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Symptoms in this phase are generally mild and many patients are asymptomatic, being often diagnosed incidentally after a routine blood test. CP may last several years and is characterized by the expansion of the myeloid cell compartment, although cells still retain the capacity to differentiate and function normally. The natural history of the disease follows a triphasic course with an initial chronic phase (CP), an intermediate accelerated phase (AP) and a final, fatal blastic phase (BP)(Fig. Clinical hallmarks of CML are leukocytosis, a left shift in the differential count, and splenomegaly. CML: The diseaseД¬ML accounts for 15вЂ“20% of all cases of leukemia in adults.

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This review summarizes the main biological acquisitions about BCR-ABL1 as a therapeutically druggable oncogenic tyrosine kinase and provides an update on drug resistance mechanisms and how they can be overcome.

Cases of acquired resistance to imatinib, however, began to be reported soon after the first clinical trials commenced вЂ“ temporarily casting shadows over the long-term efficacy of targeted therapies: might CML and cancer in general be a more tougher enemy than initially expected? Many years later, further biological and clinical advances have led to three generations of TKIs, to a life expectancy for CML patients approaching that of the general population and to the possibility to safely and permanently stop therapy in a small but significant proportion of cases - although the issue of drug resistance is not yet fully solved. The tyrosine kinase inhibitor (TKI) imatinib mesylate was approved for resistant/refractory CML patients in 2001, and for newly diagnosed patients just two years later. As a consequence, CML became the first human malignancy for whom the вЂdreamвЂ™ ofВ targeted therapy could come true.

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Between the 60s and the 90s, a series of seminal studies clarified that the deregulated activity of a tyrosine kinase, BCR-ABL1, resulting from that chromosomal abnormality, seemed to be necessary and sufficient to induce leukemia. CML has been the first human malignancy to be associated, almost 60В years ago (well before the вЂomicsвЂ™ era!) to a consistent chromosomal abnormality. However, the advances in biology and therapy of CML have set gigantic milestones in the history of anticancer precision medicine. Here we retrace the steps that have led from the biological acquisitions regarding BCR-ABL1 structure and function to the development of inhibitory strategies and we discuss drug resistance mechanism and how they can be addressed.Д¬hronic myeloid leukemia (CML) is a rare disease worldwide: its incidence is estimated to be 1вЂ“2 cases/100,000/year. The great majority of patients will have to assume TKIs indefinitely вЂ“ which raises serious pharmacoeconomic concerns and is now shifting the focus from efficacy to compliance and quality of life issues. Only a small proportion of cases may attempt therapy discontinuation without experiencing subsequent relapse. Patients achieving stable optimal responses to TKI therapy are predicted to have the same life expectancy of the general population. They are more potent molecules, but have been associated to more serious side effects and complications. Second- and third-generation TKIs were later introduced to prevent or counteract the problem of drug resistance, that may arise in a small proportion of patients. Imatinib mesylate, the first tyrosine kinase inhibitor (TKI) to be approved for therapeutic use, was hailed as a magic bullet against cancer and remains one of the safest and most effective anticancer agents ever developed. BCR-ABL1 was one of the first tyrosine kinases to be implicated in a human malignancy and the first to be successfully targeted.

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Deregulated activity of BCR-ABL1, a nonreceptor tyrosine kinase encoded by the fusion gene resulting from the t(9 22)(q34 q11) chromosomal translocation, is thought to be the driver event responsible for initiation and maintenance of chronic myeloid leukemia (CML).