ArticleCurrent genomics2011
Prader-Willi Syndrome: Obesity due to Genomic Imprinting.
Article in Current genomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
128 citing papers in PubMed, 2 syntheses or guidelines pooled it, 240 citations in OpenAlex.
- Obesogenic behaviors during structured periods among children and adolescents with intellectual and developmental disabilities: a systematic review and meta-analysis.The international journal of behavioral nutrition and physical activity · 2026Pooled it
- GrowthHormone Research Society workshop summary: consensus guidelines for recombinant human growth hormone therapy in Prader-Willi syndrome.The Journal of clinical endocrinology and metabolism · 2013Pooled it
- The Efficacy, Safety, and Pharmacology of a Ghrelin O-Acyltransferase Inhibitor for the Treatment of Prader-Willi Syndrome.The Journal of clinical endocrinology and metabolism · 2022Trial
- Transcranial direct current stimulation reduces food-craving and measures of hyperphagia behavior in participants with Prader-Willi syndrome.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2016Trial
- Dietary Modulation of Gut Microbiota Contributes to Alleviation of Both Genetic and Simple Obesity in Children.EBioMedicine · 2015Trial
- Growth hormone receptor (GHR) gene polymorphism and Prader-Willi syndrome.American journal of medical genetics. Part A · 2013Trial
- Correlations between endocrine-metabolic characteristics and body fat distribution, appetite, growth, and memory in children with Prader-Willi syndrome.Clinics (Sao Paulo, Brazil) · 2026Article
- Diagnostic Utility of Muscle Ultrasound for Sarcopenia in Prader-Willi Syndrome: A Cross-Sectional Study.Journal of cachexia, sarcopenia and muscle · 2026Observational
- Clinical Presentation, Genetics, and Laboratory Testing with Integrated Genetic Analysis of Molecular Mechanisms in Prader-Willi and Angelman Syndromes: A Review.International journal of molecular sciences · 2026Review
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- Review
- Obesity genetic association prospective cohort utilizing single center real-world evidence data.Medicine · 2025Article
- Maternal uniparental disomy of chromosome 15 with concurrent paternal non-chromosome 15 marker chromosome: a rare presentation of prader-willi syndrome.Molecular cytogenetics · 2025Article
- Comparison of Body Composition, Basal Metabolic Rate and Metabolic Outcomes of Adults with Prader-Willi Syndrome and Age- and BMI-Matched Patients with Essential Obesity.Journal of clinical medicine · 2025Article
- Footprints in the Sno: investigating the cellular and molecular mechanisms of SNORD116.Open biology · 2025Review
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- Eating behaviour and eating disorders in individuals with rare neurodevelopmental variants: current knowledge and future research directions.Frontiers in psychiatry · 2025Article
- Variant pubertal development in Prader-Willi syndrome: early and slow progression of pubarche with normal age at gonadarche.Frontiers in endocrinology · 2025Article
- Retrospective longitudinal study on the long-term impact of COVID-19 infection on polysomnographic evaluation in patients with Prader-Willi syndrome.Orphanet journal of rare diseases · 2024Article
- Serum Ghrelin and Glucagon-like Peptide 1 Levels in Children with Prader-Willi and Bardet-Biedl SyndromesJournal of clinical research in pediatric endocrinology · 2024Article
68 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prader-Willi syndrome (PWS) is a complex neurodevelopmental disorder due to errors in genomic imprinting with loss of imprinted genes that are paternally expressed from the chromosome 15q11-q13 region. Approximately 70% of individuals with PWS have a de novo deletion of the paternally derived 15q11-q13 region in which there are two subtypes (i.e., larger Type I or smaller Type II), maternal disomy 15 (both 15s from the mother) in about 25% of cases, and the remaining subjects have either defects in the imprinting center controlling the activity of imprinted genes or due to other chromosome 15 rearrangements. PWS is characterized by a particular facial appearance, infantile hypotonia, a poor suck and feeding difficulties, hypogonadism and hypogenitalism in both sexes, short stature and small hands and feet due to growth hormone deficiency, mild learning and behavioral problems (e.g., skin picking, temper tantrums) and hyperphagia leading to early childhood obesity. Obesity is a significant health problem, if uncontrolled. PWS is considered the most common known genetic cause of morbid obesity in children. The chromosome 15q11-q13 region contains approximately 100 genes and transcripts in which about 10 are imprinted and paternally expressed. This region can be divided into four groups: 1) a proximal non-imprinted region; 2) a PWS paternal-only expressed region containing protein-coding and non-coding genes; 3) an Angelman syndrome region containing maternally expressed genes and 4) a distal non-imprinted region. This review summarizes the current understanding of the genetic causes, the natural history and clinical presentation of individuals with PWS.
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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.