In normal and cancer cells, DNA is subjected to damage from many sources, including inescapable chemical reactions with oxygen and water. Other sources of DNA damage include ionizing radiation, ultraviolet radiation from the sun, and chemicals from the environment. If DNA is not repaired, genomes will gradually decay, lose normal function, and accumulate mutations (changes in DNA sequence). Such mutations are a central driving force in cancer.
Fortunately, our cells have numerous strategies for repair of DNA damage, and devote many genes and proteins to the machinery of DNA repair. It is important to understand the mechanisms of DNA repair in detail, because this process is a front-line defense against the mutations that cause cancer. Moreover, the aim of many cancer therapies is to disable tumor DNA by using radiation and drugs. It is crucial to understand exactly how cancer cells respond to DNA damage, and how to increase the effectiveness of DNA-damaging treatments.
Research in our group explores the mechanisms of genome stability and the consequences for cancer, including the biochemical mechanism of repair of cross-links between DNA strands and the DNA polymerases that help cells tolerate DNA damage.