Evidence map›Paper›PMID 25415051›Full record

ArticleeLife2014

RUNX1, a transcription factor mutated in breast cancer, controls the fate of ER-positive mammary luminal cells.

Maaike P A van Bragt, Xin Hu, Ying Xie, Zhe Li

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
4.6field-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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. RUNX1-deficiency drives immune-active ERbioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Roles and signaling pathways of CITED1 in tumors: overview and novel insights.The Journal of international medical research · 2024
    Review
  12. Article
  13. Article
  14. Proteome-wide Profiling of Asymmetric Dimethylated Arginine in Human Breast Tumors.Journal of the American Society for Mass Spectrometry · 2023
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

11 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

4 authors at 2 institutions in 2 countries.

Maaike P A van BragtDivision of Genetics, Brigham and Women's Hospital, Boston, United States.
Xin HuDivision of Genetics, Brigham and Women's Hospital, Boston, United States.
Ying XieDivision of Genetics, Brigham and Women's Hospital, Boston, United States.
Zhe LiDivision of Genetics, Brigham and Women's Hospital, Boston, United States.
Brigham and Women's Hospital · USHarvard University · US

Funding

IGF/IGF1R signaling in hematopoiesis and leukemogenesisR01HL107663 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LI, ZHE · 2011 to 2015
$1.8M
Breast cancer stem cells and their cellular originR00CA126980 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI LI, ZHE · 2009 to 2011
$735k
Breast cancer stem cells and their cellular originK99CA126980 · NCI · BOSTON CHILDREN'S HOSPITAL · PI LI, ZHE · 2007 to 2008
$274k
NCI NIH HHS K99 CA126980NCI NIH HHS K99/R00 CA126980NCI NIH HHS R00 CA126980NHLBI NIH HHS R01 HL107663
6 · The paper itself

Abstract

RUNX1 encodes a RUNX family transcription factor (TF) and was recently identified as a novel mutated gene in human luminal breast cancers. We found that Runx1 is expressed in all subpopulations of murine mammary epithelial cells (MECs) except the secretory alveolar luminal cells. Conditional knockout of Runx1 in MECs by MMTV-Cre led to a decrease in luminal MECs, largely due to a profound reduction in the estrogen receptor (ER)-positive mature luminal subpopulation, a phenotype that could be rescued by the loss of either Trp53 or Rb1. Mechanistically RUNX1 represses Elf5, a master regulatory TF gene for alveolar cells, and regulates mature luminal TF/co-factor genes (e.g., Foxa1 and Cited1) involved in the ER program. Collectively, our data identified a key regulator of the ER⁺ luminal lineage whose disruption may contribute to the development of ER⁺ luminal breast cancer when under the background of either TP53 or RB1 loss.

Indexed as

Gene Expression Regulation, NeoplasticAgingAmino Acid SequenceAnimalsApoptosis Regulatory ProteinsCell Transformation, NeoplasticCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsEpithelial CellsFemaleGene Expression Regulation, DevelopmentalHepatocyte Nuclear Factor 3-alphaIntegrasesMammary Glands, AnimalMammary Tumor Virus, MouseMiceApoptosis Regulatory ProteinsCited1 protein, mouseCore Binding Factor Alpha 2 SubunitCre recombinaseDNA-Binding ProteinsElf5 protein, mouseFoxa1 protein, mouseHepatocyte Nuclear Factor 3-alphaIntegrasesNuclear ProteinsReceptors, EstrogenRetinoblastoma ProteinRunx1 protein, mouseTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53cell fatedevelopmental biologyELF5estrogen receptorhumanhuman biologyluminal breast cancermaster regulatory transcription factormedicinemouseRUNX1stem cells

Identifiers

PMID25415051
PMCPMC4381933
OpenAlexW2147052402

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.