ArticleCell reports. Medicine2025
In vivo neutrophils hitchhiking for tumor targeting and microenvironment regulation boosts oncolytic virus therapy.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
4 citing papers in PubMed.
- Advances in oncolytic virus delivery strategies and challenges in clinical translation.Materials today. Bio · 2026Review
- A Multicellular Coordinated Network Driving Lymphovascular Space Invasion in Endometrioid Endometrial Carcinoma.Cell proliferation · 2026Article
- Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation.Experimental hematology & oncology · 2026Review
- The role and mechanism of neutrophils in oncolytic virus therapy.Experimental biology and medicine (Maywood, N.J.) · 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils constitute a substantial proportion of the immune cell population infiltrating tumors, where they play a pivotal role in establishing an immunosuppressive microenvironment to facilitate tumor growth. Our clinical investigation has unveiled that, following oncolytic virus (OV) treatment, immunosuppressive neutrophils could lead to T cell exhaustion and compromised antitumor efficacy. In this study, we devise a dual-functional conjugation strategy that enables OVs to selectively bind with circulating neutrophils and initiate their death. Prior to dysfunction, neutrophils can harbor OVs and facilitate their infiltration into tumors, leading to a 5.38-fold increase in OV levels within tumors compared to direct intravenous injection. Additionally, infiltrated neutrophils undergo dying after 8 h, which promotes T cell priming, reduces T cell exhaustion, and remodels the tumor immune microenvironment. Our findings illuminate the determinants influencing the efficacy of OVs and propose targeted solutions, thereby offering insights for the clinical translation of these therapeutic agents.
Indexed as
Identifiers
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.