Evidence map›Paper›PMID 26317761›Full record

ReviewRedox report : communications in free radical research2016

Potential scenarios leading to ovarian cancer arising from endometriosis.

Hiroshi Kobayashi

Open access · bronzeAbstract readReview
In one paragraph

Review in Redox report : communications in free radical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Hiroshi Kobayashia Department of Obstetrics and Gynecology , Nara Medical University , Japan.
Nara Medical University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe aim of this review was to highlight recent advances in our understanding of the pathogenesis of malignant transformation of endometriosis.

methodsThis study reviewed the English-language literature concerning basic science studies of the potential promotion of carcinogenesis.

resultsRepeated episodes of hemorrhage occur in endometriosis at the onset of menstruation. Extracellular hemoglobin, heme, and iron derivatives in endometriosis cause DNA damage and mutations, which create increased cellular susceptibility to oxidant-mediated cell killing. Excess DNA damage and mutations are linked to cell death, but not carcinogenesis. In response to an oxidative and inflammatory microenvironment, endometriotic cells and macrophages secrete antioxidants that control excess oxidative stress in the surrounding environment. Exposure of endometriotic cells to a sublethal level of oxidative stress may lead to carcinogenesis. Macrophages also secrete immunosuppressive factors that lead to promotion of malignant transformation. DISCUSSION: At least two potential scenarios could result in ovarian cancer arising from endometriosis. The first step: extracellular hemoglobin, heme, and iron cause cellular oxidative damage by promoting reactive oxygen species formation, which results in DNA damage and mutations (ovarian cancer initiation from endometriosis). The second step: cancer progression may be associated with persistent antioxidant production favoring a protumoral microenvironment.

Indexed as

AntioxidantsCell Transformation, NeoplasticDNA DamageEndometriosisFemaleHumansIronOvarian NeoplasmsOxidative StressReactive Oxygen SpeciesAntioxidantsIronReactive Oxygen SpeciesAntioxidantsCarcinogenesisEndometriosisOxidative stress

Identifiers

PMID26317761
PMCPMC6837701
OpenAlexW2120847569

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.