Never tear us a-PARP: Dealing with DNA lesions during mitosis

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, sub...

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Detalles Bibliográficos
Autores principales: Schoonen, Pepijn M., van Vugt, Marcel A.T.M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2017
Materias:
Author's Views
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5791853/
https://www.ncbi.nlm.nih.gov/pubmed/29404385
http://dx.doi.org/10.1080/23723556.2017.1382670
Descripción
Sumario: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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