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• W2767593721 abstract "Abstract Although PARP inhibitors (PARPi) target homologous recombination defective tumours, drug resistance frequently emerges, often via poorly understood mechanisms. Here, using genome-wide and high-density CRISPR-Cas9 “tag-mutate-enrich” mutagenesis screens, we identify close to full-length mutant forms of PARP1 that cause in vitro and in vivo PARPi resistance. Mutations both within and outside of the PARP1 DNA-binding zinc-finger domains cause PARPi resistance and alter PARP1 trapping, as does a PARP1 mutation found in a clinical case of PARPi resistance. This reinforces the importance of trapped PARP1 as a cytotoxic DNA lesion and suggests that PARP1 intramolecular interactions might influence PARPi-mediated cytotoxicity. PARP1 mutations are also tolerated in cells with a pathogenic BRCA1 mutation where they result in distinct sensitivities to chemotherapeutic drugs compared to other mechanisms of PARPi resistance ( BRCA1 reversion, 53BP1 , REV7 ( MAD2L2 ) mutation), suggesting that the underlying mechanism of PARPi resistance that emerges could influence the success of subsequent therapies." @default.
• W2767593721 created "2017-11-17" @default.
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• W2767593721 date "2018-05-10" @default.
• W2767593721 modified "2023-10-14" @default.
• W2767593721 title "Genome-wide and high-density CRISPR-Cas9 screens identify point mutations in PARP1 causing PARP inhibitor resistance" @default.
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• W2767593721 doi "https://doi.org/10.1038/s41467-018-03917-2" @default.
• W2767593721 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5945626" @default.
• W2767593721 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29748565" @default.
• W2767593721 hasPublicationYear "2018" @default.
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