Epigenetic heterogeneity in cancer


Tumour initiation entails loss of cellular identity and acquisition of uncontrolled self-renewal ability. We are interested in studying how epigenetics promote this oncogenic reprogramming process.

We are currently performing unbiased, CRISPR/Cas9-based, loss-of-function screens targeting proteins involved in establishment and recognition of DNA methylation patterns, writer, readers and erasers of chromatin marks, chromatin remodelers and proteins controlling the high-order structure of chromatin, in order to identify epigenetic regulators which either prevent (tumour suppressors) or promote (therapeutic targets) tumorigenesis.