ArticleEuropean journal of human genetics : EJHG2009
Prader-Willi syndrome.
Article in European journal of human genetics : EJHG, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00375089 (Prader-Willi Syndrome and Early-onset Morbid Obesity Natural History Clinical Protocol), which is not on this map. Cited by 210 papers, 2 of them syntheses that pooled 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.
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.
Prader-Willi Syndrome and Early-onset Morbid Obesity Natural History Clinical Protocol
Who cites it
210 citing papers in PubMed, 2 syntheses or guidelines pooled it, 588 citations in OpenAlex.
- MAGEL2-related disorders: A study and case series.Clinical genetics · 2019Pooled it
- Energy Metabolism Profile in Individuals with Prader-Willi Syndrome and Implications for Clinical Management: A Systematic Review.Advances in nutrition (Bethesda, Md.) · 2017Pooled it
- Mechanisms underlying the EEG biomarker in Dup15q syndrome.Molecular autism · 2019Trial
- Intranasal carbetocin reduces hyperphagia in individuals with Prader-Willi syndrome.JCI insight · 2018Trial
- A reduced-energy intake, well-balanced diet improves weight control in children with Prader-Willi syndrome.Journal of human nutrition and dietetics : the official journal of the British Dietetic Association · 2013Trial
- Advances and challenges of precision epigenetic therapy in treating genomic imprinting diseases.Translational pediatrics · 2026Review
- Genome-wide profiling of RNA 2'-O-methylation in neurons and identification of orphan snoRNA targets.Research square · 2026Article
- Innovative models to explore hepatic involvement in Prader-Willi syndrome.Frontiers in endocrinology · 2026Review
- Health-related Quality of Life among Children Living with Rare Diseases in China: a Nationwide Study.Applied research in quality of life · 2026Article
- Genome-wide profiling of RNA 2'-bioRxiv : the preprint server for biology · 2025Article
- Review
- Article
- Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.Epigenomics · 2025Review
- Prognostic importance of direct assignment of parent of origin via long-read genome and epigenome sequencing in retinoblastoma.JCI insight · 2024Article
- Identifying key underlying regulatory networks and predicting targets of orphan C/D box SNORD116 snoRNAs in Prader-Willi syndrome.Nucleic acids research · 2024Article
- The influence of genotype makeup on the effectiveness of growth hormone therapy in children with Prader-Willi syndrome.BMC pediatrics · 2024Article
- Genetic diversity, demographic history, and selective signatures of Silkie chicken.BMC genomics · 2024Article
- Article
- Deficiency in Prader-Willi syndrome geneiScience · 2024Article
- Investigating the correlation between genotype and phenotype in Prader-Willi syndrome: a study of 45 cases from Brazil.Orphanet journal of rare diseases · 2024Article
150 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Prader-Willi syndrome (PWS) is a highly variable genetic disorder affecting multiple body systems whose most consistent major manifestations include hypotonia with poor suck and poor weight gain in infancy; mild mental retardation, hypogonadism, growth hormone insufficiency causing short stature for the family, early childhood-onset hyperphagia and obesity, characteristic appearance, and behavioral and sometimes psychiatric disturbance. Many more minor characteristics can be helpful in diagnosis and important in management. PWS is an example of a genetic condition involving genomic imprinting. It can occur by three main mechanisms, which lead to absence of expression of paternally inherited genes in the 15q11.2-q13 region: paternal microdeletion, maternal uniparental disomy, and imprinting defect.
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.