ArticleMolecular therapy. Oncology2025
Oncolytic herpes simplex virus reprograms cancer-associated fibroblasts to enhance antitumor immunity in pancreatic cancer.
Article in Molecular therapy. Oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Overcoming melanoma drug resistance: Mechanisms and clinical progress of oncolytic viruses combined with immune checkpoint inhibitors (Review).Oncology reports · 2026Review
- Tumor-associated neutrophils in pancreatic ductal adenocarcinoma: mechanisms and therapeutic targeting.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) exhibits profound cancer-associated fibroblast (CAF)-driven immunosuppression. While oncolytic herpes simplex virus (oHSV) remodels the tumor microenvironment (TME), its direct impact on CAFs remains unclear. Here, we utilized a CAF-enriched PDAC model (1:10 KPC tumor cells:pancreatic stellate cells) to investigate oHSV therapy. Crucially, oHSV directly infects CAFs, inducing a subtype shift: it reduces immunosuppressive myofibroblastic CAFs and increases antigen-presenting CAFs. Mechanistically, oHSV upregulated major histocompatibility complex class I (MHC class I), MHC class II, and CD86 expression on CAFs; enhanced T cell activation; and significantly decreased regulatory T cells (Tregs). Furthermore, oHSV-infected CAFs boosted neutrophil recruitment and activation. Collectively, oHSV-mediated CAF reprogramming reshaped the immune landscape by reducing immunosuppression and enhancing both innate and adaptive anti-tumor immunity. This resulted in delayed tumor progression in the CAF-rich model, highlighting oHSV as a promising strategy to overcome the immunosuppressive TME in PDAC.
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Registered trials
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