ABSTRACT
INTRODUCTION A decade following the introduction of the original tyrosine kinase inhibitor (TKI), imatinib, into the clinics for the treatment of patients with chronic myeloid leukemia (CML) in chronic phase, it is abundantly clear that the overall safety and effi cacy of the drug are impressive but not optimal. It induces complete cytogenetic response (CCyR) rates of 65-85%, major molecular response (MMR; defi ned as a 3-log or more reduction in the BCR-ABL1 transcript levels compared with the baseline) rates of 40-70%, and a complete molecular response (CMR; defi ned as the absence of any detectable BCR-ABL1 transcripts) rates of 10-40%.
