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The past three decades have seen considerable advances in our understanding of the underlying mechanisms of acute myeloid leukemia (AML) and dramatic improvements in treatment. At present, decisions about therapy are largely based on prognostic factors identified at the time of diagnosis or shortly thereafter. These features include age, the karyotype of the leukemic clone, the initial leukocyte count, and the response to induction chemotherapy. Karyotypic analysis is particularly important, because it not only provides a key prognostic indicator but also serves to identify biologically distinct subgroups of AML, which in some instances require specific types of treatment.1 All-trans . . .
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Grimwade et al. (2004) studied this question.
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