Robert Wood Johnson Medical School
Department of Radiation Oncology
Cancer Institute of New Jersey
195 Little Albany Street
New Brunswick, NJ 08903
Genomic instability and tumorigenesis; DNA repair, recombination, and replication fidelity; Targets and biomarkers for DNA damage based cancer therapeutics
Genomic instability is a major driving force for tumorigenesis. Mammalian cells use several mechanisms to maintain their genomic stability, including high fidelity DNA replication in S-phase, accurate chromosome segregation in M-phase, precise and error-free repair of DNA damage throughout the cell cycle, and a series of highly coordinated cell cycle events. Homologous recombination (HR) often precisely repairs DNA double strand breaks, and restarts stalled replication forks to ensure the fidelity of DNA replication and to enable accurate chromosome segregation in mitosis. One aspect of our research focuses how HR factors work together to maintain the stability of the genome. One such protein is BCCIP (BRCA2 and CDKN1A Interacting Protein). Our works have shown that BCCIP regulates HR, cell cycle, mitosis, and other processes that are essential for the genome stability and cell viability. Currently, biochemical, cell and molecular biology, and transgenic mouse approaches are being used to further characterize BCCIP functions and activities, and to elucidate its roles in tumorigenesis and development.
Another aspect of our research focuses on characterizations of molecular targets and biomarkers that can be used to guide precision cancer therapy, especially for DNA damage based therapeutics. We are interested in developing new strategies that can differentiate cancer and normal cell sensitivities to DNA damage, and to validate new biomarkers that can predict clinical outcomes of therapeutic DNA damage.