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Pharmacogenomics. 2015;16(4):361-72. doi: 10.2217/pgs.14.179.

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

Author information

1
Department of Pharmacology, Universitätsmedizin Mainz, Obere Zahlbacher Str. 67, 55101 Mainz, Germany.

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. Original submitted 9 July 2014; Revision submitted 19 December 2014.

KEYWORDS:

RICOVER-60; SNP; anthracyclines; cardiotoxicity; clinical trial; heart failure

PMID:
25823784
DOI:
10.2217/pgs.14.179
[Indexed for MEDLINE]

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