Recently, Mueller et al[1][1] found PU.1 mutations in 7% of the 126 cases of acute myeloid leukemia (AML) they analyzed. DNA binding and transactivation of the M-CSF receptor promoter, a direct PU.1 target gene, were deficient in the 7 mutants that affected the DNA-binding domain of the PU.1. Those
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Lamandin et al. (2002) studied this question.
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