Imatinib mesylate is a new drug that can inhibit the tyrosine kinase activity of 
Bcr-Abl, the receptors for platelet-derived growth factor receptor(PDGF) and 
stem cell factor, or c-kit. Chronic myeloid leukemia (CML) is distinguished by 
the presence of a reciprocal translocation between chromosomes 9 and 22 that 
results in a shortened chromosome 22, termed the Philadelphia(Ph) chromosome. As 
a result of the translocation, a fusion gene called the Bcr-Abl gene is created 
from two normal cellular genes, encoding a chimeric Bcr-Abl protein with a 
deregulated tyrosine kinase activity. The expression of Bcr-Abl tyrosine kinase 
has been shown to be necessary and sufficient for the transformed phenotype of 
CML cells. Imatinib can block the kinase activity of Bcr-Abl, thus inhibiting 
the proliferation of Ph-positive progenitors, and has shown activity against all 
phases of CML, though responses are most substantial and durable in patients in 
the chronic phase. An international phase III study which compared the efficacy 
of imatinib with that of interferon alpha combined with low-dose cytarabine in 
newly diagnosed chronic-phase CML showed the rate of major cytogenetic response 
at 24 months was 90%, including 82% of complete cytogenetic response. These 
results indicated that imatinib was superior to interferon-containing treatment 
as a first-line therapy. More than 10,000 patients worldwide, including those in 
Japan, have been treated with imatinib in clinical trials, and a lot of 
information has been accumulated on the use of this drug. The aim of this 
article is to review the use of this drug and the practical management of 
patients with chronic myeloid leukemia.