Chronic Myeloid Leukemia by Jorge Cortes, Michael Deininger

By Jorge Cortes, Michael Deininger

power Myeloid Leukemia (CML) continues to be a key version for the enhanced knowing of the pathophysiology of a malignancy at a molecular point and has been utilized by researchers to boost various treatments and healing review tools. This concise, readable advisor assembles and synthesizes the newest advancements and traits within the therapy of CML and offers an authoritative and handy precis of the newest development in imatinib trials, the molecular tracking of CML responses, and the engineering of recent cures to beat resistance and increase sufferer care.

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Lancet 1984; 1:665– 668. 26. Passweg JR, Rowlings PA, Horowitz MM. Related donor bone marrow transplantation for chronic myelogenous leukemia. Hematol Oncol Clin North Am 1998; 12:81 – 92. 27. Monitoring treatment and survival in chronic myeloid leukemia. Italian Cooperative Study Group on Chronic Myeloid Leukemia and Italian Group for Bone Marrow Transplantation. J Clin Oncol 1999; 17:1858– 1868. 28. Gratwohl A, Brand R, Apperley J, et al. Graft-versus-host disease and outcome in HLA-identical sibling transplantations for chronic myeloid leukemia.

28. Huntly BJ, Reid AG, Bench AJ, et al. Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia. Blood 2001; 98:1732– 1738. 29. Huntly BJ, Guilhot F, Reid AG, et al. Imatinib improves but may not fully reverse the poor prognosis of patients with CML with derivative chromosome 9 deletions. Blood 2003; 102:2205– 2212. 30. Quintas-Cardama A, Kantarjian H, Talpaz M, et al. Imatinib mesylate therapy may overcome the poor prognostic significance of deletions of derivative chromosome 9 in patients with chronic myelogenous leukemia.

Patients who previously received treatment with IFN-a and sustain grade 3 or 4 neutropenia or thrombocytopenia on IM generally have a lower incidence of major or complete cytogenetic remission and shorter progression free survival than those without hematologic toxicity (74– 76). The outlook for newly diagnosed patients who sustain major degrees of hematologic toxicity is not necessarily inferior to that of those who tolerate the drug well. 0 Â 109/L. Paradoxically thrombocytopenia may on occasion also respond to G-CSF.

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