Changes

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).

The ABL1 and ABL2 genes encode tyrosine kinases which share overlapping physiological roles and ABL2 somatic or amplification mutations are more common than similar mutations in ABL1 (6).

The ABL1 and ABL2 genes encode tyrosine kinases which share overlapping physiological roles and ABL2 somatic or amplification mutations are more common than similar mutations in ABL1 (6).