ArticleFertility and sterility2015
A genome-wide screen for copy number alterations in an adolescent pilot cohort with müllerian anomalies.
Article in Fertility and sterility, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular Basis of Müllerian Agenesis Causing Congenital Uterine Factor Infertility-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Identification of Genetic Causes in Mayer-Rokitansky-Küster-Hauser (MRKH) Syndrome: A Systematic Review of the Literature.Children (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectiveTo examine whether pathogenic copy number changes (CNCs) can be identified in deoxyribonucleic acid from females with different classes of müllerian anomalies.
designWe conducted array-based copy number variant (CNV) analysis using an oligonucleotide array from deoxyribonucleic acid in 12 adolescent females with various müllerian anomalies.
settingUniversity-affiliated tertiary care institution. PATIENT(S): Twenty adolescent females with clinically confirmed müllerian anomalies. INTERVENTION(S): Array-based CNV analysis. MAIN OUTCOME MEASURE(S): Copy number changes and/or regions with absence of heterozygosity. RESULT(S): A total of 192 CNVs identified in these samples were previously annotated as polymorphic. Three CNCs that were identified in regions with minimal to no overlap with annotated polymorphisms failed significance criteria with detailed inspection. One subject harbored a 5.1-Mb region of absence of heterozygosity at Xq23 that is of unknown significance. CONCLUSION(S): We did not identify pathogenic CNCs in this small pilot cohort of patients with various müllerian anomalies, but larger studies will be needed to further investigate whether CNCs are associated with all classes of müllerian anomalies.
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