Evidence map›Paper›PMID 25473436›Full record

ArticleGenome medicine2014

Enhancer alterations in cancer: a source for a cell identity crisis.

Ken J Kron, Swneke D Bailey, Mathieu Lupien

Open access · goldAbstract read
In one paragraph

Article in Genome medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Association of Intergenic and IntragenicInternational journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. Intrinsic epigenetic state of primary osteosarcoma drives metastasis.bioRxiv : the preprint server for biology · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Ken J KronThe Princess Margaret Cancer Centre - University Health Network, Toronto, ON M5G 1 L7 Canada ; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 1 L7 Canada.
Swneke D BaileyThe Princess Margaret Cancer Centre - University Health Network, Toronto, ON M5G 1 L7 Canada ; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 1 L7 Canada.
Mathieu LupienThe Princess Margaret Cancer Centre - University Health Network, Toronto, ON M5G 1 L7 Canada ; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 1 L7 Canada ; Ontario Institute for Cancer Research, Toronto, ON M5G 0A3 Canada.
University Health Network · CAUniversity of Toronto · CA

Funding

Breast and prostate cancer risk SNPs regulate FoxA1 and nuclear receptor activityR01CA155004 · NCI · UNIVERSITY HEALTH NETWORK · PI LUPIEN, MATHIEU · 2011 to 2015
$1.2M
NCI NIH HHS R01 CA155004
6 · The paper itself

Abstract

Enhancers are selectively utilized to orchestrate gene expression programs that first govern pluripotency and then proceed to highly specialized programs required for the process of cellular differentiation. Whereas gene-proximal promoters are typically active across numerous cell types, distal enhancer activation is cell-type-specific and central to cell fate determination, thereby accounting for cell identity. Recent studies have highlighted the diversity of enhancer usage, cataloguing millions of such elements in the human genome. The disruption of enhancer activity, through genetic or epigenetic alterations, can impact cell-type-specific functions, resulting in a wide range of pathologies. In cancer, these alterations can promote a 'cell identity crisis', in which enhancers associated with oncogenes and multipotentiality are activated, while those promoting cell fate commitment are inactivated. Overall, these alterations favor an undifferentiated cellular phenotype. Here, we review the current knowledge regarding the role of enhancers in normal cell function, and discuss how genetic and epigenetic changes in enhancer elements potentiate oncogenesis. In addition, we discuss how understanding the mechanisms regulating enhancer activity can inform therapeutic opportunities in cancer cells and highlight key challenges that remain in understanding enhancer biology as it relates to oncology.

Identifiers

PMID25473436
PMCPMC4254433
OpenAlexW2152314234

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.