Abstract
AbstractBackgroundTyrosine kinase inhibitors (TKIs) are prescribed as a targeted therapy to treat chronic myeloid leukemia patients. A challenge in clinical practice is that despite excellent efficacy and improved clinical response levels acquired by imatinib, a number of patients receive TKI therapy but have a poor primary response, develop a drug resistance, or relapse after initial success. This inter-individual difference into response has increased the concern in investigating the pharmacogenetics of cancer drugs. This review discusses the influence of various factors, such as BCR-ABL point mutation, efflux and influx transporters, and others, on targeted drug response in CML. Additionally, we focus on how patients can overcome these issues.
Publisher
Springer Science and Business Media LLC