Abstract
Tumors defective in homologous recombination (HR) are highly sensitive to poly ADP-ribose polymerase (PARP) inhibition, however the cell biological mechanisms underlying this synthetic lethality remain elusive. We recently identified that PARP inhibitor-induced DNA lesions persist until mitosis, subsequently causing mitotic chromatin bridges, multinucleation and apoptosis. Here, we discuss the implications of these findings.
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Schoonen, P. M., & van Vugt, M. A. T. M. (2018). Never tear us a-PARP: Dealing with DNA lesions during mitosis. Molecular and Cellular Oncology, 5(1). https://doi.org/10.1080/23723556.2017.1382670
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