Philadelphia (Ph) chromosome is the cytogenetic hallmark of chronic myeloid 
leukemia (CML). The translocation forms a chimeric gene, bcr-abl, which 
generates BCR-ABL. This fusion protein constitutively activate ABL tyrosine 
kinase and causes CML. Imatinib mesylate is a selective tyrosine kinase 
inhibitor on ABL, c-Kit and PGDF-receptor, and functions through competitive 
inhibition at the ATP-binding site of the enzyme, which leads to growth arrest 
or apoptosis in cells that express BCR-ABL. Imatinib has revolutionized the 
management of patients with CML, and at a dose of 400 mg daily has become the 
current standard therapy for newly diagnosed patients with CML even when they 
have HLA-matched family donors. Although imatinib therapy has only a 5-year 
history, it is hoped that CML will be cured with this drug and with forthcoming 
second-generation tyrosine kinase inhibitors as well as by allogeneic stem cell 
transplantation in patients who have become resistant to these drugs.