The BCR-ABL fusion protein is primarily associated with chronic myeloid leukemia (CML) and, to a lesser extent, acute lymphoblastic leukemia (ALL). The constitutive tyrosine kinase activity of BCR-ABL leads to continuous cell signaling for growth and division, bypassing normal cellular regulatory mechanisms. This unregulated proliferation of white blood cells is a hallmark of CML and contributes significantly to disease progression.
