• N Salesi, G Bossone, G Della Longa, and B Di Cocco.
• Scuola di Specializzazione in Oncologia Medica, II Facoltà di Medicina e Chirurgia, Università degli Studi di Roma La Sapienza, Roma, Italy. salnel@libero.it
• Minerva Med. 2003 Apr 1; 94 (2): 71-6.

AbstractThe therapy of chronic myeloid leukemia, characterized by the presence of the Philadelphia chromosome in the clonal hematopoietic stem cells, has changed dramatically in the last years with the development of a specific inhibitor of the BCR-ABL tyrosine kinase: tyrosine kinase inhibitor imatinib mesylate (formerly STI571, [Glivec]). Glivec selectively blocks cellular proliferation and induces apoptosis in Philadelphia chromosome-positive (Ph+) cells harbouring the Bcr-Abl tyrosine kinase. Clinical development of imatinib mesylate began with 3 large, multicenter, phase II trials. The majority (88%) of interferon-alpha-resistant or intolerant patients in chronic-phase CML, achieved a complete hematologic response to imatinib mesylate. More importantly, approximately half of the patients achieved a major cytogenetic response, a result historically associated with improved survival. Furthermore, 21% of patients in accelerated-phase CML and 13.5% of patients in blastic-phase CML (patient populations with typically poor prognosis before the advent of imatinib mesylate) achieved major cytogenetic responses.

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