rs11057270 - SBNO1
Magnitude 2.2 · 2 studies on file
Reported associations
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A multi-ancestry genetic study of pain intensity in 598,339 veterans. - Nature medicine (2024) · Toikumo S, Vickers-Smith R, Jinwala Z, Xu H, Saini D, Hartwell EE, Pavicic M, Sullivan KA, Xu K, Jacobson DA, Gelernter J, Rentsch CT, Stahl E, Cheatle M, Zhou H, Waxman SG, Justice AC, Kember RL, Kranzler HR · PubMed 38429522
Chronic pain is a common problem, with more than one-fifth of adult Americans reporting pain daily or on most days. It adversely affects the quality of life and imposes substantial personal and economic costs. Efforts to treat chronic pain using opioids had a central role in precipitating the opioid crisis. Despite an estimated heritability of 25-50%, the genetic architecture of chronic pain is not well-characterized, in part because studies have largely been limited to samples of European ancestry. To help address this knowledge gap, we conducted a cross-ancestry meta-analysis of pain intensity in 598,339 participants in the Million Veteran Program, which identified 126 independent genetic loci, 69 of which are new. Pain intensity was genetically correlated with other pain phenotypes, lev
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Genomic and transcriptomic association studies identify 16 novel susceptibility loci for venous thromboembolism. - Blood (2020) · Lindström S, Wang L, Smith EN, Gordon W, van Hylckama Vlieg A, de Andrade M, Brody JA, Pattee JW, Haessler J, Brumpton BM, Chasman DI, Suchon P, Chen MH, Turman C, Germain M, Wiggins KL, MacDonald J, Braekkan SK, Armasu SM, Pankratz N, Jackson RD, Nielsen JB, Giulianini F, Puurunen MK, Ibrahim M, Heckbert SR, Damrauer SM, Natarajan P, Klarin D, de Vries PS, Sabater-Lleal M, Huffman JE, Bammler TK, Frazer KA, McCauley BM, Taylor K, Pankow JS, Reiner AP, Gabrielsen ME, Deleuze JF, O'Donnell CJ, Kim J, McKnight B, Kraft P, Hansen JB, Rosendaal FR, Heit JA, Psaty BM, Tang W, Kooperberg C, Hveem K, Ridker PM, Morange PE, Johnson AD, Kabrhel C, Trégouët DA, Smith NL · PubMed 31420334
Venous thromboembolism (VTE) is a significant contributor to morbidity and mortality. To advance our understanding of the biology contributing to VTE, we conducted a genome-wide association study (GWAS) of VTE and a transcriptome-wide association study (TWAS) based on imputed gene expression from whole blood and liver. We meta-analyzed GWAS data from 18 studies for 30 234 VTE cases and 172 122 controls and assessed the association between 12 923 718 genetic variants and VTE. We generated variant prediction scores of gene expression from whole blood and liver tissue and assessed them for association with VTE. Mendelian randomization analyses were conducted for traits genetically associated with novel VTE loci. We identified 34 independent genetic signals for VTE risk from GWAS meta-
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