ArticleProceedings of the National Academy of Sciences of the United States of America2026
Intravenous infusion of engineered megakaryocytes to produce oncolytic platelets in vivo for enhanced cancer immunotherapy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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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
3 citing papers in PubMed.
- Organization from cell to tissue derived delivery systems for immunotherapy.Materials today. Bio · 2026Article
- Engineering megakaryocytes with oncolytic viruses forMolecular therapy. Oncology · 2026Article
- Viral subversion of megakaryopoiesis: reshaping the landscapes of immune regulation.Infection · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Tumor-targeted delivery of oncolytic viruses (OVs) via systemic administration could not only expand virotherapy beyond primary tumors to widespread metastases, but also improve clinical adherence and convenience. We here engineer megakaryocytes encapsulating oncolytic adenovirus type 5 (M-Ad5) to produce oncolytic platelets in vivo by leveraging the thrombopoiesis process. Upon intravenous administration, M-Ad5 travels through the lungs, where it can release OVs-harbored therapeutic platelets into circulation under pulmonary turbulence microenvironments. Under the shelter of platelets, OVs resist inactivation by neutralizing antibodies and actively target widespread noninjectable cancer lesions. Intravenous infusion of M-Ad5 to mice with A549 lung cancer could significantly inhibit tumor growth and prolong survival. In multiple mouse tumor models, M-Ad5 induced a robust antitumor immune response by reprogramming the immunosuppressive tumor microenvironment, and potentiated the response to immune checkpoint inhibitors by recruiting more immune cells. We demonstrated that M-Ad5 in combination with PDL1 inhibitors activated tumor antigen-specific CD8
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