BACKGROUND: Chronic myelogenous leukemia (CML) is caused by the BCR-ABL tyrosine kinase, the product of the Philadelphia chromosome. Imatinib mesylate, formerly STI571, is a selective inhibitor of this kinase. METHODS: A total of 532 patients with late--chronic-phase CML in whom previous therapy with interferon alfa had failed were treated with 400 mg of oral imatinib daily. Patients were evaluated for cytogenetic and hematologic responses. Time to progression, survival, and toxic effects were also evaluated. RESULTS: Imatinib induced major cytogenetic responses in 60 percent of the 454 patients with confirmed chronic-phase CML and complete hematologic responses in 95 percent. After a median follow-up of 18 months, CML had not progressed to the accelerated or blast phases in an estimated 89 percent of patients, and 95 percent of the patients were alive. Grade 3 or 4 nonhematologic toxic effects were infrequent, and hematologic toxic effects were manageable. Only 2 percent of patients discontinued treatment because of drug-related adverse events, and no treatment-related deaths occurred. CONCLUSIONS: Imatinib induced high rates of cytogenetic and hematologic responses in patients with chronic-phase CML in whom previous interferon therapy had failed.
BACKGROUND:Chronic myelogenous leukemia (CML) is caused by the BCR-ABL tyrosine kinase, the product of the Philadelphia chromosome. Imatinib mesylate, formerly STI571, is a selective inhibitor of this kinase. METHODS: A total of 532 patients with late--chronic-phase CML in whom previous therapy with interferon alfa had failed were treated with 400 mg of oral imatinib daily. Patients were evaluated for cytogenetic and hematologic responses. Time to progression, survival, and toxic effects were also evaluated. RESULTS:Imatinib induced major cytogenetic responses in 60 percent of the 454 patients with confirmed chronic-phase CML and complete hematologic responses in 95 percent. After a median follow-up of 18 months, CML had not progressed to the accelerated or blast phases in an estimated 89 percent of patients, and 95 percent of the patients were alive. Grade 3 or 4 nonhematologic toxic effects were infrequent, and hematologic toxic effects were manageable. Only 2 percent of patients discontinued treatment because of drug-related adverse events, and no treatment-related deaths occurred. CONCLUSIONS:Imatinib induced high rates of cytogenetic and hematologic responses in patients with chronic-phase CML in whom previous interferon therapy had failed.
Authors: Elizabeth Dugan; Roxanne Truax; Kellen L Meadows; Andrew B Nixon; William P Petros; Justin Favaro; Nishan H Fernando; Michael A Morse; Gerard C Blobe; Herbert I Hurwitz Journal: Anticancer Res Date: 2010-04 Impact factor: 2.480
Authors: Stephane Wong; Jami McLaughlin; Donghui Cheng; Kevin Shannon; Lorraine Robb; Owen N Witte Journal: Proc Natl Acad Sci U S A Date: 2003-09-19 Impact factor: 11.205
Authors: Andreas L Petzer; Dominic Fong; Thomas Lion; Irina Dyagil; Zvenyslava Masliak; Andrija Bogdanovic; Laimonas Griskevicius; Sandra Lejniece; Stefan Goranov; Liana Gercheva; Aleksandar Stojanovic; Dontcho Peytchev; Nikolay Tzvetkov; Rasa Griniute; Atanas Stanchev; Thomas Grubinger; Marthin Kwakkelstein; Peter Schuld; Guenther Gastl; Dominik Wolf Journal: Haematologica Date: 2012-04-17 Impact factor: 9.941