Myc activation in breast cancer is due to p53-loss and sustains self-renewal of cancer stem cells (ChIP-Seq). Mus musculus

Purpose: discover the downstream pathways and the mechanism of target activation by the p53:Myc axis in normal mammary and cancer stem cells Methods: we performed ChIPseq experiments from NMuMG cells grown in adhesion under standard conditions Results: the p53:Myc axis orchestrates its transcriptional response in mammary-epithelial cells via a dual and overlapping mechanism: i) a tightly controlled epistasis driven by p53 and executed by Myc, and ii) a co-operative double occupancy of their downstream effectors at different regulatory regions Overall design: Examination p53 and Myc binding sites in murine mammary epithelial cells