Evidence map›Paper›PMID 20685852›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Research resource: genome-wide profiling of methylated promoters in endometriosis reveals a subtelomeric location of hypermethylation.

Bruno Borghese, Sandrine Barbaux, Françoise Mondon, Pietro Santulli, Guillaume Pierre, Giovanna Vinci, Charles Chapron, Daniel Vaiman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
6.5field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  7. Article
  8. Article
  9. Endometriosis in the era of precision medicine and impact on sexual and reproductive health across the lifespan and in diverse populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Review
  10. Article
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  12. Article
  13. Article
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  15. Article
  16. The Origin and Pathogenesis of Endometriosis.Annual review of pathology · 2020
    Review
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  18. Article
  19. Review
  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 3 institutions in 1 country.

Bruno BorgheseDépartement Génétique et Développement, Institut Cochin, 24 rue du Faubourg Saint-Jacques, 75014 Paris, France. bruno.borghese@inserm.fr
Sandrine Barbaux
Françoise Mondon
Pietro Santulli
Guillaume Pierre
Giovanna Vinci
Charles Chapron
Daniel Vaiman
Université Paris Cité · FRInserm · FRInstitut Cochin · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several lines of evidence indicate that endometriosis could be partially due to selective epigenetic deregulations. Promoter hypermethylation of some key genes, such as progesterone receptor and aromatase, has been associated with the silencing of these genes and might contribute to the disease. However, it is unknown whether global alterations in DNA methylation patterns occur in endometriosis and to what extent they are involved in its pathogenesis. We conducted a whole-genome scanning of methylation status in more than 25,000 promoters, using methylated DNA immunoprecipitation with hybridization to promoter microarrays. We detailed the methylation profiles for each subtype of the disease (superficial endometriosis, endometriomas, and deep infiltrating endometriosis) and compared them with the profile obtained for the eutopic endometrium. In line with the current theory of the endometrial origin of endometriosis, the overall methylation profile was highly similar between the endometrium and the lesions. It showed promoter regions consistently hypomethylated or hypermethylated (more than 1.5-times, as compared with endometrium) and others specific to one given subtype. Albeit there was no systematic correlation between promoter methylation and expression of nearby genes, 35 genes had both methylation and expressional alterations in the lesions. These genes, reported here for the first time, might be of interest in the development of endometriosis. In addition, hypermethylated regions were located at the ends of the chromosomes, whereas hypomethylated regions were randomly distributed all along the chromosomes. We postulated that this original observation might participate to the chromosomal stability and protect the endometriotic lesion against malignancy.

Indexed as

Gene Expression ProfilingPromoter Regions, GeneticChromosomes, HumanDNA MethylationDNA Restriction EnzymesEndometriosisFemaleGene Expression RegulationGenome, HumanHumansLamininOligonucleotide Array Sequence AnalysisReproducibility of ResultsReverse Transcriptase Polymerase Chain ReactionSequence Analysis, DNATelomereDNA Restriction EnzymesLamininlaminin alpha5McrBC endonucleaseTranscription Factors

Identifiers

PMID20685852
PMCPMC5417403
OpenAlexW2033961624

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.