MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state [ChIP-seq]

We address the molecular mechanisms through which MYC promotes loss of cell identity and acquisition of stem cell-like traits, favouring the onset of tumorigenesis, by performing epigenetic profile analyses in a transition from WT IMEC, IMEC over-expressing MYC and mammospeheres formed from IMEC-MYC (named M2). Overall design: ChIP-seq for H3K4me3, H3K4me1, H3K27ac and MYC binding in WT IMEC, IMEC-MYC and M2 mammospheres