• Hagop Kantarjian, Charles Sawyers, Andreas Hochhaus, Francois Guilhot, Charles Schiffer, Carlo Gambacorti-Passerini, Dietger Niederwieser, Debra Resta, Renaud Capdeville, Ulrike Zoellner, Moshe Talpaz, Brian Druker, John Goldman, Stephen G O'Brien, Nigel Russell, Thomas Fischer, Oliver Ottmann, Pascale Cony-Makhoul, Thierry Facon, Richard Stone, Carole Miller, Martin Tallman, Randy Brown, Michael Schuster, Thomas Loughran, Alois Gratwohl, Franco Mandelli, Giuseppe Saglio, Mario Lazzarino, Domenico Russo, Michele Baccarani, Enrica Morra, and International STI571 CML Study Group.
• M.D. Anderson Cancer Center, Houston, TX 77030, USA. hkantarj@mdanderson.org
• N. Engl. J. Med. 2002 Feb 28; 346 (9): 645-52.

BackgroundChronic 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.MethodsA 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.ResultsImatinib 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.ConclusionsImatinib induced high rates of cytogenetic and hematologic responses in patients with chronic-phase CML in whom previous interferon therapy had failed.

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