Chronic myeloid leukemia (CML) is caused by Bcr-Abl, a constitutively active 
tyrosine kinase that is the result of a reciprocal translocation between 
chromosomes 9 and 22 and cytogenetically evident as the Philadelphia chromosome. 
Imatinib (Glivec, Gleevec), a specific small molecule inhibitor of Bcr-Abl, has 
become the standard drug therapy for CML, and has dramatically diminished the 
use of allogeneic stem cell transplantation. Despite unprecedented rates of 
complete cytogenetic response, residual disease remains detectable in the 
majority of patients, suggesting that imatinib fails to eradicate leukemic stem 
cells. In this publication, the current perspectives for CML patients treated 
with imatinib are reviewed, focusing on the results of both standard and 
high-dose therapy. Monitoring of time-dependent prognostic factors is reviewed. 
The reasons imatinib may not be able to eradicate the disease are discussed, and 
potential strategies to achieve disease elimination are presented. Lastly, 
resistance to imatinib and the potential of second-generation Abl kinase 
inhibitors in the setting of clinical resistance are considered.