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  5. Genomic and transcriptomic association studies identify 16 novel susceptibility loci for venous thromboembolism

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Article
English
2019

Genomic and transcriptomic association studies identify 16 novel susceptibility loci for venous thromboembolism

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English
2019
Blood
Vol 134 (19)
DOI: 10.1182/blood.2019000435

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Frits R. Rosendaal
Frits R. Rosendaal

Leiden University

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Sara Lindstrӧm
Lu Wang
Erin N. Smith
+54 more

Abstract

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-analysis, of which 14 are newly reported associations. This included 11 newly associated genetic loci (C1orf198, PLEK, OSMR-AS1, NUGGC/SCARA5, GRK5, MPHOSPH9, ARID4A, PLCG2, SMG6, EIF5A, and STX10) of which 6 replicated, and 3 new independent signals in 3 known genes. Further, TWAS identified 5 additional genetic loci with imputed gene expression levels differing between cases and controls in whole blood (SH2B3, SPSB1, RP11-747H7.3, RP4-737E23.2) and in liver (ERAP1). At some GWAS loci, we found suggestive evidence that the VTE association signal for novel and previously known regions colocalized with expression quantitative trait locus signals. Mendelian randomization analyses suggested that blood traits may contribute to the underlying risk of VTE. To conclude, we identified 16 novel susceptibility loci for VTE; for some loci, the association signals are likely mediated through gene expression of nearby genes.

How to cite this publication

Sara Lindstrӧm, Lu Wang, Erin N. Smith, William Gordon, Astrid van Hylckama Vlieg, Mariza de Andrade, Jennifer A. Brody, Jack Pattee, Jeffrey Haessler, Ben Brumpton, Daniel I. Chasman, Pierre Suchon, Ming‐Huei Chen, Constance Turman, Marine Germain, Kerri L. Wiggins, James W. MacDonald, Sigrid K. Brækkan, Sebastian M. Armasu, Nathan Pankratz, Rebecca D. Jackson, Jonas B. Nielsen, Franco Giulianini, Marja Puurunen, Manal Ibrahim, Susan R. Heckbert, Scott M. Damrauer, Pradeep Natarajan, Derek Klarin, Paul S. de Vries, Maria Sabater‐Lleal, Jennifer E. Huffman, Theo K. Bammler, Kelly A. Frazer, Bryan M. McCauley, Kent D. Taylor, James S. Pankow, Alexander P. Reiner, Maiken E. Gabrielsen, Jean‐François Deleuze, Christopher J. O’Donnell, Jihye Kim, Barbara McKnight, Peter Kraft, J.-B. Hansen, Frits R. Rosendaal, John A. Heit, Bruce M. Psaty, Weihong Tang, Charles Kooperberg, Kristian Hveem, Paul M. Ridker, Pierre‐Emmanuel Morange, Andrew D. Johnson, Christopher Kabrhel, David‐Alexandre Trégouët, Nicholas L. Smith (2019). Genomic and transcriptomic association studies identify 16 novel susceptibility loci for venous thromboembolism. Blood, 134(19), pp. 1645-1657, DOI: 10.1182/blood.2019000435.

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Publication Details

Type

Article

Year

2019

Authors

57

Datasets

0

Total Files

0

Language

English

Journal

Blood

DOI

10.1182/blood.2019000435

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