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Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell disorder characterized by the fusion of the Abelson murine leukemia (ABL) gene on chromosome 9 with the breakpoint cluster region (BCR) gene on chromosome 2 which results in expression of an oncoprotein, termed BCR-ABL tyrosine kinase that plays a causal role in the pathogenesis of the disease. Until a little more than a decade ago, drug therapy for CML was limited to nonspecific agents such as busulfan, hydroxyurea, and interferon-alfa (INF-a). The landscape changed dramatically with the development of small molecule tyrosine kinase inhibitors (TKIs) that share the same therapeutic target, BCR-ABL and act by inhibiting its kinase activity. Evidence now is rising that the achievement of a reduced disease burden early in treatment with TKIs predicts a favorable long-term outcome, and that patients who show suboptimal responses to TKI therapy may benefit from treatment modifications. Therefore, the consistent use of accurate and reproducible techniques to adequately monitor treatment responses and minimal residual disease becomes a critical component of care in the management of patients with CML
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