ArticleNature communications2026
Multitrait GWAS and functional validation reveal genetic loci for gastric cancer.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Association ofFrontiers in cellular and infection microbiology · 2026Article
- VEZT promotes pancreatic cancer progression by stabilizing SLC25A24 and preserving mitochondrial function.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Gastric cancer is a leading cause of cancer-related death, particularly in East Asia, yet its genetic basis remains incompletely understood. Using genome-wide association study data from BioBank Japan, we show that gastric cancer shares significant genetic associations with 25 other phenotypes, most notably cardiovascular conditions such as angina pectoris and myocardial infarction. Mendelian randomization supports a causal role of these traits in gastric cancer risk. Multitrait analysis of GWAS reveals a novel pleiotropic locus at 12q22 (rs12814712) that is shared between gastric cancer and cardiovascular traits. Functional experiments demonstrate that the risk allele at this locus reduces transcriptional activity and downregulates the expression of nearby genes, particularly VEZT. In gastric cancer cells, overexpression of VEZT and NR2C1 suppress proliferation and migration, whereas their knockdown promotes malignancy. Our analysis identifies rs12814712 as a novel susceptibility locus for gastric cancer and underscores its regulatory role in disease-related gene networks.
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