ArticleCancer medicine2026
Shared Genetics of Kidney Function Traits and Bladder Cancer: A Genome-Wide Cross-Trait Analysis.
Article in Cancer 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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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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Abstract
backgroundClinical and epidemiological evidence has suggested a potential association between kidney dysfunction and bladder cancer (BC). One hypothesis for this comorbidity is the presence of a common genetic etiology. However, little is known about the shared genetics and causality of this association. Thus, we aimed to investigate shared genetic architecture and the causal link between kidney dysfunction and bladder cancer.
methodsLeveraging summary statistics from large-scale genome-wide association studies (GWASs) conducted on European-ancestry populations on eGFRcrea (N = 1,004,040), eGFRcys (N = 460,826), BUN (N = 852,678), UACR (N = 288,649), urate (N = 547,361) and BC (N
resultsWe found positive correlations between both BUN and urate and BC at the genome-wide level. A total of 157 significant overlapping genetic loci (range 7 to 72) were identified across five kidney function traits and BC. Among them, PSCA was prioritized as the strongest shared gene with support from MTAG, colocalization, and TWAS, whereas ZFHX3, TTC33, and ATP2A1 were considered candidates supported only by MTAG and TWAS. MR provided the most consistent support for a potential positive causal effect of BUN on BC, limited support for UACR, and exploratory evidence for urate.
conclusionsOur cross-trait analysis demonstrated a shared genetic basis underlying kidney function and BC, providing novel insights into the biological functions and molecular mechanisms underlying these complex traits.
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