ArticleTranslational oncology2025
Genetic polymorphisms of TRPA1 does affect risk of cisplatin induced nephrotoxicity in Chinese population.
Article in Translational oncology, 2025. 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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Abstract
introductionIrreversible acute kidney injury (AKI) caused by cisplatin limits its clinical use, and transient receptor potential anchor protein 1 (TRPA1) regulates cisplatin-induced nephrotoxicity (CIN) through NF-κB signaling pathway-mediated inflammation. Single nucleotide polymorphisms in TRPA1 and NF-κB1 genes may be associated with individual heterogeneous nephrotoxicity. MATERIALS AND
methodsIn this paper, we investigated the association of 17 single nucleotide polymorphisms (SNP) of TRPA1 and NF-κB1 genes with cisplatin-induced acute nephrotoxicity. Nephrotoxicity and its severity were assessed according to the Common Terminology Criteria for Adverse Events (CTCAE 5.0). SNPs were measured by 48-Plex SNPscan® high-throughput SNP typing echnology in DNA isolated from peripheral blood of 589 Chinese Han lung cancer patients (241 with CIN and 348 without CIN) treated with cisplatin regimen.
resultsTRAP1 gene rs920829 locus T allele carriers had a reduced risk of nephrotoxicity relative to C allele carriers (OR 0.684, 95 % CI 0.524-0.894, p = 0.003), and their additive and dominant models showed similar trends as well. However, the SNPs of NF-κB1 were not observed to be correlated with nephrotoxicity.
conclusionSNPs of TRPA1 have the potential as biomarkers for predicting cisplatin nephrotoxicity.
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