ArticleNature communications2022
STING agonism reprograms tumor-associated macrophages and overcomes resistance to PARP inhibition in BRCA1-deficient models of breast cancer.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 2 of them syntheses that pooled it.
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Who cites it
142 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Targeting DNA damage response to enhance cancer immunotherapy efficacy: molecular mechanisms and clinical advances.Medical oncology (Northwood, London, England) · 2025Pooled it
- Prognostic significance of STING expression in solid tumor: a systematic review and meta-analysis.Frontiers in oncology · 2023Pooled it
- Niraparib and dostarlimab for the treatment of recurrent platinum-resistant ovarian cancer: results of a Phase II study (MOONSTONE/GOG-3032).Gynecologic oncology · 2023Trial
- Dual metabolic checkpoint blockadeBioactive materials · 2027Article
- Reprogramming tumor-associated macrophages in breast cancer: from myeloid plasticity and tumor-promoting programs to CAR-macrophage therapy.Journal of hematology & oncology · 2026Review
- CCNE1 overexpression drives a cGAS-STING-dependent interferon response and sensitizes HRD-positive ovarian cancer to immune checkpoint blockade.Journal for immunotherapy of cancer · 2026Article
- The dual immune landscape of homologous recombination-deficient tumors: mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- Rejuvenating endogenous antitumor immunity via a chimeric receptor-engineered oncolytic virus targeting tumor-associated macrophages.Science advances · 2026Article
- Photothermal-driven sequential immunotherapy overcomes resistance to PARP inhibition inActa pharmaceutica Sinica. B · 2026Article
- The DNA damage response and cancer immunotherapy.Nature reviews. Cancer · 2026Review
- Self-assembled supramolecular nanoparticles ofActa pharmaceutica Sinica. B · 2026Article
- PARP inhibitor YCH1899 activates type I interferon signaling and synergizes with STING agonists in BRCA-proficient tumors.Molecular biomedicine · 2026Article
- Histone H4 lysine 20 tri-methylation safeguards breast cancer lineage fidelity and unfolded protein response.Nature communications · 2026Article
- Extracellular vesicle-mediated suppression of macrophage STING signaling promotes immune dysfunction in dedifferentiated liposarcoma.bioRxiv : the preprint server for biology · 2026Article
- Cell Selective STING-Activating Polysaccharide Immunomodulators for Cancer Therapy.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026Article
- Discovery of a non-canonical TREM2-S100A9 axis that drives pro-tumorigenic macrophage polarization and sensitizes ovarian clear cell carcinoma to IL-17 blockade.Cell death discovery · 2026Article
- Insights from three decades of BRCA1/2 modeling in mice.Nature genetics · 2026Review
- Tumor cell intrinsic dsRNA innate immune response triggered by PARP inhibitor is compromised in BRCA1-deficient breast cancer by repressing IRF3.Protein & cell · 2026Article
- C92, a proton channel-blocking allosteric STING agonist generates robust antitumor activity.Journal for immunotherapy of cancer · 2026Article
82 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
PARP inhibitors (PARPi) have drastically changed the treatment landscape of advanced ovarian tumors with BRCA mutations. However, the impact of this class of inhibitors in patients with advanced BRCA-mutant breast cancer is relatively modest. Using a syngeneic genetically-engineered mouse model of breast tumor driven by Brca1 deficiency, we show that tumor-associated macrophages (TAMs) blunt PARPi efficacy both in vivo and in vitro. Mechanistically, BRCA1-deficient breast tumor cells induce pro-tumor polarization of TAMs, which in turn suppress PARPi-elicited DNA damage in tumor cells, leading to reduced production of dsDNA fragments and synthetic lethality, hence impairing STING-dependent anti-tumor immunity. STING agonists reprogram M2-like pro-tumor macrophages into an M1-like anti-tumor state in a macrophage STING-dependent manner. Systemic administration of a STING agonist breaches multiple layers of tumor cell-mediated suppression of immune cells, and synergizes with PARPi to suppress tumor growth. The therapeutic benefits of this combination require host STING and are mediated by a type I IFN response and CD8
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