1 Introduction</h5> Chronic myeloid leukemia (CML) is a hematopoietic stem cell cancer that arises following a reciprocal genetic translocation between chromosomes 9 and 22  , resulting in the short Philadelphia (Ph) chromosome carrying the Bcr-Abl (Breakpoint cluster region-Abelson leukemia) oncogene [2–4] . The understanding of the central role played by Bcr-Abl in the pathogenesis of CML gave birth to the so-called “targeted therapy”  . In 2001, Imatinib (Gleevec™, Fig. 1 ), a potent Bcr-Abl inhibitor, was approved for the treatment of CML serves as validation of the concept that therapeutic agents targeting cancer-specific pathways can offer significative improvements over traditional chemotherapeutic agents  . Imatinib is now considered as a first-line therapy for the majority of CML cases due to its high efficacy and relatively mild side effects  .</P>However, the initial enthusiasm generated by the high response rate to this drug has been dampened by the development of resistance, accounting for 16% in newly diagnosed chronic phase CML and more than 50% in more advanced stages  . Mutations in the kinase domain of Bcr-Abl are the major mechanism of acquired Imatinib resistance [9–11] . To date, at least 50 different point mutations that encode
European Journal of Medicinal Chemistry – Elsevier
Published: May 1, 2013
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