Status of bcr-abl tyrosine kinase inhibitors in chronic myelogenous leukemia

Citation
Me. O'Dwyer et Bj. Druker, Status of bcr-abl tyrosine kinase inhibitors in chronic myelogenous leukemia, CURR OPIN O, 12(6), 2000, pp. 594-597
Citations number
21
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
CURRENT OPINION IN ONCOLOGY
ISSN journal
10408746 → ACNP
Volume
12
Issue
6
Year of publication
2000
Pages
594 - 597
Database
ISI
SICI code
1040-8746(200011)12:6<594:SOBTKI>2.0.ZU;2-J
Abstract
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.