FLT3 activating mutations are in general rare in ALL, but have been detected in approximately 20% of ALL specimens, with rearrangement of the MLL gene,37,79,80 25% of hyperdiploid ALL,8081 and in the rare subset of CD117/KIT-positive, CD3-positive ALL.82 Interestingly, the internal tandem duplication of the FLT3 gene, commonly detected in AML, has thus far not been seen in ALL. FLT3 inhibitors (e.g., PKC412 and CEP-701) can suppress FLT3--positive ALL cells in vitro and therefore warrant clinical trials.79 83

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