In APL patients, focal somatic mutations or germinal SNP in cis-regulatory regions disrupt MYB binding, reduce H3K27ac/H3K4me chromatin signatures of active enhancers, and disrupt interaction with the proximal promoter, all yielding WT1 repression.
In APL patients, focal somatic mutations or germinal SNP in cis-regulatory regions disrupt MYB binding, reduce H3K27ac/H3K4me chromatin signatures of active enhancers, and disrupt interaction with the proximal promoter, all yielding WT1 repression.