The bcr-abl fusion protein is present in the vast majority of cases of chro
nic myelogenous leukemia, and the deregulated tyrosine kinase activity of t
his protein is essential for leukemic transformation. Thus, bcr-abl is an i
deal target for pharmacologic inhibition. In preclinical studies, STI571 (f
ormerly CGP57148B), an abl-specific, tyrosine kinase inhibitor, selectively
killed bcr-abl-expressing cells both in vitro and in vivo. In early clinic
al trials of STI571, encouraging results have been obtained, and there is a
lready a suggestion that STI571 may soon need to be incorporated into treat
ment algorithms for chronic myelogenous leukemia. Curr Opin Oncol 2000, 12:
594-597 (C) 2000 Lippincott Williams & Wilkins, Inc.