OBJECTIVE: To summarize the use of tyrosine kinase inhibitors (TKIs) for 
treatment of patients with chronic myeloid leukemia (CML) and provide practical 
information for patient management.
DATA SOURCES: Literature was retrieved from PubMed (2000-January 2011), using 
the search terms chronic myeloid leukemia and tyrosine kinase inhibitor. 
Abstracts presented at the 2008-2010 annual meetings of the American Society of 
Hematology and the American Society of Clinical Oncology, reference citations 
from identified publications, as well as the manufacturers' full prescribing 
information for cited drugs, also were reviewed.
STUDY SELECTION AND DATA EXTRACTION: Articles evaluating the efficacy and safety 
of the TKIs imatinib, nilotinib, and dasatinib were evaluated. Focus was placed 
on publications supporting management of patients with CML in the chronic phase. 
Reports presenting clinical trial information of TKIs in development also were 
included.
DATA SYNTHESIS: The discovery of targeted tyrosine kinase inhibition of BCR-ABL 
kinase dramatically changed the treatment of CML. Imatinib, the first TKI 
approved for treatment of patients with Philadelphia chromosome--positive CML, 
demonstrated significant superiority over the previous standard of care: 
interferon plus cytarabine. The newer, more potent TKIs, nilotinib and 
dasatinib, have demonstrated improved efficacy over imatinib as first-line 
therapy and provide an effective option for patients with resistance or 
intolerance to imatinib.
CONCLUSIONS: To maximize efficacy of TKI therapy, close patient management, 
involving frequent monitoring of patient response, is essential. Given the 
importance of continuing TKI therapy, early recognition and management of 
adverse events are critical to optimizing outcomes in patients with CML. In 
addition to the safety profile and considerations of comorbidities, additional 
factors can affect therapeutic selection, including drug-drug and drug-food 
interactions. Research investigating new therapies, particularly for patients 
harboring the T315I mutation-which remains refractory to current TKIs-continues 
in the quest to improve outcomes in patients with CML.