ArticleMaterials today. Bio2025
Light-controlled pyroptosis via redox-responsive microneedles enhances photodynamic-epigenetic immunotherapy in breast cancer.
Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Localized immunotherapy via dissolving microneedles for the prevention of breast cancer recurrence.Drug delivery and translational research · 2026Review
- Review
- Microneedle-Assisted Delivery of Biologics: From Large Molecules to Cancer Vaccines.AAPS PharmSciTech · 2026Review
- Estrogen Receptor-Low Positive (ER-Low) Breast Cancer: A Unique Clinical and Pathological Entity.Current oncology (Toronto, Ont.) · 2026Review
- Smart Nanoformulations for Oncology: A Review on Overcoming Biological Barriers with Active Targeting, Stimuli-Responsive, and Controlled Release for Effective Drug Delivery.Pharmaceutics · 2026Review
- The molecular mechanisms of pyroptosis and its implications in tumor immunotherapy.Molecular cancer · 2026Review
- Advances in porphyrin-based photosensitizers for photodynamic therapy of A549 lung cancer.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the potential of photodynamic therapy in breast cancer treatment, inadequate immunogenicity and inefficient pyroptosis induction remain critical limitations. To address this, we developed dissolvable microneedles (MNs) for localized co-delivery of decitabine (DEC) and glutathione (GSH)-responsive photosensitizer nanoparticles (HPPH-ss-NPs), aiming to potentiate immunogenic pyroptosis in breast cancer. The MNs enabled spatiotemporal control of DEC (dissolution-dependent release) and HPPH-ss-NPs (GSH-triggered activation), enhancing tumor drug levels with reduced systemic exposure. Mechanistically, DEC restored pyroptosis executioner gasdermin E (GSDME) expression, while HPPH-ss-NPs depleted intracellular GSH and generated caspase-3-activating ROS under light irradiation. The synergistic action triggered GSDME-dependent pyroptosis, releasing immunostimulatory DAMPs that increased mature dendritic cells and tumor-infiltrating CD8
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Registered trials
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