ArticleBlood advances2024
Genetic variants in canonical Wnt signaling pathway associated with pediatric immune thrombocytopenia.
Article in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Increased percentages of circulating T follicular helper cells associate with disease subtype and activity in pediatric immune cytopenias.Haematologica · 2026Article
- DNA Methylation Variation in Blood Cells may Impact Platelet Function.TH open : companion journal to thrombosis and haemostasis · 2026Article
- Ubiquitous dysregulation of the Wnt pathway in immune thrombocytopenia genetic susceptibility.Blood vessels, thrombosis & hemostasis · 2025Article
- Tapering and Sustained Remission of Thrombopoietin Receptor Agonists (TPO-RAs): Is it Time for Paediatric ITP?Advances in therapy · 2024Review
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Authors and funding
18 authors.
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Abstract
abstractThrough the use of genetic sequencing, molecular variants driving autoimmunity are increasingly identified in patients with chronic and refractory immune cytopenias. With the goal of discovering genetic variants that predispose to pediatric immune thrombocytopenia (ITP) or increase risk for chronic disease, we conducted a genome-wide association study in a large multi-institutional cohort of pediatric patients with ITP. A total of 591 patients were genotyped using an Illumina Global Screening Array BeadChip. Six variants met genome-wide significance in comparison between children with ITP and a cohort of healthy children. One variant in NAV2 was inversely associated with ITP (adjusted odds ratio [aOR], 0.52; P = 3.2 × 10-11). Two other variants in close proximity to NKD1 were also inversely associated with ITP (aOR, 0.43; P = 8.86 × 10-15; aOR, 0.48; P = 1.84 × 10-16). These genes have been linked to the canonical Wnt signaling pathway. No variants met genome-wide significance in comparison of those with ITP that self-resolved in <1 year versus those who developed chronic ITP. This study identifies genetic variants that may contribute to ITP risk and raises a novel pathway with a potential role in ITP pathogenesis.
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