A reciprocal translocation between chromosomes 22 and 9 produces the BCR-ABL fusion oncoprotein, which is found in patients with chronic myelogenous leukemia (CML). Although there are various versions, p210 is the most commonly found BCR-ABL form. The fusion to BCR, results in deregulated/constitutively active tyrosine kinase activity of BCR-ABL which is sufficient of oncogenic transformation of myeloid cells. Inhibition of BCR-ABL oncogenic activity by the ABL-kinase inhibitor STI-571 (also known as gleevec, imatinib) became the first and best example for successful targeted therapy of cancer, and specifically CML. In recent years, several mutations (such as the T351I mutation) were found in CML patients that resulted in STI-571 resistance and the need for additional drug development.
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