Evidence map›Paper›PMID 27872195›Full record

ReviewReproductive sciences (Thousand Oaks, Calif.)2017

Estrogen Receptors and Signaling in Fibroids: Role in Pathobiology and Therapeutic Implications.

Mostafa A Borahay, Mehmet R Asoglu, Aymara Mas, Sarah Adam, Gokhan S Kilic, Ayman Al-Hendy

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Reproductive sciences (Thousand Oaks, Calif.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

18 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 5 institutions in 1 country.

Mostafa A Borahay1 Department of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Mehmet R Asoglu2 Department of Obstetrics & Gynecology, The University of Texas Medical Branch, Galveston, TX, USA.
Aymara Mas3 Department of Obstetrics & Gynecology, Georgia Regents University, Augusta, GA, USA.
Sarah Adam4 Department of Obstetrics & Gynecology, Mercer University, Macon, GA, USA.
Gokhan S Kilic2 Department of Obstetrics & Gynecology, The University of Texas Medical Branch, Galveston, TX, USA.
Ayman Al-Hendy3 Department of Obstetrics & Gynecology, Georgia Regents University, Augusta, GA, USA.
The University of Texas Medical Branch at Galveston · USAugusta University · USGeorgia Regents Medical Center · USJohns Hopkins Medicine · USMercer University · US

Funding

UTMB Clinical and Translational Science AwardUL1TR000071 · NCATS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BRASIER, ALLAN R. · 2012 to 2014
$14.4M
NCATS NIH HHS UL1 TR000071
6 · The paper itself

Abstract

Uterine fibroids are the most common gynecologic tumors with a significant medical and financial burden. Several genetic, hormonal, and biological factors have been shown to contribute to the development and growth of fibroid tumors. Of these factors, estrogen is particularly critical since fibroids are considered estrogen dependent because no prepubertal cases have been described in the literature and tumors tend to regress after menopause. Understanding the role of estrogen in fibroids is not only important for understanding the pathobiology of fibroids but also for the development of successful therapeutics. In this review, we discuss the types and structure of estrogen receptors (nuclear and membrane bound, including α and β receptors and G protein-coupled estrogen receptor 1 GPER1). Estrogen-signaling pathways in fibroids include genomic (direct and indirect) and nongenomic including Ras-Raf-MEK (MAPK/Erk Kinase)-mitogen-activated protein kinase (MAPK) and phosphatidylinositide 3-kinase (PI3K)-phosphatidylinositol-3,4,5-trisphosphate (PIP3)-Akt (Protein kinase B)-mammalian target of rapamycin (mTOR) pathways; shortly Ras-Raf-MEK-MAPK and PI3K-PIP3-Akt-mTOR pathways. Several aberrations in estrogen receptors and signaling pathways are implicated in fibroid pathobiology. Current therapeutic and research agents targeting ERs/signaling include gonadotropin-releasing hormone (GnRH) agonists, GnRH antagonists, aromatase inhibitors, selective ER modulators, gene therapy, and others. Future research can identify potential targets for the development of novel treatments. In particular, epigenomics of estrogen activity and individualized (precision) medicine appear to be attractive areas for future research.

Indexed as

AnimalsFemaleHumansLeiomyomaMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, EstrogenSignal TransductionUterine NeoplasmsMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Estrogenestrogenestrogen receptorfibroidsignalingtreatmentuterine leiomyoma

Identifiers

PMID27872195
PMCPMC6344829
OpenAlexW2552911241

What OpenQuestion holds

Textmetadata
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.