CML Research Aims to Improve a "Magic Bullet"

Jane De Lartigue, PhD
Published: Friday, Apr 10, 2020
Approval of imatinib (Gleevec) almost 20 years ago heralded the arrival of the targeted therapy era in oncology and thrust the ABL1 kinase into the limelight.1 A fusion involving the ABL1 gene is present in the vast majority of patients with chronic myeloid leukemia (CML), and aberrant ABL1 kinase activity is the central oncogenic driver in this cancer type.2

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The ABL1 gene was first described in 1970 as the normal cellular counterpart of a virally encoded gene found in a mouse leukemia virus that could transform normal mouse lymphocytes and fibroblasts. The viral protein was shown to have tyrosine kinase activity.16,17

About 10 years earlier, investigators had discovered an unusual chromosome in the leukocytes of patients with CML, dubbed the Philadelphia chromosome after the city in which it was first described. Through a series of seminal studies, it was shown that the Philadelphia chromosome is the result of a chromosomal translocation involving chromosomes 22 and 9, the latter containing the human ABL1 gene (Figure 1).17,18

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