ArticleOncology research2025
Oncolytic adenovirus H101 enhances the anti-tumor effects of PD-1 blockade via CD47 downregulation in tumor cells.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrating oncolytic adenoviruses into combination cancer therapy: Mechanisms, advances and clinical outlook.Clinical and translational medicine · 2026Review
- Review
- Overcoming immune resistance in advanced esophageal squamous cell carcinoma with recombinant human adenovirus type 5 by impacting the immune microenvironment: a case report.Frontiers in immunology · 2025Article
- Immunotherapy in Gastrointestinal Cancers: Current Insights.Clinical pharmacology : advances and applications · 2025Review
- Combination of oncolytic viruses and immune checkpoint inhibitors for treatment of high-grade gliomas.Frontiers in neurologyReview
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To investigate the anti-tumor effects of an E1B55KD-deleted oncolytic adenovirus, H101, in combination with a humanized anti-PD-1 (Programmed cell death protein 1) monoclonal antibody, Camrelizumab. Methods: Anti-tumor efficacy of intratumoral injection of H101 or/and intraperitoneal injection of Camrelizumab were evaluated in an immune system humanized NOD Results: Combining H101 with Camrelizumab demonstrated more potent anti-tumor effects than monotherapy in mouse S.C. tumor model. Increased tumor-infiltrating T cells were observed in the combined treatment group. H101 infection decreased the expression of CD47 in cancer cells, thereby promoting macrophages to phagocytose cancer cells. Following the H101-mediated activation of macrophages, increased levels of cytokines, including TNF, IL-12 and IFN-γ were observed. Moreover, when induced THP-1 cells were co-cultured with H101-treated cancer cells, expression of IFN-γ was increased in T cells. Elimination of IL-12 using an anti-IL-12 antibody abolished IFN-γ production from T cells. In addition, infection with H101 increased PD-L1 expression in YTS-1 cells. These results suggested that H101 may act synergistically to enhance the therapeutic efficacy of PD-1 blockade in cancer via suppressing CD47 signaling, which may promote macrophages to phagocytose tumor cells and activate CD8 Conclusion: The combination of H101 with PD-1 blockade exhibits potential as a novel strategy for the treatment of cancer.
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