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The BCR-Abl protein is a fusion oncoprotein resulting from the translocation between the BCR gene on chromosome 22 and the ABL1 gene on chromosome 9, forming the Philadelphia chromosome. It exhibits constitutive tyrosine kinase activity, leading to uncontrolled cell proliferation and survival, primarily associated with chronic myelogenous leukemia (CML) and some cases of acute lymphoblastic leukemia (ALL). Targeting its aberrant kinase activity is the basis for therapies such as imatinib.
Tyrosine kinase inhibition
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