Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

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Items 901–1,000 of 1,042

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  9. Inhibitors of PARP: Number crunching and structure gazing
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  10. Outcome of triple-negative breast cancer in patients with or without deleterious BRCA mutations
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  15. Endogenous DNA 3′ Blocks Are Vulnerabilities for BRCA1 and BRCA2 Deficiency and Are Reversed by the APE2 Nuclease
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  16. Ten-year survival after epithelial ovarian cancer is not associated with BRCA mutation status
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  17. CtIP-mediated resection is essential for viability and can operate independently of BRCA1
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  18. The Predominant Role of Surgery in the Prevention and New Trends in the Surgical Treatment of Women With BRCA1/2 Mutations
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  51. DNA Repair Proteins as Molecular Targets for Cancer Therapeutics
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  52. A phosphorylation–deubiquitination cascade regulates the BRCA2–RAD51 axis in homologous recombination
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  53. An update on PARP inhibitors for the treatment of cancer
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  54. The DNA damage signalling kinase ATM is aberrantly reduced or lost in BRCA1/BRCA2-deficient and ER/PR/ERBB2-triple-negative breast cancer
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  59. Doubling Down on the PI3K-AKT-mTOR Pathway Enhances the Antitumor Efficacy of PARP Inhibitor in Triple Negative Breast Cancer Model beyond BRCA-ness
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