SynthesisJournal of thrombosis and thrombolysis2024
No evidence for a genetic causal effect of breast cancer on venous thromboembolism: a mendelian randomization study.
Synthesis in Journal of thrombosis and thrombolysis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 1 citations in OpenAlex.
- Thrombopoiesis meets tumorigenesis: unlocking the diagnostic and prognostic potential of platelet indices in breast cancer- a narrative review.Annals of medicine and surgery (2012) · 2026Review
- Thromboinflammatory pathways in breast cancer: clinical and molecular insights into venous thromboembolism risk - a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Causal relationships between risk of venous thromboembolism and 18 cancers: a bidirectional Mendelian randomization analysis.International journal of epidemiology · 2024Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Active cancer is known to contribute to venous thromboembolism (VTE), but the cause-and-effect association of breast cancer on VTE is not yet clear. In order to investigate the possible causal relationships, we used a Mendelian randomization analysis. Data for generically predicted breast cancer were identified based on the BCAC consortium. A meta-analysis of genome-wide association study (GWAS) comprising 1,500,861 participants for VTE as well as data from the FinnGen study for VTE, DVT and PE was used for the causal-effect estimation. Our primary method was inverse-variance weighted (IVW), and our supplementary methods included weighted median and MR-Egger. We also carried out sensitivity analysis for the study. No evidence of causal-effect was detected of overall breast cancer on VTE in both the GWAS meta-analysis (OR=1.01, 95%CI:0.98-1.04, p = 0.495) and the FinnGen consortium (OR=1.00,95%CI:0.96-1.04, p = 0.945). In addition, the presence of ER-positive or ER-negative disease did not significantly influence the incidence of VTE and its subtypes. In conclusion, no genetic cause-and-effect of breast cancer on VTE risk was detected in the large MR analysis.
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