Katerina I. Leonova

This paper investigates why oncogenic mutations often fail to induce cancer by showing that normal cells undergo a transient, plastic state but are constrained by lineage-specific barriers preventing stable transformation.

The paper introduces an image-based method to measure chromatin accessibility using DNA-binding fluorescent molecules and finds higher accessibility in tumor compared to normal cells.

The paper compares the cellular response to DNA damage and chromatin damage using bleomycin and curaxin, finding distinct p53-dependent and -independent effects.

The paper shows that chromatin destabilizing drugs like curaxin induce an interferon response (TRAIN) through repeat transcription, independent of p53 status, and may prevent cancer by eliminating epigenetically unstable cells.