Research in our lab is focused on the DNA Double Strand Break (DSB) repair response in mammalian cells. DNA DSB’s are critical lesions for a cell and can lead to cell death if left unrepaired. Alternatively, if repaired incorrectly, a DSB can result in mutagenic consequences leading normal cells down a path to tumorigenesis.
We are currently investigating the role BRCA2 (breast cancer susceptibility gene 2) plays in the DSB response as well as its role in homologous recombination (HR). People who inherit a deleterious mutation in the BRCA2 gene are at an incredibly high lifetime risk for breast, ovarian, and other types of cancer. We are particularly interested in the molecular pathogenic events that lead to such a high risk for cancer in the absence of functional BRCA2.
- Biochemical and genetic characterization of tumor associated mutations in the BRCA2 gene.
- Genetic screens to further understand the molecular pathogenesis leading to tumor formation in BRCA2 carriers.
- Proteomic strategies to identify novel proteins that interact with BRCA2 after DNA damage.
- Identifying mechanisms and proteins that govern the regulatory decision between HR and NHEJ after a DSB is generated in mammalian cells.