Research interests: Studies of my research group are aimed at molecular details and interactions of the processes that generate mutations in the genome, particularly via the bypass of DNA damage during replication. The accumulation of mutations in somatic cells is essential for tumorigenesis. Often, cells acquire a mutator phenotype through the inactivation or modification of DNA damage tolerance pathways that enables them to accumulate further mutations in key cancer genes. Several distinct cellular mechanisms exist that enable the bypass of DNA damage during replication. We are studying each of these mechanisms using a range of biochemical, genetic and genomic approaches. We pioneered the use of whole genome sequencing in cell lines to measure the mutagenic effect of the loss of various DNA repair capabilities. We use cell culture experiments to model the mutagenic processes that take place in tumours, to help treatment selection based on the cancer mutation patterns. We also work with clinicians on the analysis of tumour genomic data to better understand the aetiology, the effect of mutagenic treatments and the evolution of resistance.