Chronic myeloid leukemia (CML) is caused by the BCR-ABL oncogene. The 
Philadelphia chromosome (Ph) from a reciprocal translocation, t(9;22) (q34;q11) 
causes a fusion gene, BCR-ABL, that encodes a constitutively active tyrosine 
kinase. Treatment of CML by imatinib is effective to control the tyrosyl 
phosphorylation of the protein related to the cell signaling. BCR-ABL mRNA is 
overexpressed in the minimal residual disease (MRD), known as an early sign of 
relapse. Between December 2005 and June 2008, we measured BCR-ABL mRNA levels in 
the bone marrow (BM) from patients by quantitative real-time polymerase chain 
reaction (RQ-PCR) in Aomori Prefectural Central Hospital. Eighty-six samples 
from 26 patients were collected. Among the 26 CML patients, 11 patients (42%) 
were in the pretreatment group. Seven (64%) of the 11 patients achieved complete 
molecular response (CMR). In the post-treatment group consisting of the 
remaining 15 patients, 9 (60%) patients achieved CMR. The patients receiving 
imatinib at a dose over 300 mg per day required 13 (6-77) months [median 
(range)] to achieve CMR. On the other hand, the patients receiving a dose below 
300 mg per day required 29.5 (11-84) months [median (range)]. When BCR-ABL mRNA 
was detected during the treatment course of patients with CMR, careful 
observation of BCR-ABL mRNA was useful for tracking the clinical course of 
patients. In conclusion, the BCR-ABL mRNA level was useful for monitoring the 
clinical course in 26 patients with CML.