الفهرس 
INTRODUCTION
CHRONIC MYELOID LEUKAEMIAOnly 14 pages are availabe for public view
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Abstract
The tyrosine kinase inhibitor Imatinib was the first BCR-ABL targeted agent approved in 2001 for the treatment of patients with CML. Unfortunately, resistance to Imatinib has become a clinically significant problem that limits the long-term benefits of the drug. The mechanisms that underlie Imatinib resistance are multifactorial. Experimental evidence indicates that targeting BCR-ABL is not sufficient for elimination of minimal residual disease found within the bone marrow. Thus curative strategies will likely need to focus on strategies where BCR-ABL inhibitors are given in combination with agents that specifically target the leukaemic stem cell. One potential target to be exploited is the JAK/STAT3 pathway. Recently using STAT3 conditional knock-out mice, it was shown that STAT3 is critical for initiating the disease. The aim of this work is to assess the level of p-STAT3 Tyr705 expression in different stages of the disease i.e. chronic and advanced phases and to evaluate its relation to imatinib resistance and the level of BCR-ABL gene expression. A total of 70 subjects were enrolled in this study. They were classified into 2 groups; one group included 50 CML patients. The other group included 20 age matched healthy subjects as controls. Flowcytometry analysis was carried out to evaluate the expression of the p-STAT3 Tyr705 using fluorochrome labeled monoclonal antibodies against p-STAT3 Tyr705 and BCR-ABL quantitation by real time PCR also carried out for confirmation of diagnosis & assessment of the treatment response.