Investigators

Summary

DNA double-strand breaks (DSBs) are the most deleterious of DNA lesions and must be timely and accurately repaired to prevent genome instability. Telomeres, the ends of our linear chromosomes, resemble DSBs and must be protected from improper DNA damage signaling and repair. Telomeres also shorten with every cell division, which provides a tumor suppressor function, but critically short telomeres activate senescence and aging phenotypes. How DSBs are recognized and repaired but telomeres are protected from an improper DNA damage response is a major question in both cancer and aging biology. My laboratory combines cell biology, biochemistry, and single-molecule microscopy to answer these fundamental questions in order to understand the growth of cancer cells and develop new therapeutic avenues for targeting tumors.