- 2007 - Ph.D. - Cellular and Molecular Biology - University of Michigan
- 2000 - B.A. - Biology - Lawrence University
Research & Grants
Double-strand breaks (DSBs) can arise in DNA from endogenous sources and exogenous toxins, and DNA damaging agents are used as chemotherapeutics to selectively target cancer cells. In the typical cell, DSBs are commonly induced by reactive oxygen species generated by metabolism. These, as well as breaks caused by ionizing radiation and other clastogens used in cancer chemotherapy, are typically complex, often containing clusters of damaged bases at their termini. My current work focuses on how complex lesions affect the initiation of DSB repair by homologous recombination.