My broad goal is to understand the mechanisms of homologous recombination and DNA repair in human cells and translate the basic studies’ results into development of novel cancer therapies. I have more than 20 years of experience in the field of homologous recombination and DNA repair, with specific expertise in the biochemistry of homologous recombination proteins, including RAD51, RAD52, and RAD54. Homologous recombination is responsible for repairing the most harmful type of DNA damage, double-stranded breaks and inter-strand cross-links, faithful homologous chromosome segregation during meiosis, and telomere maintenance. As a postdoc at the University of California Davis, I studied several key homologous recombination proteins. As a faculty at Drexel University College of Medicine, I focus my research program on understanding the mechanisms of HR in humans and the development of small-molecule inhibitors of the major HR proteins, RAD51, RAD52, and RAD52, for anticancer therapy. As a PI or co-PI on several NIH, Leukemia and Lymphoma Society, KECK Foundation, Basser Foundation, Coulter program, and Drexel-funded grants, I laid the groundwork for future research by developing the biochemical and cellular assays that are required for the analysis of the mechanisms of HR and development of small molecule inhibitors. We have produced multiple peer-reviewed publications from each project and have authored or co-authored 36 papers over the past 10 years, including those published in Nature, Molecular Cell, Nature Structural and Molecular Biology, Nature Communications, Genes and Development, and PNAS. I have trained 18 pre-doctoral and 9 postdoctoral fellows in my lab. I have an extensive experience in collaborative research. In particular, I have more than 5 years of collaboration experience with Dr. Du, the PI of the current proposal. At UT Health San Antonio, I continue my nationally recognized program in understanding the mechanisms of DNA repair in human cells and the development of specific inhibitors as novel cancer therapeutics with a specific focus on BRCA-deficient breast and ovarian cancer. The current proposal is an extension of my research on the development of specific inhibitors of RAD52, whose inactivation induces synthetic lethality in BRCA-deficient cancers. I am the recipient of a Recruitment of Established Investigators Award from the Cancer Prevention and Research Institute of Texas (CPRIT). I have established a strong collaboration with Drs. Patrick Sung, Weixing Zhao and Sandeep Burma, co-leaders of this project, as evidenced by our joint publications. I also have regular (at least once a month) video conferences with Drs. Dipanjan Chowdhury and Panagiotis Konstantinopoulos, co-leaders of Project 1, with whom we discuss the experimental design of the proposed studies and our recent results supporting the current proposal. In summary, I have the expertise, leadership, and motivation to conduct collaborative research on DNA repair and tumorigenesis.