Evidence map›Paper›PMID 27535958›Full record

ArticleBiology of reproduction2016

Aberrant Endometrial DNA Methylome and Associated Gene Expression in Women with Endometriosis.

Sahar Houshdaran, Camran R Nezhat, Kim Chi Vo, Zara Zelenko, Juan C Irwin, Linda C Giudice

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 3 pooled it
18.0field-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

54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Pathogenesis of Endometriosis and Endometriosis-Associated Cancers.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. New concepts on the etiology of endometriosis.The journal of obstetrics and gynaecology research · 2023
    Article
  17. Article
  18. Review
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

Sahar HoushdaranDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of California San Francisco, San Francisco, California.
Camran R NezhatCenter for Special Minimally Invasive and Robotic Surgery, Palo Alto, California.
Kim Chi VoDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of California San Francisco, San Francisco, California.
Zara ZelenkoDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of California San Francisco, San Francisco, California.
Juan C IrwinDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of California San Francisco, San Francisco, California.
Linda C GiudiceDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of California San Francisco, San Francisco, California linda.giudice@ucsf.edu.
University of California, San Francisco · USCenter for Special Minimally Invasive and Robotic Surgery · US

Funding

Project 4: Human Endometrial Programming for Successful ImplantationP50HD055764 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GIUDICE, LINDA C · 2014 to 2022
$16.4M
Trophoblast Differentiation in In Vivo and In Vitro Fertilized EmbryosU54HD055764 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TRAN, NAM D · 2007 to 2013
$11.5M
NICHD NIH HHS P50 HD055764NICHD NIH HHS U54 HD055764
6 · The paper itself

Abstract

Endometriosis is an estrogen-dependent, progesterone-resistant disorder largely derived from retrograde transplantation of menstrual tissue/cells into the pelvis, eliciting an inflammatory response, pelvic pain, and infertility. Eutopic endometrium (within the uterus), giving rise to pelvic disease, displays cycle-dependent transcriptomic, proteomic, and signaling abnormalities, and although its DNA methylation profiles dynamically change across the cycle in healthy women, studies in endometriosis are limited. Herein, we investigated the DNA methylome and associated gene expression in three phases of the cycle in eutopic endometrium of women with severe endometriosis versus controls, matched for ethnicity, medications, smoking, and no recent contraceptive steroid use. Genome-wide DNA methylation and gene expression were coassessed in each sample. Cycle phase was determined by histology, serum hormone levels, and unsupervised principal component and hierarchical cluster analyses of microarray data. Altered endometrial DNA methylation in endometriosis was most prominent in the midsecretory phase (peak progesterone), with disruption of the normal pattern of cycle-dependent DNA methylation changes, including a bias toward methylation of CpG islands, suggesting wide-range abnormalities of the chromatin remodeling machinery in endometriosis. DNA methylation changes were associated with altered gene expression relevant to endometrial function/dysfunction, including cell proliferation, inflammation/immune response, angiogenesis, and steroid hormone response. The data provide insight into epigenetic reprogramming and steroid hormone actions in endometrium contributing to the pathogenesis and pathophysiology of endometriosis.

Indexed as

DNA MethylationGene ExpressionAdultCpG IslandsEndometriosisEndometriumEpigenesis, GeneticFemaleGene Expression RegulationHumansMenstrual CycleProteomicsDNA methylationendometriosisendometriumepigenetics

Identifiers

PMID27535958
PMCPMC5178151
OpenAlexW2513803129

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.