deregulation of transcriptional networks. One understudied source of transcriptional regulators are transposable elements (TEs), whose aberrant usage could contribute to oncogenic transcriptional circuits. However, the regulatory influence of TEs and their links to AML pathogenesis remain unexplored. Here we identify six endogenous retrovirus (ERV) families with AML-associated enhancer chromatin signatures that are enriched in binding of key regulators of hematopoiesis and AML pathogenesis. Using both locus-specific genetic editing and simultaneous epigenetic silencing of multiple ERVs, we demonstrate that ERV deregulation directly alters the expression of adjacent genes in AML. Strikingly, deletion or epigenetic silencing of an ERV-derived enhancer suppresses cell growth by inducing apoptosis in leukemia cell lines. This work reveals that ERVs are a previously unappreciated source of AML enhancers that may be exploited by cancer cells to help drive tumour heterogeneity and evolution.

Indexed as

AnimalsCell LineChromatinDNA Transposable ElementsEndogenous RetrovirusesEpigenesis, GeneticGene Regulatory NetworksGenome, HumanHumansInterspersed Repetitive SequencesLeukemia, Myeloid, AcuteChromatinDNA Transposable Elements

Identifiers

PMID32665538
PMCPMC7360734
OpenAlexW3043041775

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.