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Chronic Myeloid Leukemia: Current Management Challenges
Chronic Myeloid Leukemia: Current Management Challenges Tariq Mughal, MD
Much of the current progress in “targeted” treatments of cancers has resulted from the lessons learned from the successful application of our understanding of the molecular basis of chronic myeloid leukemia (CML) resulting in the introduction of imatinib into the clinics in 1998. The drug rapidly became the treatment of choice for the majority of patients with CML in chronic phase (CP). Remarkably, the lessons from patients with CML have continued with the understanding of the molecular mechanisms of imatinib resistance. Many efforts have focused on strategies to circumvent drug resistance and we now have a growing arsenal of various treatments for patients with CML. In this supplement to Clinical Lymphoma and Myeloma dedicated to some of the therapeutic advances, various specialists address pertinent topics ranging from the optimal management of the new patient in CP to drug resistance and emerging treatments. The major shifts in the therapeutic algorithm for the newly diagnosed patient with CML in CP are highlighted by Mughal and Goldman. This article discusses the current place of imatinib and the need for additional therapy for those patients who do not fare so well or are unable to tolerate the drug because of side effects. Giralt addresses the current place of allogenic stem cell transplantation, which remains
the sole treatment that results in long-term molecular remissions and perhaps cure. Atallah et al discuss the safety issues of the tyrosine kinase inhibitors and speculate on some of the long-term concerns, such as myocardial toxicity and the remote possibility of secondary malignancies related to imatinib. Swords and colleagues address the current role of tyrosine kinase inhibitors in the management of the advanced phases of CML and Philadelphia chromosome–positive acute lymphoblastic leukemia. O’Hare et al focus on the significance of Abl kinase domain mutations and strategies to overcome drug resistance, particularly against the T315I mutation which is almost always accompanied by a significant degree of resistance not only to imatinib, but also dasatinib, nilotinib, and bosutinib (SKI-606). It is, indeed, a privilege to be part of the global efforts to improve outcomes for patients afflicted with CML. I hope that the readers find the information herein useful.
Tariq Mughal, MD Supplement Editor
Dr Mughal has no relevant relationships to disclose.
S94 • Clinical Lymphoma & Myeloma Vol 7 Suppl 3 March 2007
Much of the current progress in “targeted” treatments of cancers has resulted from the lessons learned from the successful application of our understanding of the molecular basis of chronic myeloid leukemia (CML) resulting in the introduction of imatinib into the clinics in 1998. The drug rapidly became the treatment of choice for the majority of patients with CML in chronic phase (CP). Remarkably, the lessons from patients with CML have continued with the understanding of the molecular mechanisms of imatinib resistance. Many efforts have focused on strategies to circumvent drug resistance and we now have a growing arsenal of various treatments for patients with CML. In this supplement to Clinical Lymphoma and Myeloma dedicated to some of the therapeutic advances, various specialists address pertinent topics ranging from the optimal management of the new patient in CP to drug resistance and emerging treatments. The major shifts in the therapeutic algorithm for the newly diagnosed patient with CML in CP are highlighted by Mughal and Goldman. This article discusses the current place of imatinib and the need for additional therapy for those patients who do not fare so well or are unable to tolerate the drug because of side effects. Giralt addresses the current place of allogenic stem cell transplantation, which remains
the sole treatment that results in long-term molecular remissions and perhaps cure. Atallah et al discuss the safety issues of the tyrosine kinase inhibitors and speculate on some of the long-term concerns, such as myocardial toxicity and the remote possibility of secondary malignancies related to imatinib. Swords and colleagues address the current role of tyrosine kinase inhibitors in the management of the advanced phases of CML and Philadelphia chromosome–positive acute lymphoblastic leukemia. O’Hare et al focus on the significance of Abl kinase domain mutations and strategies to overcome drug resistance, particularly against the T315I mutation which is almost always accompanied by a significant degree of resistance not only to imatinib, but also dasatinib, nilotinib, and bosutinib (SKI-606). It is, indeed, a privilege to be part of the global efforts to improve outcomes for patients afflicted with CML. I hope that the readers find the information herein useful.
Tariq Mughal, MD Supplement Editor
Dr Mughal has no relevant relationships to disclose.
S94 • Clinical Lymphoma & Myeloma Vol 7 Suppl 3 March 2007