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The **breakpoint cluster region protein** (BCR) is a multidomain enzyme with serine/threonine kinase activity, GTPase-activating protein (GAP) activity, and guanine nucleotide exchange factor (GEF) activity for the Rho family of GTPases, including Rac1 and RhoA[1][2][3][8]. BCR plays important roles in cellular signaling pathways that regulate cytoskeletal organization and cell migration. Clinical significance arises predominantly from chromosomal translocation t(9;22) leading to the BCR-ABL1 fusion gene, which encodes a constitutively active tyrosine kinase and is the hallmark of chronic myeloid leukemia and some acute leukemias. BCR itself participates in various signaling interactions, but it is as the BCR-ABL1 fusion oncoprotein that it is targeted therapeutically[1][2][3][8].
Tyrosine kinase inhibition (by targeting the abnormal BCR-ABL1 fusion protein activity, which drives unregulated cell growth)
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