Institute website

My group has a long-standing interest in a transcription factor called Myc, which is also an important oncogene in human cancer. We use Myc as a paradigm to understand how specific chromatin environments – or epigenetic states – determine recognition of transcription factor-binding sites in the human and mouse genomes, and how transcription factors further modify chromatin to regulate gene expression. When its activity becomes uncontrolled, Myc deregulates cell cycle progression and induces malignant transformation, but concomitantly elicits compensatory tumor suppressor mechanisms (apoptosis, senescence and DNA damage responses). We are particularly interested in the role of chromatin-modifying enzymes, such as histone acetyl- and methyl-transferases, in those biological responses.