Chronic myelogenous leukemia (CML) is a clonal malignant myeloproliterative disorder believed to be originated from a single abnormal haemopoietic stem cell. It's course of diseases gets worse slowly . Half of the patients who were not cured lived for about 3 years. The pathologic hallmark of this disease is the Philadelphia chromosome that is caused by a t(9;22) chromosomal trans location, which exists in over 90% of CML patients. The resulting Bcr-Abl fusion gene encodes a novel cytoplasmic protein with constitutive tyrosine kinase, which is a significant cancer gene in CML disease.Gleevec (STI-571) which came into the market in 2001, is the first recognized selectivity inhibitor of Bcr-Abl tyrosine kinase. Inhibition of the constitutively active Bcr-Abl tyrosine kinase by Gleevec(STI-571) has been proven to be a highly effective treatment for CML. However, Gleevec(STI-571) is only transiently effective in blast crisis, and drug resistance emerges by amplification of or development of mutational changes in Bcr-Abl. Although the clinical success of Gleevec(STI-571) has validated the importance of Bcr-Abl as a therapeutic target for the treatment of CML, the emerging problem of Bcr-Abl tyrosine kinase resistance has highlighted the need for continuing efforts to develop more effective treatments for this universally fatal disease.This article studied the overriding resistance of Bcr-Abl tyrosine kinase...
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