ArticleNature communications2024
Plasticity-induced repression of Irf6 underlies acquired resistance to cancer immunotherapy in pancreatic ductal adenocarcinoma.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 26 citations in OpenAlex.
- Immune-pressure redistribution in resistance to PD-1/PD-L1 blockade: mechanisms, biomarkers, and therapeutic design.Molecular cancer · 2026Review
- Targeted Cepharanthine-Mediated Dual-Pathway Inhibition Sensitizes Pancreatic Cancer to Gemcitabine.Life (Basel, Switzerland) · 2026Article
- Plasticity of Non-Apoptotic Residual Tumor Cells After Neoadjuvant Immunochemotherapy: Epigenetic and Microenvironmental Determinants.Biomolecules · 2026Review
- Penicophenone F from an Arctic Fungus Against UVB-Induced Corneal Damage via Inhibiting the ROS-EphA2 Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- Epithelial-mesenchymal transition and immunosuppression: Two sides of the same coin.Cellular and molecular life sciences : CMLS · 2026Review
- Identification, functional insights and therapeutic targeting of EMT tumour states.Nature reviews. Cancer · 2026Review
- Targeting IL-12 for pancreatic cancer immunotherapy: advances in delivery strategies and clinical translation.Frontiers in immunology · 2026Review
- Review
- Allostery in Disease: Anticancer Drugs, Pockets, and the Tumor Heterogeneity Challenge.Journal of molecular biology · 2025Review
- Interpretable Transfer Learning for Cancer Drug Resistance: Candidate Target Identification.Current issues in molecular biology · 2025Article
- Multidrug Resistance: Are We Still Afraid of the Big Bad Wolf.Pharmaceuticals (Basel, Switzerland) · 2025Review
- IRF6 controls Epstein-Barr virus (EBV) lytic reactivation and differentiation in EBV-infected epithelial cells.PLoS pathogens · 2025Article
- Drug resistance and tumor heterogeneity: cells and ensembles.Biophysical reviews · 2025Review
- Looking Beyond Checkpoint Inhibitor Monotherapy: Uncovering New Frontiers for Pancreatic Cancer Immunotherapy.Molecular cancer therapeutics · 2025Review
- The role of interferon regulatory factors in atherosclerosis.Frontiers in cardiovascular medicine · 2025Review
- Neutrophil Extracellular Traps Promote Pancreatic Cancer Progression via the STING Pathway.Gastroenterology research and practice · 2025Article
- Review
- Cancer cell plasticity defines response to immunotherapy in cutaneous squamous cell carcinoma.Nature communications · 2024Article
- The Role of Interferon Regulatory Factors in Liver Diseases.International journal of molecular sciences · 2024Review
Corrections and comments
- Update of
Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
Acquired resistance to immunotherapy remains a critical yet incompletely understood biological mechanism. Here, using a mouse model of pancreatic ductal adenocarcinoma (PDAC) to study tumor relapse following immunotherapy-induced responses, we find that resistance is reproducibly associated with an epithelial-to-mesenchymal transition (EMT), with EMT-transcription factors ZEB1 and SNAIL functioning as master genetic and epigenetic regulators of this effect. Acquired resistance in this model is not due to immunosuppression in the tumor immune microenvironment, disruptions in the antigen presentation machinery, or altered expression of immune checkpoints. Rather, resistance is due to a tumor cell-intrinsic defect in T-cell killing. Molecularly, EMT leads to the epigenetic and transcriptional silencing of interferon regulatory factor 6 (Irf6), rendering tumor cells less sensitive to the pro-apoptotic effects of TNF-α. These findings indicate that acquired resistance to immunotherapy may be mediated by programs distinct from those governing primary resistance, including plasticity programs that render tumor cells impervious to T-cell killing.
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What OpenQuestion holds
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.