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Our laboratory focuses on understanding the molecular mechanisms of DNA double-strand break repair in mammalian cells, which has a significant impact on cancer etiology and cancer treatment.

Genome instability is a hallmark of cancer cells and DNA double-strand breaks are a major source to induce genome instability. We have established a series of unique EGFP-based reporters to monitor different DSB repair pathways. Using a combination of genetics and molecular and cellular biology approaches, we study not only the major DSB repair pathways commonly used in normal cells, but also error-prone alternative DSB pathways often elevated during oncogenesis. In this process, we have identified new targets in double-strand break repair network that can be used for synthetic-lethality strategies of targeted cancer treatment. We are also developing our reporter systems for screening and working with experts in chemistry and structural biology to identify leads of small molecule inhibitors for translational research.