The Bcr‑Abl tyrosine kinase drives chronic myeloid leukemia (CML) and is the target of imatinib therapy, which induces complete cytogenetic responses in most patients. However, relapse is often associated with acquired BCR‑ABL mutations. This dissertation examines kinase domain mutations in patients with stable responses, regulatory domain mutations outside the kinase domain, and catalytically inactive Bcr‑Abl deletion mutants. While mutations were frequent during imatinib treatment, their effects varied, with limited predictive value for relapse and diverse impacts on drug resistance and sensitivity.
