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The human translocation (t8;21) is associated with approximately 12% of the
cases of acute myelogenous leukemia. Two genes, AML1 and ETO, are fused together
at the translocation breakpoint, resulting in the _expression_ of a chimeric
protein called AML1-ETO. AML1-ETO is thought to interfere with normal AML1
function, although the mechanism by which it does so is unclear. Here, we have
used Drosophila genetics to investigate two models of AML1-ETO function. In the
first model, AML1-ETO is a constitutive transcriptional repressor of AML1 target
genes...
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