The genome of every cell is constantly exposed to endogenous and exogenous factors that directly damage DNA. Their misrepair can trigger genome rearrangements that cause a plethora of inherited human syndromes with life-threatening complications including cancer, immunodeficiency and premature ageing. To prevent catastrophic changes to the information encoded in our DNA a complex network of proteins has evolved to maintain genome integrity. A characteristic feature of cancer cells is a breakdown of the repair processes, which leads to the genome becoming unstable, a process that is essential for tumourigenesis.
Our research focuses on understanding the basic molecular mechanisms by which cells detect and repair damaged DNA, and how to exploit this knowledge to improve cancer therapies.
We are particularly interested in how the repair of damaged DNA is executed during the process of genome duplication, and how chromosomal stability is achieved under stressful conditions. To address these questions, we employ state-of-the art techniques including monitoring of DNA replication at the single molecule level in living cells, isolation of proteins on newly replicated DNA (to identify novel components of the replication machinery) and super-resolution microscopy for live-cell imaging.
A long-term goal of our research is to elucidate the mechanisms by which cells maintain integrity of their genetic information and translate these basic scientific findings into the development of novel therapies for cancer.