Cellular function depends on genome integrity, which must be preserved, at great metabolic and other cost, for the entire lifespan of an organism. Defects in the way cells repair or respond to different DNA damages are associated with increased genomic instability and have been linked to human pathology, heritable cancers, and premature aging syndromes with severe neurological abnormalities.

Our research focuses on the investigation of cellular DNA damage responses and their impact on genetic and epigenetic defects and the mechanisms of aging and disease.

Research covers the study of the molecular events that couple arrest of active transcription to chromatin alteration and repair in healthy versus disease situations. In particular, we are interested to identify the regulatory cascades involved in the interplay between genomic stability and active transcription with ultimate goal to gain in depth knowledge of the underlying causes of related disorders and explain their clinical features.
Moreover, our studies involve the exploration of the role of transcription in chemotherapeutic agent-driven cytotoxicity. In addition, the role of tumor-driven chromatin modifications in gene expression, DNA repair efficacy and cellular chemosensitivity is under investigation.
Employing advanced proteomics and high-throughput genomic approaches, we aim to decipher the mechanisms underlying genetic versus epigenetic mechanisms in oncogenesis and cancer therapy.

Fousteri research