Given the large interindividual variability in developing
anthracycline-induced cardiomyopathy,
additional markers for risk stratification have been
identified. Genetic studies have identified SNPs in
SLC28A3 and several other genes that are significantly
associated with anthracycline therapyinduced
cardiotoxicity in children [29]. Other studies
have also shown that there may be a genetic
component leading to individual differences in
anthracycline pharmacodynamics in patients
receiving low-to-moderate doses of anthracyclines.
Functional polymorphisms in CBR1 and CBR3
modulate the synthesis of anthracycline alcohol
metabolites. Myocardial accumulation of anthracycline
alcohol metabolites may influence the course
of cardiomyopathy. Patients with varying polymorphisms
in CRB1 and CRB3 may synthesize alcohol
metabolites at differing rates, therefore affecting the
likelihood of the development of anthracyclineinduced
cardiomyopathy [30]. Individual studies noted hemachromatosis gene mutations and P450
oxidoreductase polymorphisms conferred a high
risk for anthracycline-induced cardiotoxicity, but
need to be further validated