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May inform future risk stratification for anthracycline cardiotoxicity; leaves open prospective validation before any clinical adoption.
The solute carrier superfamily comprises of uptake transporters that can contribute to the absorption and elimination of a broad array of clinically important drugs. Recent studies have suggested that the tissue-specific expression of these transporters may have important consequences for an individual's susceptibility to drug-induced organ damage or to drug-drug interactions. Polymorphic variants have been identified in genes encoded by this family, and some of these have been associated with functional changes in transport function and response to anthracycline-induced toxicity and efficacy. Here, we review recent advances in the role solute carrier transporters play in anthracycline-induced cardiotoxicity, highlight potential implications of genetic variants that may contribute to drug response and discuss novel technologies to study mechanisms of anthracycline transport.
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Huang et al. (2018) studied this question.
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