Evidence map›Paper›PMID 31683028›Full record

ReviewJournal of minimally invasive gynecology2020

Should Genetics Now Be Considered the Pre-eminent Etiologic Factor in Endometriosis?

Grant W Montgomery, Sally Mortlock, Linda C Giudice

Open access · greenAbstract readReview
In one paragraph

Review in Journal of minimally invasive gynecology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.6field-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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Building Disease Models for Endometriosis: iPSCs as Game-Changers.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. The long road of drug development for endometriosis - Pains, gains, and hopes.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Review
  7. Review
  8. Endometriosis in the era of precision medicine and impact on sexual and reproductive health across the lifespan and in diverse populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Oocyte-Secreted Serum Biomarkers GDF9 and BMP15 in Women with Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023
    Article
  13. New concepts on the etiology of endometriosis.The journal of obstetrics and gynaecology research · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Abdominal wall endometriosis: a case report.The Pan African medical journal · 2022
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Grant W MontgomeryInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia (Drs. Montgomery and Mortlock). Electronic address: g.montgomery1@uq.edu.au.
Sally MortlockInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia (Drs. Montgomery and Mortlock).
Linda C GiudiceDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, San Francisco, California (Dr. Giudice).
The University of Queensland · AUUniversity of California, San Francisco · US

Funding

Integrative Analysis of Genomic, Epigenomic and Phenotypic Data for Disease Stratification of EndometriosisR01HD089511 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GIUDICE, LINDA C, MISSMER, STACEY ANN · 2016 to 2020
$3.0M
NICHD NIH HHS R01 HD089511
6 · The paper itself

Abstract

Endometriosis is a common, estrogen-dependent, inflammatory disorder characterized by the growth of endometrial-like tissue at extrauterine locations. Its pathogenesis and mechanisms underlying its pathophysiology are poorly understood, although genetic variation is strongly implicated in these processes. Genetic studies reveal that approximately 50% of risk for endometriosis is due to genetic factors and the other 50% likely owing to environmental factors. As with other complex diseases, genetic variants in the DNA sequence increasing endometriosis risk all have small effects, unlike most single-gene disorders. It is the combinations of these variants adding together that contribute to higher risks for individual women. In addition, recent data on disease lesions demonstrate a high frequency of somatic (likely acquired) mutations, some of which are present in the eutopic endometrium and specifically in the epithelial cell compartment, raising the possibility that abnormal epithelial progenitors in the eutopic endometrium give rise to ectopic disease. Discovery in this field is occurring at a rapid pace, and further definitions of genetic (germline) and environmental (somatic) contributions to the pathogenesis and pathophysiology of this disorder are anticipated soon. These discoveries are expected to increase diagnostic, therapeutic, and preventive strategies to minimize disease and its associated morbidities.

Indexed as

Genetic TestingDiagnosis, DifferentialDiagnostic Techniques, Obstetrical and GynecologicalEndometriosisEndometriumEstrogensFemaleGenetic Predisposition to DiseaseHumansMutationPeritoneal DiseasesRisk FactorsEstrogensDisease modelGenetic risk factorsSomatic mutations

Identifiers

PMID31683028
PMCPMC7863762
OpenAlexW2987191598

What OpenQuestion holds

Textmetadata
LicenceTDM
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.