Evidence map›Paper›PMID 23818951›Full record

ArticlePloS one2013

Genome-wide DNA methylation analysis reveals a potential mechanism for the pathogenesis and development of uterine leiomyomas.

Ryo Maekawa, Shun Sato, Yoshiaki Yamagata, Hiromi Asada, Isao Tamura, Lifa Lee, Maki Okada, Hiroshi Tamura, Eiichi Takaki, Akira Nakai and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
8.7field-weighted citation impact, top 2% 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, 104 citations in OpenAlex.

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  7. UTERINE FIBROIDS.Physiological reviews · 2025
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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

11 authors at 1 institution in 1 country.

Ryo MaekawaDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Shun Sato
Yoshiaki Yamagata
Hiromi Asada
Isao Tamura
Lifa Lee
Maki Okada
Hiroshi Tamura
Eiichi Takaki
Akira Nakai
Norihiro Sugino
Yamaguchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pathogenesis of uterine leiomyomas, the most common benign tumor in women, remains unclear. Since acquired factors such as obesity, hypertension and early menarche place women at greater risk for uterine leiomyomas, uterine leiomyomas may be associated with epigenetic abnormalities that are caused by unfavorable environmental exposures. PRINCIPAL

findingsProfiles of genome-wide DNA methylation and mRNA expression were investigated in leiomyomas and in myometrium with and without leiomyomas. Profiles of DNA methylation and mRNA expression in the myometrium with and without leiomyomas were quite similar while those in leiomyomas were distinct. We identified 120 genes whose DNA methylation and mRNA expression patterns differed between leiomyomas and the adjacent myometrium. The biological relevance of the aberrantly methylated and expressed genes was cancer process, including IRS1 that is related to transformation, and collagen-related genes such as COL4A1, COL4A2 and COL6A3. We also detected 22 target genes of estrogen receptor (ER) alpha, including apoptosis-related genes, that have aberrant DNA methylation in the promoter, suggesting that the aberrant epigenetic regulation of ER alpha-target genes contributes to the aberrant response to estrogen.

conclusionsAberrant DNA methylation and its related transcriptional aberration were associated with cancer processes, which may represent a critical initial mechanism that triggers transformation of a single tumor stem cell that will eventually develop into a monoclonal leiomyoma tumor. The aberrant epigenetic regulation of ER alpha-target genes also may contribute to the aberrant response to estrogen, which is involved in the development of uterine leiomyomas after menarche.

Indexed as

DNA MethylationAdultApoptosis Regulatory ProteinsChromosomes, Human, XCollagen Type IVCollagen Type VIFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInsulin Receptor Substrate ProteinsLeiomyomaMiddle AgedReceptors, EstrogenApoptosis Regulatory ProteinsCOL4A1 protein, humanCOL4A2 protein, humanCollagen Type IVCollagen Type VIInsulin Receptor Substrate ProteinsIRS1 protein, humanReceptors, Estrogen

Identifiers

PMID23818951
PMCPMC3688587
OpenAlexW2057883358

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Registered trials

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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.