ArticleBMC research notes2018
Methylation analysis of HOXA10 regulatory elements in patients with endometriosis.
Article in BMC research notes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Deconvolution of DNA methylation data reveals cell type-specific epigenomic signatures in endometriosis and eutopic endometrium.Molecular human reproduction · 2026Article
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- The Role of Adenogenesis Factors in the Pathogenesis of Endometriosis.International journal of molecular sciences · 2025Review
- A Systematic Review of Epigenetics of Endometriosis.F&S reviews · 2024Article
- A Lifelong Impact on Endometriosis: Pathophysiology and Pharmacological Treatment.International journal of molecular sciences · 2023Review
- Endometriosis: A Disease with Few Direct Treatment Options.Molecules (Basel, Switzerland) · 2022Review
- Current Knowledge on Endometriosis Etiology: A Systematic Review of Literature.International journal of women's health · 2021Review
- Expression of nm23-H1, p53, and integrin β1 in endometriosis and their clinical significance.International journal of clinical and experimental pathology · 2020Article
- The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights.International journal of molecular sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe pathogenesis of endometriosis is still mysterious, being retrograde menstruation and coelomic metaplasia the most accepted hypotheses. Recently, it has been proposed that endometriosis is caused by fine-tuning alterations of the female genital system development during the foetal life and that in utero exposition to endocrine disruptors can be one of the factors causing the disease, possibly acting on the methylation status of the genome. In this study, we have evaluated the methylation status of HOXA10 gene regulation regions in a cohort of 22 endometriosis patients respect to a control group of 6 healthy women.
resultsThe methylation study was carried out on three CpG islands, previously described hypermethylated in the endometrium of endometriosis patients and include 22 CpG sites, 21 CpG sites and 10 CpG sites, respectively identified through the online platform MethPrimer. The analysis did not find significant differences between patients with endometriosis and healthy control individuals. These results confirm previous studies on genome wide methylation analysis in endometriosis patients. Therefore, other epigenetically altered genes should be considered more related to the pathogenesis of endometriosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.