Back

A Population-Specific PARP1 Gene Variation Modulates PARP Trapping

Cai, J.; Billur, R.; Cohen, M. S.; Ladurner, A. G.; Black, B. E.

2025-11-13 cancer biology
10.1101/2025.11.11.687916 bioRxiv
Show abstract

Poly-(ADP-ribose) polymerase inhibitors (PARPi) block NAD+-binding pocket of PARP1, inhibiting PAR synthesis. However, they differ in their ability to retain PARP1 on damaged DNA to induce synthetic lethality in homologous recombination-deficient (HRD) cancer. Allosteric enzymatic activation requires destabilization of the helical domain (HD) of PARP1 and is indispensable for activation and chromatin retention induced by distinct PARPi. Here we report that the effect of the clinical PARPi talazoparib is robustly impacted by a common human polymorphism within the HD. PARP1V762 greatly enhanced talazoparib-driven allosteric retention on chromatin, prolonged XRCC1 recruitment, and enhanced cell killing. Talazoparib switches from Type-II PARPi behavior in PARP1A762 to allosteric, pro-retention Type-I behavior for PARP1V762. Thus, both PARPi efficacy and dose-limiting tolerability depends on PARP1 allele, motivating variant-guided cancer therapies. TEASEROne of the four FDA-approved PARPi drugs, talazoparib, is modulated by a PARP1 SNP that is widespread in the population.

Matching journals

The top 3 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.