PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors

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...

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Main Authors: Anna D. Staniszewska, Joshua Armenia, Matthew King, Chrysiis Michaloglou, Avinash Reddy, Maneesh Singh, Maryann San Martin, Laura Prickett, Zena Wilson, Theresa Proia, Deanna Russell, Morgan Thomas, Oona Delpuech, Mark J. O’Connor, Elisabetta Leo, Helen Angell, Viia Valge-Archer
Format: Article
Language:English
Published: Taylor & Francis Group 2022-12-01
Series:OncoImmunology
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Online Access:https://www.tandfonline.com/doi/10.1080/2162402X.2022.2083755
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author Anna D. Staniszewska
Joshua Armenia
Matthew King
Chrysiis Michaloglou
Avinash Reddy
Maneesh Singh
Maryann San Martin
Laura Prickett
Zena Wilson
Theresa Proia
Deanna Russell
Morgan Thomas
Oona Delpuech
Mark J. O’Connor
Elisabetta Leo
Helen Angell
Viia Valge-Archer
author_facet Anna D. Staniszewska
Joshua Armenia
Matthew King
Chrysiis Michaloglou
Avinash Reddy
Maneesh Singh
Maryann San Martin
Laura Prickett
Zena Wilson
Theresa Proia
Deanna Russell
Morgan Thomas
Oona Delpuech
Mark J. O’Connor
Elisabetta Leo
Helen Angell
Viia Valge-Archer
author_sort Anna D. Staniszewska
collection DOAJ
description 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.
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spelling doaj-art-42e14e70567c4dc0ac16e7566635a8442025-08-20T02:56:37ZengTaylor & Francis GroupOncoImmunology2162-402X2022-12-0111110.1080/2162402X.2022.2083755PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumorsAnna D. Staniszewska0Joshua Armenia1Matthew King2Chrysiis Michaloglou3Avinash Reddy4Maneesh Singh5Maryann San Martin6Laura Prickett7Zena Wilson8Theresa Proia9Deanna Russell10Morgan Thomas11Oona Delpuech12Mark J. O’Connor13Elisabetta Leo14Helen Angell15Viia Valge-Archer16Early Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Boston, MA, USAEarly Oncology, Oncology R&D, AstraZeneca, Boston, MA, USAEarly Oncology, Oncology R&D, AstraZeneca, Boston, MA, USAEarly Oncology, Oncology R&D, AstraZeneca, Boston, MA, USAEarly Oncology, Oncology R&D, AstraZeneca, Alderley Park, Macclesfield, UKEarly Oncology, Oncology R&D, AstraZeneca, Boston, MA, USAEarly Oncology, Oncology R&D, AstraZeneca, Boston, MA, USAEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKEarly Oncology, Oncology R&D, AstraZeneca, Cambridge, UKPARP 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.https://www.tandfonline.com/doi/10.1080/2162402X.2022.2083755PARP inhibitorolaparibcGAS-STINGimmune checkpoint blockadeBRCA
spellingShingle Anna D. Staniszewska
Joshua Armenia
Matthew King
Chrysiis Michaloglou
Avinash Reddy
Maneesh Singh
Maryann San Martin
Laura Prickett
Zena Wilson
Theresa Proia
Deanna Russell
Morgan Thomas
Oona Delpuech
Mark J. O’Connor
Elisabetta Leo
Helen Angell
Viia Valge-Archer
PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors
OncoImmunology
PARP inhibitor
olaparib
cGAS-STING
immune checkpoint blockade
BRCA
title PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors
title_full PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors
title_fullStr PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors
title_full_unstemmed PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors
title_short PARP inhibition is a modulator of anti-tumor immune response in BRCA-deficient tumors
title_sort parp inhibition is a modulator of anti tumor immune response in brca deficient tumors
topic PARP inhibitor
olaparib
cGAS-STING
immune checkpoint blockade
BRCA
url https://www.tandfonline.com/doi/10.1080/2162402X.2022.2083755
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