Association of NADPH oxidase polymorphisms with anthracycline-induced cardiotoxicity in the RICOVER-60 trial of patients with aggressive CD20(+) B-cell lymphoma

2015 | journal article; research paper. A publication with affiliation to the University of Göttingen.

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​Association of NADPH oxidase polymorphisms with anthracycline-induced cardiotoxicity in the RICOVER-60 trial of patients with aggressive CD20(+) B-cell lymphoma​
Reichwagen, A.; Ziepert, M.; Kreuz, M.; Gödtel-Armbrust, U.; Rixecker, T.; Poeschel, V. & Toliat, M. R. et al.​ (2015) 
Pharmacogenomics16(4) pp. 361​-372​.​ DOI: https://doi.org/10.2217/PGS.14.179 

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Authors
Reichwagen, Annegret; Ziepert, Marita; Kreuz, Markus; Gödtel-Armbrust, Ute; Rixecker, Tanja; Poeschel, Viola; Toliat, Mohammad Reza; Nürnberg, Peter; Tzvetkov, Mladen ; Deng, Shiwei; Trümper, Lorenz ; Hasenfuss, Gerd ; Pfreundschuh, Michael; Wojnowski, Leszek
Abstract
Aim: To identify gene variants responsible for anthracycline-induced cardiotoxicity. Patients & methods: Polymorphisms of the NADPH oxidase subunits and of the anthracycline transporters ABCC1, ABCC2 and SLC28A3 were genotyped in elderly patients (61-80 years) treated for aggressive CD20(+) B-cell lymphomas with CHOP-14 with or without rituximab and followed up for 3 years. Results: The accumulation of RAC2 subunit genotypes TA/AA among cases was statistically significant upon adjustment for gender, age and doxorubicin dose in a multivariate logistic regression analysis (OR: 2.3, p = 0.028; univariate: OR: 1.8, p = 0.077). RAC2 and CYBA genotypes were significantly associated with anthracycline-induced cardiotoxicity in a meta-analysis of this and a similar previous study. Conclusion: Our results support the theory that NADPH oxidase is involved in anthracycline-induced cardiotoxicity.
Issue Date
2015
Journal
Pharmacogenomics 
ISSN
1462-2416
eISSN
1744-8042
Language
English

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