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[Different mechanisms for CBF?-MYH11 function in acute myeloid leukemia with inv(16) have been proposed such as tethering of RUNX1 outside the nucleus, interference with transcription factor complex assembly and recruitment of histone deacetylases, all resulting in transcriptional repression of RUNX1 target genes.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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