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• W4283076616 abstract "PARP inhibitors are synthetically lethal with BRCA1/2 mutations, and in this setting, accumulation of DNA damage leads to cell death. Because increased DNA damage and subsequent immune activation can prime an anti-tumor immune response, we studied the impact of olaparib ± immune checkpoint blockade (ICB) on anti-tumor activity and the immune microenvironment. Concurrent combination of olaparib, at clinically relevant exposures, with ICB gave durable and deeper anti-tumor activity in the Brca1m BR5 model vs. monotherapies. Olaparib and combination treatment modulated the immune microenvironment, including increases in CD8+ T cells and NK cells, and upregulation of immune pathways, including type I IFN and STING signaling. Olaparib also induced a dose-dependent upregulation of immune pathways, including JAK/STAT, STING and type I IFN, in the tumor cell compartment of a BRCA1m (HBCx-10) but not a BRCA WT (HBCx-9) breast PDX model. In vitro, olaparib induced BRCAm tumor cell-specific dendritic cell transactivation. Relevance to human disease was assessed using patient samples from the MEDIOLA (NCT02734004) trial, which showed increased type I IFN, STING, and JAK/STAT pathway expression following olaparib treatment, in line with preclinical findings. These data together provide evidence for a mechanism and schedule underpinning potential benefit of ICB combination with olaparib." @default.
• W4283076616 created "2022-06-19" @default.
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• W4283076616 date "2022-06-18" @default.
• W4283076616 modified "2023-10-12" @default.
• W4283076616 title "PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors" @default.
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• W4283076616 doi "https://doi.org/10.1080/2162402x.2022.2083755" @default.
• W4283076616 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35756843" @default.
• W4283076616 hasPublicationYear "2022" @default.
• W4283076616 type Work @default.
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