The main objective of our research is to better understand the molecular mechanisms responsible for the maintenance of genome stability. These controls are lost in cancer, which is characterized by genomic instability.

Specifically, we are studying:

• The mechanism of DNA double-strand break (DSB) repair, in particular the early processing events that are critical to determine repair pathway choice. We utilize biochemical approaches in cell-free extracts derived from the eggs of the vertebrate, Xenopus laevis, proteomics analysis as well as small molecules that regulate the response to DSBs.
• The mechanism(s) of DNA Inter-strand Crosslink (ICL) repair. These lesions are generated by several classes of successful chemotherapeutic drugs. Understanding signaling from these lesions and their modes of repair is critical to develop more effective compounds and to circumvent resistance.
• DNA replication stress and DNA damage resulting from oncogene activation. We are focusing on the case of c-Myc