Evidence map›Paper›PMID 41529867›Full record

ArticleKorean journal of family medicine2026

Assessing the impact of metabolomic markers on gastric cancer risk: a two-sample Mendelian randomization study.

Tung Hoang, Van Mai Truong, Tho Thi Anh Tran

Abstract read
In one paragraph

Article in Korean journal of family medicine, 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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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

3 authors.

Tung HoangFaculty of Pharmacy, University of Health Sciences, Vietnam National University, Ho Chi Minh City, Vietnam. htung@uhsvnu.edu.vn.
Van Mai TruongFaculty of Odonto-Stomatology, University of Health Sciences, Vietnam National University, Ho Chi Minh City, Vietnam.
Tho Thi Anh TranDepartment of Gastroenterology and Hepatology, Nghe An Oncology Hospital, Nghe An, Vietnam.

Funding

Vietnam National University Ho Chi Minh City C2024-44-34Vingroup Innovation Foundation VINIF.2023.TS.119
6 · The paper itself

Abstract

Background: This study aimed to examine the relationship between genetically predicted metabolite levels and gastric cancer (GC) risk using Mendelian randomization (MR), and to identify the metabolic pathways potentially involved. Methods: We selected genetic instruments for metabolites from 64 genome-wide association studies covering 362,750 participants. A two-sample MR design was applied to evaluate the associations with GC using summary-level data from a combined analysis of the UK Biobank and FinnGen. The primary analysis relied on the inverse-variance weighted method, while the median-weighted and MR-Egger methods were used to account for potential violations of instrumental variable assumptions and provide the estimate even when a subset of instruments was invalid. The MR-Egger intercept test was performed to detect directional pleiotropy. Metabolites showing significant associations with GC were further examined using pathway enrichment analysis to identify relevant metabolic and lipid processes. Results: MR analyses identified 25 and 17 metabolites that were positively and inversely associated with GC risk, respectively. Notably, hexanoylcarnitine and cis-4-decenoylcarnitine were strongly associated with increased risk, whereas pregnanediol disulfate, acetylcarnitine, prolyl-hydroxyproline, and X-18914 were associated with reduced risk, with no evidence of heterogeneity or directional pleiotropy. Enrichment analyses highlighted key metabolic pathways, including cysteine and methionine catabolism, beta-oxidation of pristanoyl-CoA (coenzyme A), oxidation of branched-chain fatty acids, and peroxisomal lipid metabolism. Conclusion: This study identified a set of genetically predicted metabolites associated with GC risk, highlighting the potential utility of metabolite panels and lipid-based biomarkers for risk stratification and early detection. However, further standardization and extensive validation are necessary prior to clinical application.

Indexed as

Gastric CancerMendelian RandomizationMetabolitesPathways

Identifiers

PMID41529867
PMCPMC13424861

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