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Somatically acquired translocations play a major role in the pathogenesis of human leukemias. These rearrangements frequently alter the structure or expression of genes encoding key regulatory proteins involved in normal hematopoiesis. Analysis of these proteins in the human leukemias and in genetically manipulated mouse models has greatly increased our understanding of the mechanisms of leukemogenesis. This information also has led to improvements in our ability to deliver the optimal treatment intensity to individual patients and to the development of novel leukemia-specific therapies.
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Rubnitz et al. (1998) studied this question.
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