Evidence map›Paper›PMID 26056044›Full record

ArticleOncotarget2015

Combined estrogenic and anti-estrogenic properties of estetrol on breast cancer may provide a safe therapeutic window for the treatment of menopausal symptoms.

Céline Gérard, Mélanie Mestdagt, Ekaterine Tskitishvili, Laudine Communal, Anne Gompel, Elisabete Silva, Jean-François Arnal, Françoise Lenfant, Agnès Noel, Jean-Michel Foidart and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Estetrol and Mammary Gland: Friends or Foes?Journal of mammary gland biology and neoplasia · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
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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

11 authors at 5 institutions in 3 countries.

Céline GérardLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, Liège, Belgium.
Mélanie MestdagtLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, Liège, Belgium.
Ekaterine TskitishviliLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, Liège, Belgium.
Laudine CommunalGynaecological Endocrinology Unit, Paris Descartes University, Hôpitaux Universitaires, Paris, France.
Anne GompelGynaecological Endocrinology Unit, Paris Descartes University, Hôpitaux Universitaires, Paris, France.
Elisabete SilvaInstitute of Environment, Health and Societies, Brunel University London, Uxbridge, United Kingdom.
Jean-François ArnalINSERM U1048, Institut des Maladies Métaboliques et Cardiovasculaires, University of Toulouse, UPS, Toulouse, France.
Françoise LenfantINSERM U1048, Institut des Maladies Métaboliques et Cardiovasculaires, University of Toulouse, UPS, Toulouse, France.
Agnès NoelLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, Liège, Belgium.
Jean-Michel FoidartLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, Liège, Belgium.
Christel PéqueuxLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, Liège, Belgium.
University of Liège · BEUniversité Toulouse III - Paul Sabatier · FRBrunel University of London · GBInserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased risk of breast cancer is a critical side effect associated with the use of a menopausal hormone therapy (MHT). Estetrol (E4) is a natural estrogen produced by the human fetal liver and is a promising compound for clinical use in MHT. However, its impact on breast cancer is controversial and poorly defined. In this preclinical study, we show that E4 acts as a weak estrogen by stimulating the growth of hormone-dependent breast cancer only at concentrations exceeding menopausal therapeutic needs. E4 presents also an antitumor activity by decreasing the strong proliferative effect of estradiol (E2). While estrogen receptor alpha (ERα) is the predominant receptor mediating its effects, the dual weak-estrogenic/anti-estrogenic feature of E4 results from differential signaling pathways activation. Both nuclear and rapid extra-nuclear signaling pathway are necessary for a complete estrogenic effect of E4. However, the antitumor action of E4 is not due to a capacity to antagonize E2-induced nuclear activity. Altogether, our results highlight that E4 has a limited impact on breast cancer and may offer a safe therapeutic window for the treatment of menopausal symptoms.

Indexed as

AnimalsBlotting, WesternBreast NeoplasmsCell Line, TumorCell ProliferationEstetrolEstrogen Replacement TherapyFemaleFluorescent Antibody TechniqueHeterograftsHumansMiceReal-Time Polymerase Chain ReactionEstetrolbreast cancerestetrolestrogen receptormenopauseSERM

Identifiers

PMID26056044
PMCPMC4627333
OpenAlexW1821983332

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.