ArticleHuman molecular genetics2024
A multi-ancestry genome-wide association study in type 1 diabetes.
Article in Human molecular genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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
26 citing papers in PubMed.
- Development and application of type 1 diabetes polygenic scores across diverse populations.Diabetologia · 2026Review
- Genetic basis of Asian diabetes.Journal of diabetes investigation · 2026Review
- Article
- Development and validation of a trans-ancestry polygenic risk score for type 1 diabetes.Diabetologia · 2026Article
- Toward Personalized Medicine in Type 1 Diabetes: Understanding How Patient Heterogeneity Influences Therapeutic Efficacy.Diabetes, obesity & metabolism · 2026Review
- ALGI: Sparse Convolutional Denoising Autoencoder Utilizing Local Genomic Information for Genotype Imputation.Animals : an open access journal from MDPI · 2026Article
- Interpreting artificial neural networks to detect genome-wide association signals for complex traits.NAR genomics and bioinformatics · 2026Article
- Integrated histopathology of the human pancreas throughout stages of type 1 diabetes progression.Nature communications · 2026Article
- Advances in haplotype phasing and genotype imputation.Nature reviews. Genetics · 2026Review
- HLA-focused type 1 diabetes genetic risk prediction in populations of diverse ancestry.Diabetologia · 2026Article
- Article
- Immune cell-based transcriptomic Mendelian randomization and colocalization study on type 1 diabetes.BMC medicine · 2025Article
- Bridging pharmacovigilance and genetic insight: investigating drugs and indications for breast cancer risk in women with autoimmune diseases.Journal of translational medicine · 2025Article
- Preclinical Diagnosis of Type 1 Diabetes: Reality or Utopia.Biomedicines · 2025Review
- Biallelic SH2B3 germline variants are associated with a neonatal myeloproliferative disease and multisystemic involvement.European journal of human genetics : EJHG · 2025Article
- Methods for multiancestry genome-wide association study meta-analysis.Annals of human genetics · 2025Review
- Metabolome-wide Mendelian randomisation reveals causal links between circulating metabolites and type 1 diabetes.EBioMedicine · 2025Article
- Type 1 Diabetes Polygenic Scores Improve Diagnostic Accuracy in Pediatric Diabetes Care.Hormone research in paediatrics · 2025Article
- Type 1 Diabetes Genetics Consortium.The Journal of clinical endocrinology and metabolism · 2025Review
- Integrated histopathology of the human pancreas throughout stages of type 1 diabetes progression.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Type 1 diabetes (T1D) is an autoimmune disease caused by destruction of the pancreatic β-cells. Genome-wide association (GWAS) and fine mapping studies have been conducted mainly in European ancestry (EUR) populations. We performed a multi-ancestry GWAS to identify SNPs and HLA alleles associated with T1D risk and age at onset. EUR families (N = 3223), and unrelated individuals of African (AFR, N = 891) and admixed (Hispanic/Latino) ancestry (AMR, N = 308) were genotyped using the Illumina HumanCoreExome BeadArray, with imputation to the TOPMed reference panel. The Multi-Ethnic HLA reference panel was utilized to impute HLA alleles and amino acid residues. Logistic mixed models (T1D risk) and frailty models (age at onset) were used for analysis. In GWAS meta-analysis, seven loci were associated with T1D risk at genome-wide significance: PTPN22, HLA-DQA1, IL2RA, RNLS, INS, IKZF4-RPS26-ERBB3, and SH2B3, with four associated with T1D age at onset (PTPN22, HLA-DQB1, INS, and ERBB3). AFR and AMR meta-analysis revealed NRP1 as associated with T1D risk and age at onset, although NRP1 variants were not associated in EUR ancestry. In contrast, the PTPN22 variant was significantly associated with risk only in EUR ancestry. HLA alleles and haplotypes most significantly associated with T1D risk in AFR and AMR ancestry differed from that seen in EUR ancestry; in addition, the HLA-DRB1*08:02-DQA1*04:01-DQB1*04:02 haplotype was 'protective' in AMR while HLA-DRB1*08:01-DQA1*04:01-DQB1*04:02 haplotype was 'risk' in EUR ancestry, differing only at HLA-DRB1*08. These results suggest that much larger sample sizes in non-EUR populations are required to capture novel loci associated with T1D risk.
Indexed as
Identifiers
What Socratic 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 Socratic graph.