| Autor: |
Schoonen PM; Department of Medical Oncology, University Medical Center Groningen, University of Groningen. Hanzeplein 1, Groningen, the Netherlands., van Vugt MATM; Department of Medical Oncology, University Medical Center Groningen, University of Groningen. Hanzeplein 1, Groningen, the Netherlands. |
| Jazyk: |
angličtina |
| Zdroj: |
Molecular & cellular oncology [Mol Cell Oncol] 2017 Oct 31; Vol. 5 (1), pp. e1382670. Date of Electronic Publication: 2017 Oct 31 (Print Publication: 2018). |
| DOI: |
10.1080/23723556.2017.1382670 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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