​Epigenetic plasticity has been associated with nongenomic adaptive resistance in multiple tumor types. It leads to a highly dynamic phenotypic evolution of cancer cells in response to physical and molecular perturbations, significantly confounds interpretations of therapy responses, and contributes to the resistance development.

Using joint information theoretic approaches, coupled with single cell multi-omics analysis as well as epigenetic sequencing technologies, we interrogate the detailed molecular machinery of the drug-induced epigenetic remodeling and identify effective drug targets to arrest the tumor epigenetic plasticity.