Resumen
The effectiveness and safety of the anti-cancer agent doxorubicin (anthracycline group medicine) depend on the metabolism and retention of the drug in the human organism. Polymorphism of cytochrome p450 (CYP)-encoding genes and detoxifying enzymes such as CYP3A4 and CYP2D6 were found responsible for variations in the doxorubicin metabolism. Transmembrane transporters such as p-glycoproteins were reported to be involved in cancer tissue retention of doxorubicin. ATP-binding cassette (ABC) family members, including ABCB1 transporters (also known as Multi-Drug Resistance 1 (MDR1)) proteins, were determined to pump out doxorubicin from breast cancer cells, therefore reducing the drug effectiveness. This study critically discusses the latest data about the role of CYP3A4, CYP2D6, and ABCB1 gene polymorphism in the regulation of doxorubicin?s effects in breast cancer patients. The assessment of genetic differences in the expression of doxorubicin metabolizing and transporting enzymes should be explored for the development of personalized medical treatment of breast cancer patients.