Evidence map›Paper›PMID 31479615›Full record

ReviewAnnual review of pathology2020

The Origin and Pathogenesis of Endometriosis.

Yeh Wang, Kristen Nicholes, Ie-Ming Shih

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 5 pooled it
32.5field-weighted citation impact, top 1% 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

238 citing papers in PubMed, 5 syntheses or guidelines pooled it, 447 citations in OpenAlex.

  1. Alterations in Cellular Immunity in Patients With Endometriosis: Systematic Review and Meta-Analysis.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Pooled it
  2. Pooled it
  3. Expression ofInternational journal of molecular sciences · 2023
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Predictive markers of endometriosis: a future perspective.Archives of gynecology and obstetrics · 2026
    Review
  15. Article
  16. Article
  17. Building Disease Models for Endometriosis: iPSCs as Game-Changers.International journal of molecular sciences · 2026
    Review
  18. Article
  19. Review
  20. Article

178 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

3 authors at 2 institutions in 1 country.

Yeh WangPathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA; email: ywang354@jhmi.edu, knicho28@jhmi.edu, ishih@jhmi.edu.
Kristen NicholesPathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA; email: ywang354@jhmi.edu, knicho28@jhmi.edu, ishih@jhmi.edu.
Ie-Ming ShihPathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA; email: ywang354@jhmi.edu, knicho28@jhmi.edu, ishih@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

Role of cancer-associated mutations in endometriosisR01HD096147 · NICHD · JOHNS HOPKINS UNIVERSITY · PI SEGARS, JAMES H., SHIH, IE-MING · 2019 to 2023
$3.4M
NICHD NIH HHS R01 HD096147
6 · The paper itself

Abstract

Recent molecular genetic findings on endometriosis and normal endometrium suggest a modified model in which circulating epithelial progenitor or stem cells intended to regenerate uterine endometrium after menstruation may become overreactive and trapped outside the uterus. These trapped epithelium-committed progenitor cells form nascent glands through clonal expansion and recruit polyclonal stromal cells, leading to the establishment of deep infiltrating endometriosis. Once formed, the ectopic tissue becomes subject to immune surveillance, resulting in chronic inflammation. The inflammatory response orchestrated by nuclear factor-κB signaling is exacerbated by aberrations in the estrogen receptor-β and progesterone receptor pathways, which are also affected by local inflammation, forming a dysregulated inflammation-hormonal loop. Glandular epithelium within endometriotic tissue harbors cancer-associated mutations that are frequently detected in endometriosis-related ovarian cancers. In this review, we summarize recent advances that have illuminated the origin and pathogenesis of endometriosis and have provided new avenues for research that promise to improve the early diagnosis and management of endometriosis.

Indexed as

EndometriosisEndometriumEstrogen Receptor betaFemaleHumansMenstruationOvarian NeoplasmsReceptors, ProgesteroneSignal TransductionStromal CellsUterusEstrogen Receptor betaReceptors, Progesteronechronic inflammationendocrine dysregulationendometriosisgenetic and epigenetic alterationsimmune dysregulationovarian cancerstem cell

Identifiers

PMID31479615
PMCPMC7980953
OpenAlexW2971693998

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.