Background: Chronic myelogenous leukemia is a myeloproliferative disease, due to reciprocal translocations of chromosome 9 and 22, resulting to Bcr-Abl fusion gene. This gene has important role in chronic myelogenous leukemia development with activation of tyrosine kinase. In the era of tyrosine kinase inhibitor drugs, chronic myelogenous leukemia survival has improved greatly but unfortunately tyrosine kinase inhibitor resistence emerge as a treatment problem. It is important to determine the type, pattern and combination of Bcr-Abl kinase domain gene mutations that occur in chronic myelogenous leukemia patients with positive Bcr-Abl which hadincomplete molecular response to imatinib, a first generation tirozin kinase inhibitor. Objective: To determine the point mutations C944T, T1052C, T932C in kinase domain of the Bcr-Abl gene and the influence of the number of point mutations to Bcr-Abl/G6PDH Methods: Observational clinical and laboratories study of 40 Chronic Phase- chronic myelogenous leukemia patients Bcr-Abl positive, who received treatment for more than 18 months in. Venous blood sampling was done for point mutations C944T, T1052C, T932C and Bcr-Abl/G6PD ratio. Results: 90% of patients achieve complete Hematologic Response and majority of patients (60%) achieve Complete Molecular Response. Sixteen (40%) patients, who did not achieve chronic myelogenous leukemia , had point mutations in C944T, T 932C, and T1052C. Eight of the have 3 point mutations in C944T, T 932C, and T1052C, while 5 patients have T932 and T1052C, and 1 patient has mutation in T1052. The new finding in this study are the incidence of T932C mutations are quite high. The type of the Bcr-Abl transcripts will affect the increase of leukocytes and the number of mutations in the Bcr-Abl kinase domain affects blast number and the ratio of Bcr-Abl/G6PDH. Conclusion: Most of the responses to treatment is first-generation tyrosine kinase inhibitors provides a complete hematologic response and most of the molecular response is undetectable
