Evidence map›Paper›PMID 26456077›Full record

ReviewThe Journal of pathology2016

Models of endometriosis and their utility in studying progression to ovarian clear cell carcinoma.

Claire M King, Cynthia Barbara, Andrew Prentice, James D Brenton, D Stephen Charnock-Jones

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

Review in The Journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.5field-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

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

  1. Pooled it
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  8. Case report: A germlineFrontiers in oncology · 2024
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  17. Experimental and therapeutic medicine · 2020
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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

5 authors at 3 institutions in 1 country.

Claire M KingDepartment of Obstetrics and Gynaecology, University of Cambridge, The Rosie Hospital, Cambridge, UK.
Cynthia BarbaraDepartment of Obstetrics and Gynaecology, University of Cambridge, The Rosie Hospital, Cambridge, UK.
Andrew PrenticeDepartment of Obstetrics and Gynaecology, University of Cambridge, The Rosie Hospital, Cambridge, UK.
James D BrentonFunctional Genomics of Ovarian Cancer Laboratory, CR-UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge, UK.
D Stephen Charnock-JonesDepartment of Obstetrics and Gynaecology, University of Cambridge, The Rosie Hospital, Cambridge, UK.
Rosie Hospital · GBUniversity of Cambridge · GBNational Institute for Health Research · GB

Funding

Cancer Research UK 13095Cancer Research UK 15601Cancer Research UK A13095Cancer Research UK A15601
6 · The paper itself

Abstract

Endometriosis is a common benign gynaecological condition affecting at least 10% of women of childbearing age and is characterized by pain--frequently debilitating. Although the exact prevalence is unknown, the economic burden is substantial (∼$50 billion a year in the USA alone) and it is associated with considerable morbidity. The development of endometriosis is inextricably linked to the process of menstruation and thus the models that best recapitulate the human disease are in menstruating non-human primates. However, the use of these animals is ethically challenging and very expensive. A variety of models in laboratory animals have been developed and the most recent are based on generating menstrual-like endometrial tissue that can be transferred to a recipient animal. These models are genetically manipulable and facilitate precise mechanistic studies. In addition, these models can be used to study malignant transformation in epithelial ovarian carcinoma. Epidemiological and molecular evidence indicates that endometriosis is the most plausible precursor of both clear cell and endometrioid ovarian cancer (OCCA and OEA, respectively). While this progression is rare, understanding the underlying mechanisms of transformation may offer new strategies for prevention and therapy. Our ability to pursue this is highly dependent on improved animal models but the current transgenic models, which genetically modify the ovarian surface epithelium and oviduct, are poor models of ectopic endometrial tissue. In this review we describe the various models of endometriosis and discuss how they may be applicable to developing our mechanistic understanding of OCCA and OEA.

Indexed as

Disease Models, AnimalAdenocarcinoma, Clear CellAnimalsCarcinoma, Ovarian EpithelialCell Transformation, NeoplasticDisease ProgressionEndometrial NeoplasmsEndometriosisFemaleHumansMenstruationNeoplasms, Glandular and EpithelialOvarian NeoplasmsPrimatesRabbitsRodentiaanimal modelclear cell ovarian cancerendometrioid ovarian cancerendometriosismenstruation

Identifiers

PMID26456077
PMCPMC4855629
OpenAlexW1920069294

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.