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Background Tyrosine 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.
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Zaker et al. (2023) studied this question.
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