Chronic myelogenous leukaemia - new therapeutic principles

The deregulated tyrosine kinase activity of the BCR-ABL fusion protein is t he cause of malignant transformation in almost all cases of chronic myeloge nous leukaemia (CML), malting BCR-ABL an ideal target for pharmacological i nhibition. Signal transduction inhibitor (STI571) (formerly CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encourageing a nd STI571 promises to be an important addition to the therapy of CML.