The cause of chronic myeloid leukemia (CML) is a constitutivelyactive BCR-ABL tyrosine kinase. Imatinib inhibits this kinase.This is a retrospective analysis to detect the relative efficacy ofimatinib mesylate in achieving complete hematologic and molecularresponse for newly diagnosed patients of CML in the chronic phasewho attended kasr el Aini center of radiation oncology and nuclearmedicine (NEMROCK),during the period from March 2003 toDec.2005, giving an estimate of progression-free survival and overall survival.The standard monitoring of response includes full blood counts,clinical examination, cytogenetic examination and molecularexamination by quantitative RT-PCR for BCR/ABL mRNA.The median follow up of patients was 17.3 months.The median dose of imatinib mesylate was 370 mg/d (range from346 to 400 mg/d).Q RT-PCR has provided extremely valuable for assessing andmonitoring minimal residual disease after treatment with imatinibmesylate.Imatinib induces a very rapid hematologic response (average 4weeks) as compared to other treatment options. This response wasachieved in all patients of this study. 14 patient out of 17 (82.4%) achieved molecular response, byQ RT-PCR, among the responders 41.2% > 2 log reduction, 23.5% (4patients) showed at least 3 log reduction, 41.2% < 2 log reductionand 17.6% showed no response.There were no correlation between the risk staging andhematologic or molecular response.The analysis of responses was complicated by the high rate ofinterruption and discontinuation of treatment.Long term of clinical significance of a reduction in the amountof BCR-ABL transcript during the period of follow up is not clearand it is too early to predict the survival advantage of this response.No one of our patients had progressed to accelerated phase orblastic crisis.Imatinib now seems to be the initial treatment of choice forpatients with CML who do not have a suitable bone marrow donor orwho are not candidates for transplantation.