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• W2769136370 abstract "Abstract Transplantable murine models of ovarian high grade serous carcinoma (HGSC) remain an important research tool. We previously showed that ID8, a widely-used syngeneic model of ovarian cancer, lacked any of the frequent mutations in HGSC, and used CRISPR/Cas9 gene editing to generate derivatives with deletions in Trp53 and Brca2 . Here we have used one ID8 Trp53 −/− clone to generate further mutants, with additional mutations in Brca1 , Pten and Nf1 , all of which are frequently mutated or deleted in HGSC. We have also generated clones with triple deletions in Trp53 , Brca2 and Pten . We show that ID8 Trp53 −/− ; Brca1 −/− and Trp53 −/− ; Brca2 −/− cells have defective homologous recombination and increased sensitivity to both platinum and PARP inhibitor chemotherapy compared to Trp53 −/− . By contrast, loss of Pten or Nf1 increases growth rate in vivo , and reduces survival following cisplatin chemotherapy in vivo . Finally, we have also targeted Trp53 in cells isolated from a previous transgenic murine fallopian tube carcinoma model, and confirmed that loss of p53 expression in this second model accelerates intraperitoneal growth. Together, these CRISPR-generated models represent a new and simple tool to investigate the biology of HGSC, and the ID8 cell lines are freely available to researchers." @default.
• W2769136370 created "2017-12-04" @default.
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• W2769136370 date "2017-12-04" @default.
• W2769136370 modified "2023-10-18" @default.
• W2769136370 title "CRISPR/Cas9-derived models of ovarian high grade serous carcinoma targeting Brca1, Pten and Nf1, and correlation with platinum sensitivity" @default.
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• W2769136370 doi "https://doi.org/10.1038/s41598-017-17119-1" @default.
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