Overview
We study polymerase theta (POLQ) and the error-prone microhomology-mediated end-joining pathway to uncover synthetic lethal interactions that can be exploited in homologous-recombination-deficient (HRD) tumors.
Approach
Tumors that lose homologous recombination become dependent on backup repair pathways such as POLQ-mediated end joining. Disabling that backup is selectively lethal to the cancer cell while sparing normal tissue.
This strategy complements PARP inhibition and our DNA Damage Repair & PARP-Immunotherapy program, offering a route to extend benefit in HRD tumors and to address PARP resistance.