Evidence map›Paper›PMID 30657901›Full record

ReviewEndocrinology2019

Epithelial Mutations in Endometriosis: Link to Ovarian Cancer.

Serdar E Bulun, Yong Wan, Daniela Matei

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
13.0field-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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Review
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  14. TET3-overexpressing macrophages promote endometriosis.The Journal of clinical investigation · 2024
    Article
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  16. Review
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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

3 authors at 1 institution in 1 country.

Serdar E BulunDepartment of Obstetrics and Gynecology, Division of Reproductive Medicine in Science, Feinberg School of Medicine at Northwestern University, Chicago, Illinois.
Yong WanDepartment of Obstetrics and Gynecology, Division of Reproductive Medicine in Science, Feinberg School of Medicine at Northwestern University, Chicago, Illinois.
Daniela MateiDepartment of Obstetrics and Gynecology, Division of Reproductive Medicine in Science, Feinberg School of Medicine at Northwestern University, Chicago, Illinois.
Northwestern University · US

Funding

Endometriosis and RetinoidsR37HD038691 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BULUN, SERDAR E. · 2010 to 2019
$4.5M
Interplay between ER and TGF-b in carcinogenesisR01CA202948 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WAN, YONG · 2016 to 2021
$1.4M
NCI NIH HHS R01 CA202948NICHD NIH HHS R37 HD038691
6 · The paper itself

Abstract

Epidemiologic and histopathologic associations between endometriosis and epithelial ovarian cancer have been reported; however, the underlying molecular and cellular mechanisms are not well understood. A possible genetic link has been suggested in recent publications. Driver mutations in PIK3CA, KRAS, ARID1A, and other genes have been found in the epithelium of intrauterine endometrial tissue, ovarian and extraovarian pelvic endometriosis tissue, ovarian cancers associated with endometriosis (i.e., clear cell and endometrioid type), and other epithelial ovarian cancers. This makes sense because pelvic endometriosis occurs primarily as a result of retrograde menstruation and implantation of endometrial tissue fragments in ovarian inclusion cysts or extraovarian peritoneal or subperitoneal sites. Unlike epithelial cells, endometriotic stromal cells are mutation free but contain widespread epigenetic defects that alter gene expression and induce a progesterone-resistant and intensely inflammatory environment, driven by estrogen via estrogen receptor-β. The resulting increased estrogenic action in the stroma drives inflammation and sends paracrine signals to neighboring epithelial cells to enhance proliferation. In addition, massively high concentrations of estrogen in the ovary may exert an additional and direct genotoxic effect on DNA and cause accumulation of additional mutations and malignant transformation in initially mutated endometriotic epithelial cells in an ovarian endometrioma, which may initiate epithelial ovarian cancer. The same epithelial mutations and inflammatory processes in stroma are seen in extraovarian deep-infiltrating endometriosis, but carcinogenesis does not occur. We provide a focused review of the literature and discuss the implications of recent genetic breakthroughs linking endometriosis and ovarian cancer.

Indexed as

Carcinoma, Ovarian EpithelialEndometriosisFemaleHumansOvarian Neoplasms

Identifiers

PMID30657901
PMCPMC6382454
OpenAlexW2910391678

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.