Variation in the human genome is a most important cause of variable response to drugs. Different patients respond in different ways to the same medication. There are many inter-individual differences in drug response owing to the sequence variants of genes that encode drug-metabolizing enzymes, drug transporters, or drug targets. Many studies have shown that genetic factors greatly contribute to influence the variability in drug effects. Current advances in the biology of cancer and emergence of high-throughput sequencing for genome analysis are expected to provide new approaches for optimizing treatment and lead the future direction for personalized medicine. Chemotherapy is an impor tant adjuvant systemic therapeutic approach for the successful treatment of
breast cancer and, during early stage breast cancer, has been demonstrated to improve survival rate. Most of the drug-metabolizing enzymes and transporters have a broad range of genetic polymorphisms, which may cause inter-individual variability with different concentrations of drugs. In addition, anticancer therapies are known to have a narrow therapeutic range; a high concentration in a patient’s body increases the toxicity, and a low concentration decreases the effect of the drug. Various combinations of cytotoxic chemotherapeutic drugs such as cyclophosphamide, anthracyclines, and taxanes are an integral part of the systemic treatment of
breast cancer patients. Genetic variations such as single nucleotide polymorphisms (SNPs) are present across individuals and might affect pharmacokinetics and pharmacodynamics of drugs. In this review, we highlight obtained from recent studies on genetic variants associated to pharmacokinetics and pharmacodynamics of most of the important drugs used in
neo-adjuvant chemotherapy of
breast cancer like cyclophosphamide, doxorubicin, Epirubicin, paclitaxel, docetaxel and 5-fluorouracil.