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Genetic polymorphisms of TRPA1 does affect risk of cisplatin induced nephrotoxicity in Chinese population
Cong Wang1, Guifei Deng1, Siyu Niu2
1Department of Nephrology, Yibin Traditional Chinese Medicine Hospital. Yibin, Sichuan 644600, China.
Introduction:
Irreversible 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 Methods:
In 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.
Results:
TRAP1 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.
Conclusion:
SNPs of TRPA1 have the potential as biomarkers for predicting cisplatin nephrotoxicity.
Insights
Single nucleotide polymorphisms (SNPs) in the TRPA1 gene are associated with reduced risk of cisplatin-induced nephrotoxicity. These TRPA1 SNPs may serve as biomarkers for predicting kidney damage in patients receiving cisplatin treatment.
Area of Science:
- Pharmacogenomics
- Nephrology
- Oncology
Background:
- Cisplatin chemotherapy can cause irreversible acute kidney injury (AKI), limiting its clinical application.
- Transient receptor potential anchor protein 1 (TRPA1) plays a role in cisplatin-induced nephrotoxicity (CIN) via NF-κB signaling and inflammation.
- Genetic variations, specifically single nucleotide polymorphisms (SNPs) in TRPA1 and NF-κB1 genes, may influence individual susceptibility to kidney damage.
Purpose of the Study:
- To investigate the association between specific SNPs in the TRPA1 and NF-κB1 genes and the occurrence of cisplatin-induced acute nephrotoxicity.
- To identify potential genetic biomarkers for predicting kidney toxicity in patients undergoing cisplatin-based chemotherapy.
Main Methods:
- Genotyping of 17 SNPs in TRPA1 and NF-κB1 genes using high-throughput SNPscan technology.
- Analysis of DNA from 589 Chinese Han lung cancer patients treated with cisplatin.
- Assessment of nephrotoxicity severity based on the Common Terminology Criteria for Adverse Events (CTCAE 5.0).
Main Results:
- Carriers of the T allele at the TRPA1 gene rs920829 locus showed a significantly reduced risk of nephrotoxicity compared to C allele carriers (OR 0.684, p=0.003).
- Additive and dominant genetic models for TRPA1 rs920829 also indicated a protective effect.
- No significant correlation was found between the studied NF-κB1 gene SNPs and cisplatin-induced nephrotoxicity.
Conclusions:
- SNPs within the TRPA1 gene, particularly at the rs920829 locus, demonstrate potential as predictive biomarkers for cisplatin-induced nephrotoxicity.
- Further validation of TRPA1 SNPs could aid in personalized treatment strategies to mitigate kidney damage.
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