The hallmark of chronic myeloid leukemia is the existence of the cytogenetic evidence of the Phyladelphia chromosome (reciprocal translocation between chromosome 9 and 22, and is specifically designated t(9;22)(q34;q11). The result of the translocation is the oncogenic BCR-ABL gene fusion, located on the shorter derivative 22 chromosome. This gene encodes the Bcr-abl fusion protein the BCR-ABL tyrosine kinase - a protein that is continuously activated. The result of this unregulated activation is an unregulated neoplastic type cell division - chronic myeloid leukemia. The first targeted molecular treatment operating in cancer- inhibitor of the BCR-ABL tyrosine kinase, Imatinib mesylate, is the standard of care for chronic myeloid leukemia (CML) Methods. A retrospective review of patients in one department of hematology with a diagnosis of Ph/BCR-ABL positive CML and received imatinib. Results. From 2002 to 2012, 66 patients in CML-CP received imatinib were introduced in the study. 22 (33%) patients received imatinib as upfront therapy, the others as second or third line treatment. The cytogenetic response (CyR) achieved was major in 62% with 56% complete cytogenetic response (CCR), no CyR in 17 patients (25%). The molecular response was complete in 13 (20%) and major in 16 (24%) patients. Better cytogenetic and molecular responses were achieved by those with low and intermediary risk (Sokal) Seven patients developed under imatinib additional cytogenetic anomalies: supplemental chromosome 8 (6), duplication of Ph1 (2), trisomy 17 and 19 (1). The median of follow-up was 69 months (range 18-180) and under imatinib was 52 months (range 3-126). The Sokal score was a better predictor of survival than Hasford's. Conclusions. Imatinib remains the best first line treatment, but there are still a significant number of patients who did not achieve a CyR. The responses and survival were not influenced by the previous treatments but the earlier introduction of imatinib is better. The Sokal score seems to have a better prognostic role. The survival of patients with CML is evidently improuved by tyrosin kynase inhibitors. [ABSTRACT FROM AUTHOR]