Chromatin interactions of the EVI1 oncogene in myeloid leukaemia (ChIP-Seq)

EVI1 expression is associated with poor prognosis in myeloid leukaemia. Aberrant expression can result from Chr.3q alterations, which cause juxtaposition of enhancers that induce EVI1 activation via long-range chromatin interactions. More often, however, EVI1 expression occurs unrelated to 3q alterations, and it is unclear if its expression underlies similar dependencies as 3q+ cells. As enhancers regulate promoters by physical interaction/chromatin looping, we explored if the EVI1 promoter in EVI1+3q- cells interacts with distally located chromatin and if these intereactions promote EVI1 expression. To monitor if these interactions involve active chromatin, we further performed H3K27ac-ChIP-Seq. Overall design: For this sample set, we performed ChIP-Seq using H3K27ac antibodies (abcam ab4729) as previously described (Boulianne et al, doi:10.1016/j.celrep.2017.01.057) using formaldehyde crosslinked DNA from CML patients' leukaemia cells.