Chronic myeloid leukemia (CML) is characterized by the presence of a BCR-ABL 
fusion gene, which is the result of a reciprocal translocation between 
chromosomes 9 and 22, and is cytogenetically visible as a shortened chromosome 
22 (Philadelphia). Research during the past two decades has established that 
BCR-ABL is probably the pathogenetic pathway leading to CML, and that 
constitutive tyrosine kinase activity is central to BCR-ABL capacity to 
transform hematopoietic cells in vitro and in vivo. The tyrosine kinase 
inhibitor imatinib mesylate was introduced into the treatment regimen for CML in 
1998. During the last few years, reports on chromosomal changes during imatinib 
treatment have been described. In this study, we evaluated the random aneuploidy 
rate with chromosomes 9 and 18 in bone marrow from treated and untreated 
patients. We found higher aneuploidy rates in both treated and untreated 
patients compared to the control group. In three patients who were treated with 
imatinib mesylate for more than 1.5 years, triploidy also appeared in some 
nuclei. To our knowledge, this is the first report on new chromosomal changes 
such as random aneuploidy and triploidy under imatinib treatment, but more 
studies are needed to investigate the long-term effect of the imatinib treatment 
on genetic instability.