By far the most common ABL1 alteration associated with cancer is the BCR-ABL1 fusion, a reciprocal translocation between chromosome 22 (BCR locus) and chromosome 9 (ABL1 locus) produces the Philadelphia chromosome t(9;22)(q34.1;q11.2), which is prevalent in Chronic Myeloid Leukemia (1, 2) and to a lesser extent in B-cell Acute Lymphoblastic Leukemia and T-cell Acute Lymphoblastic Leukemia. The head to tail arrangement of the BCR-ABL1 fusion gene results in an activated tyrosine kinase activity.
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A number of other gene fusion partners have been identified with ABL1 and linked to other hematological cancers, but at a much smaller prevalence than BCR-ABL1.