ReviewClinical & translational immunology2017
Type 1 diabetes genome-wide association studies: not to be lost in translation.
Review in Clinical & translational immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.
- Genome-wide search for genes affecting the age at diagnosis of type 1 diabetes.Journal of internal medicine · 2021Pooled it
- Systematic Review of Polygenic Risk Scores for Type 1 and Type 2 Diabetes.International journal of molecular sciences · 2020Pooled it
- ProtectiveiScience · 2026Article
- MDA5 and the integrated stress response control sex-specific type 1 diabetes onset in NOD mice.bioRxiv : the preprint server for biology · 2026Article
- Toward Personalized Medicine in Type 1 Diabetes: Understanding How Patient Heterogeneity Influences Therapeutic Efficacy.Diabetes, obesity & metabolism · 2026Review
- Personalized medicine as a novel therapeutic approach for autoimmune diseases: new insights and future prospects.Osong public health and research perspectives · 2026Article
- Impact of Parabacteroides distasonis colonization on host microbiome, metabolome, immunity, and diabetes onset.Journal of molecular endocrinology · 2025Article
- Type 1 Diabetes: A Guide to Autoimmune Mechanisms for Clinicians.Diabetes, obesity & metabolism · 2025Review
- A Historical and Epistemological Review of Type 1 Diabetes Mellitus.Journal of clinical medicine · 2025Review
- Protocol for the development of a core outcome set for type 1 diabetes risk screening.BMJ open · 2025Article
- The perfect storm: unraveling the interplay of genetic predisposition and viral triggers in type 1 diabetes pathogenesis.Frontiers in endocrinology · 2025Review
- HBI: a hierarchical Bayesian interaction model to estimate cell-type-specific methylation quantitative trait loci incorporating priors from cell-sorted bisulfite sequencing data.Genome biology · 2024Article
- A functional variant rs912304 for late-onset T1D risk contributes to islet dysfunction by regulating proinflammatory cytokine-responsive gene STXBP6 expression.BMC medicine · 2024Article
- Public Attitudes, Interests, and Concerns Regarding Polygenic Embryo Screening.JAMA network open · 2024Article
- Deep learning captures the effect of epistasis in multifactorial diseases.Frontiers in medicine · 2024Article
- Nutrigenomics and redox regulation: Concepts relating to the Special Issue on nutrigenomics.Redox biology · 2023Review
- The beta cell-immune cell interface in type 1 diabetes (T1D).Molecular metabolism · 2023Review
- Pediatric Type 1 Diabetes: Mechanisms and Impact of Technologies on Comorbidities and Life Expectancy.International journal of molecular sciences · 2023Review
- Biobank-scale methods and projections for sparse polygenic prediction from machine learning.Scientific reports · 2023Article
- Type 1Micromachines · 2023Review
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
Genetic studies have identified >60 loci associated with the risk of developing type 1 diabetes (T1D). The vast majority of these are identified by genome-wide association studies (GWAS) using large case-control cohorts of European ancestry. More than 80% of the heritability of T1D can be explained by GWAS data in this population group. However, with few exceptions, their individual contribution to T1D risk is low and understanding their function in disease biology remains a huge challenge. GWAS on its own does not inform us in detail on disease mechanisms, but the combination of GWAS data with other omics-data is beginning to advance our understanding of T1D etiology and pathogenesis. Current knowledge supports the notion that genetic variation in both pancreatic β cells and in immune cells is central in mediating T1D risk. Advances, perspectives and limitations of GWAS are discussed in this review.
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.