ArticleNature communications2023
PARP14 inhibition restores PD-1 immune checkpoint inhibitor response following IFNγ-driven acquired resistance in preclinical cancer models.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- PARP7 inhibitors enhance the immunogenic effects of radiation in pancreatic cancer cells.Molecular therapy. Oncology · 2026Article
- Inflammatory cytokines induce new cancer dependencies.Nature genetics · 2026Article
- Structure, function, regulation, evolution, and therapeutic implications of PARP14.Genes & development · 2026Review
- Immune checkpoint inhibitors in dMMR-MSI-H colorectal cancer: rationale, progress and prospects.Frontiers in immunology · 2026Review
- Transcriptome-wide Mendelian randomization and single-cell analysis during CD4NPJ precision oncology · 2025Article
- Targeting MARylation and DePARylation in Cancer Therapy: New Promising Therapeutic Opportunities.Cancers · 2025Review
- PARP‑1 in liver diseases: Molecular mechanisms, therapeutic potential and emerging clinical applications (Review).Molecular medicine reports · 2025Review
- Sigma1 inhibitor suppression of adaptive immune resistance mechanisms mediated by cancer cell derived extracellular vesicles.Cancer biology & therapy · 2025Article
- Systemic immunosuppression from ultraviolet radiation exposure inhibits cancer immunotherapy.Journal for immunotherapy of cancer · 2025Article
- Article
- BALs are prognostic biomarkers and correlate with malignant behaviors in breast cancer.BMC cancer · 2025Article
- Mono-ADP-ribosylating PARP enzymes in cellular signaling and disease.Journal of cell science · 2025Review
- PARP14-mediated glycolysis enhances Tamoxifen resistance in estrogen receptor + breast cancer cells.Discover oncology · 2025Article
- PARP7 inhibits type I interferon signaling to prevent autoimmunity and lung disease.The Journal of experimental medicine · 2025Article
- Interferon-induced PARP14-mediated ADP-ribosylation in p62 bodies requires the ubiquitin-proteasome system.The EMBO journal · 2025Article
- Gut microbiota affects PD-L1 therapy and its mechanism in melanoma.Cancer immunology, immunotherapy : CII · 2025Review
- Intratumoral Collagen Deposition Supports Angiogenesis Suggesting Anti-angiogenic Therapy in Armored and Cold Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Combined PARP14 inhibition and PD-1 blockade promotes cytotoxic T cell quiescence and modulates macrophage polarization in relapsed melanoma.Journal for immunotherapy of cancer · 2025Article
- Current trends in sensitizing immune checkpoint inhibitors for cancer treatment.Molecular cancer · 2024Review
- PARP enzymes and mono-ADP-ribosylation: advancing the connection from interferon-signalling to cancer biology.Expert reviews in molecular medicine · 2024Review
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 2 countries.
Funding
Abstract
Resistance mechanisms to immune checkpoint blockade therapy (ICBT) limit its response duration and magnitude. Paradoxically, Interferon γ (IFNγ), a key cytokine for cellular immunity, can promote ICBT resistance. Using syngeneic mouse tumour models, we confirm that chronic IFNγ exposure confers resistance to immunotherapy targeting PD-1 (α-PD-1) in immunocompetent female mice. We observe upregulation of poly-ADP ribosyl polymerase 14 (PARP14) in chronic IFNγ-treated cancer cell models, in patient melanoma with elevated IFNG expression, and in melanoma cell cultures from ICBT-progressing lesions characterised by elevated IFNγ signalling. Effector T cell infiltration is enhanced in tumours derived from cells pre-treated with IFNγ in immunocompetent female mice when PARP14 is pharmacologically inhibited or knocked down, while the presence of regulatory T cells is decreased, leading to restoration of α-PD-1 sensitivity. Finally, we determine that tumours which spontaneously relapse in immunocompetent female mice following α-PD-1 therapy upregulate IFNγ signalling and can also be re-sensitised upon receiving PARP14 inhibitor treatment, establishing PARP14 as an actionable target to reverse IFNγ-driven ICBT resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.