ArticleDiscover oncology2025
Causal relationships between gut microbiota and urothelial carcinoma mediated by inflammatory cytokines and blood cell traits identified through Mendelian randomization analysis.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- The Urinary Microbiota and the Gut-Bladder Axis in Bladder Cancer.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of gut microbiota in tumorigenesis has gained significant attention in recent years. This study aimed to investigate the causal relationship between gut microbiota and three types of urothelial carcinoma (renal pelvic cancer [RPC], urothelial carcinoma [UC], and bladder cancer [BC]), and to explore potential underlying mechanisms.
methodsTwo-sample Mendelian randomization (MR) analysis was conducted using GWAS data to identify gut microbiota-associated SNPs and evaluate their causal effects on the three cancers. Sensitivity analysis, reverse MR analysis, and mediation MR analysis were further performed to examine the roles of gut microbiota, inflammatory factors, and blood cells in cancer development.
resultsMediation MR analysis revealed that Bacillaceae A significantly increased RPC risk by elevating IL-6 levels; CAG-452 promoted RPC by reducing SCF levels; and Succiniclasticum increased RPC risk by lowering platelet reactivity (WNR_Isobutyric_A._PLT_SD_SFL) (mediation effect ratio: 34.01%). Conversely, UCG-010 sp003150215 reduced RPC risk by increasing platelet reactivity (mediation effect ratio: 30.51%). For UC, Syntrophorhabdaceae promoted UC development by lowering IL-4 levels (mediation effect ratio: 22.46%), while Prevotella sp002437285 increased UC risk through modulation of WNR_Captopril_PLT_SD_SSC (mediation effect ratio: 30.58%).
conclusionThis research identifies causal relationships between gut microbiota and RPC, UC, and BC, and elucidates their impact on cancer development through mediation by inflammatory factors and blood cells. These findings provide new perspectives and a foundation for the potential application of gut microbiota in cancer prevention and treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.