ArticleAmerican journal of cancer research2025
Causal impact of genetically determined metabolites on kidney cancer and its subtypes: an integrated mendelian randomization and metabolomic study.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Blood metabolomic signatures linking air pollution to lung cancer in the Cancer Prevention Studies.Nature communications · 2026Article
- Article
- Causal relationships between neuroimaging phenotypes and the risk of early and late-onset alzheimer's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Causal Relationships Between Plasma Metabolites and Risk of Dermatomyositis.Clinical, cosmetic and investigational dermatology · 2025Article
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11 authors.
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Abstract
Metabolic dysregulation is a hallmark of kidney cancer, yet the causal roles of specific metabolites in its major subtypes remain unclear. This study aimed to elucidate the causal relationships between circulating metabolites and the three primary subtypes of kidney cancer - clear cell renal cell carcinoma (ccRCC), papillary RCC (pRCC), and chromophobe RCC (chRCC) - and to identify potential diagnostic and therapeutic targets. A total of 1,400 circulating metabolites and metabolic ratios were evaluated as exposures, with kidney cancer outcomes derived from the FinnGen database. Genetic instruments were selected from genome-wide association studies (GWAS) and harmonized with outcome data. Mendelian randomization (MR) analyses were conducted using the inverse-variance weighted (IVW) method as the primary approach, supported by multiple sensitivity analyses, including Cochran's Q test, MR-Egger regression, leave-one-out analysis, and MR-PRESSO. To correct for multiple testing, metabolites were stratified into absolute levels and metabolic ratios, and the Benjamini-Hochberg false discovery rate (FDR) procedure was applied separately within each category. Causally associated metabolites were further analyzed via KEGG pathway enrichment. For clinical validation, untargeted metabolomic profiling was performed on paired tumors and adjacent normal tissues from 48 patients with ccRCC. In total, 85 metabolites were found to be causally associated with kidney cancer, including 57 for ccRCC, 71 for pRCC, and 51 for chRCC. After FDR correction, three metabolites remained statistically significant: carnitine (overall RCC: OR = 1.25, P
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