ArticleAmerican journal of obstetrics and gynecology2015
Evidence for pelvic organ prolapse predisposition genes on chromosomes 10 and 17.
Article in American journal of obstetrics and gynecology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The trial behind it
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Who cites it
16 citing papers in PubMed.
- Admixture mapping of pelvic organ prolapse in African Americans from the Women's Health Initiative Hormone Therapy trial.PloS one · 2017Trial
- Verification of the Chromosome Region 9q21 Association with Pelvic Organ Prolapse Using RegulomeDB Annotations.BioMed research international · 2015Trial
- The bidirectional association between hemorrhoidal disease and varicose veins: a nationwide population-based cohort study.International journal of colorectal disease · 2025Article
- Review
- Genetics of Female Pelvic Organ Prolapse: Up to Date.Biomolecules · 2024Review
- Exploring risk factors of pelvic organ prolapse at eastern of Democratic Republic of Congo: a case-control study.BMC women's health · 2024Article
- The polymorphisms of extracellular matrix-remodeling genes are associated with pelvic organ prolapse.International urogynecology journal · 2022Article
- Advances in molecular mechanisms of pelvic organ prolapse (Review).Experimental and therapeutic medicine · 2021Review
- Genome-Wide Association Study of Pelvic Organ Prolapse Using the Michigan Genomics Initiative.Female pelvic medicine & reconstructive surgery · 2021Article
- Collagen type 1A1, type 3A1, and LOXL1/4 polymorphisms as risk factors of pelvic organ prolapse.BMC research notes · 2021Article
- Genome‑wide DNA methylation analysis of uterosacral ligaments in women with pelvic organ prolapse.Molecular medicine reports · 2019Article
- Collagen XVIII and LOXL-4 polymorphisms in women with and without advanced pelvic organ prolapse.International urogynecology journal · 2018Article
- Can pelvic floor dysfunction after vaginal birth be prevented?International urogynecology journal · 2016Article
- Biological findings from the PheWAS catalog: focus on connective tissue-related disorders (pelvic floor dysfunction, abdominal hernia, varicose veins and hemorrhoids).Human genetics · 2016Article
- Elastin density: Link between histological and biomechanical properties of vaginal tissue in women with pelvic organ prolapse?International urogynecology journal · 2016Article
- Genetic Determinants of Pelvic Organ Prolapse among African American and Hispanic Women in the Women's Health Initiative.PloS one · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
objectiveWe conducted a genomewide linkage analysis to identify pelvic organ prolapse (POP) predisposition genes using a resource of high-risk POP pedigrees. STUDY
designCases are defined as women who reported bothersome symptoms of POP based on standardized symptom questions (Pelvic Floor Distress Inventory, moderately or quite bothered), and/or received treatment for POP documented in medical records. Our complete pedigree resource contains 299 familial POP cases in 83 high-risk pedigrees. Genotype data were obtained from Illumina HumanHap550, 610Q, the Human1M-Duo, Human Omni1-Quad, or the Human Omni 2.5 platforms. A set of single nucleotide polymorphism markers common to all platforms was identified and markers in high linkage disequilibrium were removed. We performed a genomewide linkage analysis under general dominant and recessive models using a Markov chain, Monte Carlo linkage analysis method implemented in MCLINK (University of Utah) software. Because 70 individuals in 32 pedigrees were used in a previously published linkage analysis for a phenotype of POP requiring treatment/surgery, we also performed linkage only including the 225 newly recruited and genotyped cases in 61 pedigrees.
resultsLinkage analysis using our complete pedigree resource for the loosened criteria of bothersome POP showed evidence for significant genomewide linkage on chromosome 10q24-26 (recessive model, maximum heterogeneity logarithm of odds 3.4); suggestive evidence was identified on chromosomes 6 and 17, and an additional region on chromosome 10. In the subset of only the newly recruited familial POP cases, significant evidence for genomewide linkage was observed on chromosome 17q25 (recessive model, maximum heterogeneity logarithm of odds 3.3), and suggestive evidence for linkage was observed on chromosomes 10 and 11. Neither analysis duplicated the previously published linkage evidence for the POP requiring treatment/surgery phenotype observed on chromosome 9.
conclusionWhile the etiology of this common condition is unknown, this study provides evidence that loci on chromosomes 10q and 17q may contribute to POP etiology.
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