Evidence map›Paper›PMID 33603851›Full record

ReviewExperimental and therapeutic medicine2021

Ovarian endometriosis, a precursor of ovarian cancer: Histological aspects, gene expression and microRNA alterations (Review).

Adriana Ioana Gaia-Oltean, Cornelia Braicu, Diana Gulei, Razvan Ciortea, Dan Mihu, Horace Roman, Alexandru Irimie, Ioana Berindan-Neagoe

Open access · diamondAbstract readReview
In one paragraph

Review in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
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  11. Review
  12. Review
  13. Article
  14. Article
  15. Assessment ofInternational journal of molecular sciences · 2023
    Article
  16. The Expression ofInternational journal of molecular sciences · 2023
    Article
  17. Article
  18. miR 31-3p Has the Highest Expression in Cesarean Scar Endometriosis.International journal of molecular sciences · 2022
    Article
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

Adriana Ioana Gaia-OlteanDepartment of Oncological Surgery, Iuliu Hatieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania.
Cornelia BraicuResearch Center for Functional Genomics and Translational Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 40015 Cluj-Napoca, Romania.
Diana GuleiMedFuture-Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 40015 Cluj-Napoca, Romania.
Razvan CiorteaSecond Department of Obstetrics and Gynecology, Iuliu Hatieganu University of Medicine and Pharmacy, 400124 Cluj-Napoca, Romania.
Dan MihuSecond Department of Obstetrics and Gynecology, Iuliu Hatieganu University of Medicine and Pharmacy, 400124 Cluj-Napoca, Romania.
Horace RomanCenter of Endometriosis, Clinique Tivoli-Ducos, 33000 Bordeaux, France.
Alexandru IrimieDepartment of Oncological Surgery, Iuliu Hatieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania.
Ioana Berindan-NeagoeResearch Center for Functional Genomics and Translational Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 40015 Cluj-Napoca, Romania.
Iuliu Hațieganu University of Medicine and Pharmacy · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian endometriosis is a frequent chronic gynecological disease with an uncertain evolution regarding its progression or association with ovarian malignant lesions. The present review summarized the histological aspects, gene expression and microRNA (miRNA/miR) alterations associated with ovarian endometriosis and cancer and their possible interaction. The endometriosis-ovarian cancer interaction has been proposed by certain researchers as a single entity. Histological results indicated that endometriosis has been in different circumstances coexisting with ovarian cancer, with reference to endometrioid and clear cell carcinoma. Endometriosis with moderate and severe atypia can influence cell proliferation and architecture, resulting in a possible malignant transformation. Gene expression analysis indicated that the pathologies of both endometriosis and ovarian cancer are characterized by genetic instability from a molecular point of view, as several important genetic mutations, including ARID1A, PI3KCA, PTEN, BRCA1, BRCA2, TP53 and KRAS genes, were identified. miRNA alterations have been implicated in the regulation of gene expression. Common dysregulated miRNAs, such as miR-331, miR-335, miR-891, miR-548, miR-124, miR-148, miR-215, miR-192, miR-337, miR-153, miR-155, miR-144, miR-221 and miR-3688 were extensively investigated in understanding endometriosis and ovarian cancer evolution. From a combined viewpoint including histological aspects, gene expression and miRNA alterations, it is reasonable to speculate that endometriosis is associated with ovarian cancer. Ovarian endometriosis lesions may present a risk for ovarian malignant lesions, which supports a model of endometriosis as a malignant precursor. However, the endometriosis-ovarian cancer association is not widely accepted in the literature and additional studies are required to validate this association.

Indexed as

gene expressionhistologymiRNAsovarian cancerovarian endometriosis

Identifiers

PMID33603851
PMCPMC7851621
OpenAlexW3124429930

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.