Zonneville et al. show that p53 mutant cancers express high levels of the Base Excision Repair (BER) pathway and that deoxyuridine analogues induce DNA damage in p53-mutant TNBC cells. They exploit this genetic liability for therapeutic purposes using a combination of fluorinated deoxyuridine analogues and PARP1 inhibitors to target the BER pathway, inducing cytotoxicity and suppressing tumor growth in mice.
- Justin Zonneville
- Moyi Wang
- Andrei V. Bakin
