Chronic myeloid leukemia (CML) originates from the hematopoietic stem cell and 
is characterized by the reciprocal translocation t(9;22)(q34;q11), which results 
in the BCR-ABL fusion gene on chromosome 22q-, also known as the Philadelphia 
chromosome. This chimeric gene codes for a cytoplasmic protein with constitutive 
tyrosine-kinase activity, responsible for cellular transformation and 
leukemogenesis in CML. The aim of this observational cohort study was to 
discriminate and quantify BCR-ABL transcripts in the peripheral blood of 
patients with CML who were treated with imatinib mesylate (Glivec, Novartis). 
Twenty-two patients were followed for six months during treatment. Quantitative 
real time polymerase chain reaction was performed before treatment and after 3 
and 6 months from treatment initiation. As compared with the third month, there 
was a significant decrease in BCR-ABL expression in the sixth month of treatment 
(P = 0.0002). At the sixth month, there was a significant difference in the 
levels of the two major transcripts of BCR-ABL, B2A2 and B3A2 (P = 0.0347), 
indicating that B2A2 may be more sensitive to imatinib. The results of our study 
indicate that imatinib is able to modify the natural history of CML, and raise 
the hypothesis that patients who express the B2A2 transcript may have a better 
prognosis.