Evidence map›Paper›PMID 39762845›Full record

ArticleJournal of translational medicine2025

Association of genetically proxied cancer-targeted drugs with cardiovascular diseases through Mendelian randomization analysis.

Chuchun Fang, Xuewei Liu, Chen Yu, Songlin Li, Xueying Liu, Shifeng Qiu, Hongbin Liang, Caiwen Ou, Jiancheng Xiu

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Advances in Molecular and Translational Medicine: 2nd Edition.International journal of molecular sciences · 2025
    Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Chuchun Fang *Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Xuewei Liu *The First School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, China.
Chen YuDepartment of Cardiology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.
Songlin LiDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Xueying LiuDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Shifeng QiuDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Hongbin LiangDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Caiwen OuThe First School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, China. oucaiwen@smu.edu.cn.
Jiancheng XiuDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. xiujch@163.com.ORCID 0000-0001-5433-2586

Funding

Clinical Research Program of Nanfang Hospital, Southern Medical University 2021CR007Guangzhou Key Research and Development Program 202206080014National Key R&D Program of China 2018YFC1312803
6 · The paper itself

Abstract

backgroundCancer-targeted therapies are progressively pivotal in oncological care. Observational studies underscore the emergence of cancer therapy-related cardiovascular toxicity (CTR-CVT), impacting patient outcomes. We aimed to investigate the causal relationship between different types of cancer-targeted therapies and cardiovascular disease (CVD) outcomes through a two-sample Mendelian randomization (MR) study.

methodsThis genome-wide association study was conducted using a two-sample Mendelian randomization framework. Genetic instruments for drug target gene expression were extracted from the eQTLGen consortium (31684 individuals, 37 cohorts). Genome-wide association study (GWAS) summary statistics for 19 cardiovascular diseases were derived from the FinnGen database. Primary analysis was carried out using the summary-data-based MR (SMR) method, with sensitivity analysis for validation. Colocalization analysis identifies shared causal variants between exposure eQTLs and CVD-associated single-nucleotide polymorphisms (SNPs).

resultsAmong the 39 drug target genes, 8 were identified with detectable cis-eQTLs and were subsequently validated through positive control analysis for further investigation. In the SMR and sensitivity analyses, genetically proxied VEGFA inhibition showed significantly strong association with stroke (odds ratio [OR] = 1.17, 95% confidence interval [CI] = 1.09-1.26, p = 1.33 × 10

conclusionsThis genetic association study revealed evidence supporting the genetic association between the use of VEGFA inhibitors and increased stroke risk, highlighting the need for enhanced pharmacovigilance. These findings underscore the delicate balance between cardiovascular toxicity risk and the benefits of cancer-targeted therapy.

Indexed as

Antineoplastic AgentsCardiovascular DiseasesGenome-Wide Association StudyMendelian Randomization AnalysisPolymorphism, Single NucleotideHumansMolecular Targeted TherapyNeoplasmsQuantitative Trait LociVascular Endothelial Growth Factor AAntineoplastic AgentsVascular Endothelial Growth Factor ACancer-targeted therapyCardiovascular diseaseseQTLMendelian randomization

Identifiers

PMID39762845
PMCPMC11702226

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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.