Targeting the BCR-ABL Tyrosine Kinase in Chronic Myeloid Leukemia

Abstract

Chronic myeloid leukemia (CML) is one of the most remarkable cancers.^1,2 It was probably the first type of leukemia to be recognized, in the 1840s, as a distinct entity. A landmark was the discovery of the Philadelphia (Ph) chromosome in 1960.³ This led to the identification in CML cells of the BCR-ABL fusion gene and its corresponding protein, which is now firmly established as the unique cause of the initial, or “chronic,” phase of CML. ABL and BCR, which are located on chromosomes 9 and 22, respectively, are normal genes whose function is still unknown. The ABL gene encodes . . .