SynthesisBMC gastroenterology2024
Human blood metabolites and gastric cancer: a Mendelian randomization analysis.
Synthesis in BMC gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- Assessing the impact of metabolomic markers on gastric cancer risk: a two-sample Mendelian randomization study.Korean journal of family medicine · 2026Article
- Article
- A multicenter retrospective study on the risk factors of stricture formation after moderate circumferential defect resection in esophageal endoscopic submucosal dissection.Surgical endoscopy · 2026Observational
- Exploring the causal relationship between matrix metalloproteinases and adrenocortical carcinoma: A Mendelian randomization study.Medicine · 2025Article
- METTL3-Mediated m6A Modification of COL5A2 Inhibits Ferroptosis Through an IGF2BP3-dependent Mechanism in Gastric Cancer.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
backgroundGastric cancer (GC) remains one of the predominant malignant tumors within the digestive tract, yet its underlying biological mechanisms remain elusive. The primary objective of this study is to delineate the causal relationship between circulating metabolites and GC.
methodThe primary Mendelian randomization (MR) analysis was based on three large GWAS datasets. While the inverse variance weighted served as the primary analysis technique for investigating causal relationships, additional sensitivity analyses were facilitated through methods such as MR-PRESSO, the weighted median, and MR-Egger. Subsequently, replication, meta-analysis, and multivariable MR were executed using another GC GWAS.
resultsThe results of this study indicated significant associations between three metabolites 3-methyl-2-oxovalerate (OR 5.8, 95%CI: 1.53-22.05, p = 0.0099), piperine (OR 2.05, 95%CI: 1.13-3.7, p = 0.0175), Phe-Phe dipeptide (OR 0.16, 95%CI: 0.03-0.93, p = 0.0409) and GC.
conclusionThe present study provides evidence supporting a causal relationship between these three circulating metabolites and GC risk. Elevated levels of 3-methyl-2-oxovalerate and piperine may increase the risk of GC, while Phe-Phe dipeptide may have a protective effect. By integrating genomics and metabolomics, we offer a novel perspective on the biological mechanisms underlying GC. Such insights have the potential to enhance strategies for the screening, prevention, and treatment of GC.
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