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One of Dr Hirai's major research projects was elucidation of the mechanisms of action of the AML1/Runx1 gene product. Through the study of certain leukemias with t(12;21)(p13;q22), including myelodysplastic syndrome (MDS) or progression of chronic myelogenous leukemia to blastic crisis, he and his colleagues identified the AML1-Evi-1 fusion gene. This finding was reported in the EMBO Journal (1994). Subsequently, the group studied the function of the AML1 gene, and found that the AML1-Evi-1 fusion protein binds to the promoters of AML1-target genes, but that it interferes with the transcriptional activity of native AML1. Although its functional importance is still not fully understood, the research team also found that AML1 is phosphorylated by ERK upon stimulation by growth factors. Recently, Dr Hirai became interested in the in vivo function of AML1 during the process of hematopoiesis. Despite his untimely death, some interesting studies using tissue-specific gene targeting in mice are continuing.
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European Journal of Cancerno. SUPnan (2014): 142-143
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