ArticleHuman molecular genetics2010
Genome-wide association study identifies a susceptibility locus for biliary atresia on 10q24.2.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 80 papers, 4 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
80 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- The correlation between rs2501577 gene polymorphism and biliary atresia: a systematic review and meta-analysis.Pediatric surgery international · 2023Pooled it
- Trans-ethnic meta-analysis of genome-wide association studies for Hirschsprung disease.Human molecular genetics · 2016Pooled it
- Genetic variant in MTRR, but not MTR, is associated with risk of congenital heart disease: an integrated meta-analysis.PloS one · 2014Pooled it
- The SNP rs402710 in 5p15.33 is associated with lung cancer risk: a replication study in Chinese population and a meta-analysis.PloS one · 2013Pooled it
- Another ciliopathy? Uncovering the ciliary basis of biliary atresia.Hepatology international · 2026Review
- HCMV infection disrupts barrier functions and promotes epithelial-mesenchymal transition in a cholangiocyte organoid model.Nature communications · 2026Article
- Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026Review
- Amyloid precursor protein as a fibrosis marker in infants with biliary atresia.Pediatric research · 2025Article
- Genetic background and biliary atresia.World journal of pediatric surgery · 2025Review
- Multiple susceptibility enhancer variants increasingFrontiers in genetics · 2025Article
- Organoids in biliary atresia.World journal of pediatric surgery · 2025Review
- Immunology of Biliary Atresia.Seminars in pediatric surgery · 2024Review
- Mechanism of biliary atresia caused by T follicular helper cells-induced immune injury.BMC pediatrics · 2024Article
- Biliary atresia.Nature reviews. Disease primers · 2024Review
- Article
- Diseases of bile duct in children.World journal of gastroenterology · 2024Review
- Biliary atresia: the role of gut microbiome, and microbial metabolites.Frontiers in cellular and infection microbiology · 2024Review
- Biliary atresia is associated with polygenic susceptibility in ciliogenesis and planar polarity effector genes.Journal of hepatology · 2023Article
- A fetal wound healing program after intrauterine bile duct injury may contribute to biliary atresia.Journal of hepatology · 2023Article
- Contribution ofInternational journal of molecular sciences · 2023Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedChen, Guo [corrected to Cheng, Guo]
Authors and funding
26 authors.
Funding
Abstract
Biliary atresia (BA) is characterized by the progressive fibrosclerosing obliteration of the extrahepatic biliary system during the first few weeks of life. Despite early diagnosis and prompt surgical intervention, the disease progresses to cirrhosis in many patients. The current theory for the pathogenesis of BA proposes that during the perinatal period, a still unknown exogenous factor meets the innate immune system of a genetically predisposed individual and induces an uncontrollable and potentially self-limiting immune response, which becomes manifest in liver fibrosis and atresia of the extrahepatic bile ducts. Genetic factors that could account for the disease, let alone for its high incidence in Chinese, are to be investigated. To identify BA susceptibility loci, we carried out a genome-wide association study (GWAS) using the Affymetrix 5.0 and 500 K marker sets. We genotyped nearly 500 000 single-nucleotide polymorphisms (SNPs) in 200 Chinese BA patients and 481 ethnically matched control subjects. The 10 most BA-associated SNPs from the GWAS were genotyped in an independent set of 124 BA and 90 control subjects. The strongest overall association was found for rs17095355 on 10q24, downstream XPNPEP1, a gene involved in the metabolism of inflammatory mediators. Allelic chi-square test P-value for the meta-analysis of the GWAS and replication results was 6.94 x 10(-9). The identification of putative BA susceptibility loci not only opens new fields of investigation into the mechanisms underlying BA but may also provide new clues for the development of preventive and curative strategies.
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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.