Evidence map›Paper›PMID 41572223›Full record

ArticleBMC cancer2026

The causal association between systolic blood pressure and breast cancer: a two sample Mendelian randomization study.

Zainab Awada, Nabila Kazmi, Hannah J Jones, Sarah J Lewis

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Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Zainab AwadaDepartment of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
Nabila KazmiDepartment of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
Hannah J JonesDepartment of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
Sarah J LewisDepartment of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK. s.j.lewis@bristol.ac.uk.

Funding

Cancer Research UK C18281/A29019
6 · The paper itself

Abstract

backgroundBreast cancer (BC) is the leading cause of cancer incidence worldwide. Observational studies have suggested that hypertension may be a risk factor for BC. We tested whether systolic blood pressure (SBP) may influence BC and BC subtypes using a Mendelian randomisation (MR) approach.

methodsWe used 334 genetic variants associated with SBP as an instrumental variable. Effect estimates were obtained from the UK biobank (n = 469,767; SNP-exposure estimates) and the Breast Cancer Association Consortium (BCAC) (122,977 cases and 105,974 controls; SNP-outcome estimates). We assessed BC sub-types including: Triple-negative breast cancer (TNBC), human epidermal growth factor receptor 2 (HER2) positive, Luminal-A, Luminal-B, and Luminal-B HER2 negative. We used inverse variance weighted (IVW) as our primary analysis but conducted a series of sensitivity analyses to test the robustness of our findings. We created a restricted subset of SNPs by excluding SNPs associated with body mass index (BMI) and those with small effect sizes on the exposure, we also conducted multivariable mendelian randomisation analysis to control for adiposity as a potential confounder.

resultsFor each 1 mm/Hg increase in SBP the estimated effect was OR 1.00 (0.93, 1.08) for overall BC, analyses of BC sub-types results also did not support a causal effect of SBP. Similarly, results of our sensitivity analyses did not show strong evidence of an association.

conclusionThe results of our study did not support a causal effect of SBP on overall BC or its sub-types.

Indexed as

Blood PressureBreast NeoplasmsHypertensionFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMendelian Randomization AnalysisMiddle AgedPolymorphism, Single NucleotideRisk FactorsBreast cancerCancer epidemiologySystolic blood pressureTwo-sample Mendelian randomisation

Identifiers

PMID41572223
PMCPMC12914972

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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.