The ABL1 gene encodes for a non-receptor tyrosine kinase that is ubiquitously expressed and involved in a large number of cellular processes (see '''[https://www.ncbi.nlm.nih.gov/gene/25#reference-sequences "NCBI Gene]'''). By far the most prevalent ABL1 alteration associated with cancer are the fusions of the ABL1 gene with a number of parters, but especially with the BCR gene. 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 (6). | The ABL1 gene encodes for a non-receptor tyrosine kinase that is ubiquitously expressed and involved in a large number of cellular processes (see '''[https://www.ncbi.nlm.nih.gov/gene/25#reference-sequences "NCBI Gene]'''). By far the most prevalent ABL1 alteration associated with cancer are the fusions of the ABL1 gene with a number of parters, but especially with the BCR gene. 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 (6). |