1) Genome instability gene functions in mitochondria, which we found suppress inflammation. We examine how breast cancer susceptibility genes (BRCA) and Fanconi Anemia suppressors function at mitochondrial DNA replication forks to control the immune response and metabolism, and how patient mutations can derail such control.
2) The molecular cause for Fanconi Anemia and hereditary heme malignancies for insights on cancer biology. We test patient samples and have established an exciting Fanconi Anemia mouse model recapitulating key features of the human disease to understand cause and effect.
3) BRCA/p53 collaborations at the DNA replication fork. We identified unexpected roles for BRCA and p53 in replication stability. We are investigating how genome stability proteins function at the replication fork and how this determines therapy response and resistance.