ArticleJournal of virology2011
Vesicular stomatitis virus expressing tumor suppressor p53 is a highly attenuated, potent oncolytic agent.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 49 citations in OpenAlex.
- Vesicular Stomatitis Virus-Based Oncolytic Virotherapy: Recent Progress and Emerging Trends.Current oncology (Toronto, Ont.) · 2025Review
- Engineering of Vesicular Stomatitis Virus (VSV) for Modulating Cell Death and Antitumor Immunity.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- The chicken chorioallantoic membrane model for isolation of CRISPR/cas9-based HSV-1 mutant expressing tumor suppressor p53.PloS one · 2023Article
- Win or loss? Combination therapy does improve the oncolytic virus therapy to pancreatic cancer.Cancer cell international · 2022Review
- Immunovirotherapy Based on Recombinant Vesicular Stomatitis Virus: Where Are We?Frontiers in immunology · 2022Review
- Review
- The role of NK cells in oncolytic viral therapy: a focus on hepatocellular carcinoma.Journal of translational genetics and genomics · 2021Article
- Experimental Evolution Generates Novel Oncolytic Vesicular Stomatitis Viruses with Improved Replication in Virus-Resistant Pancreatic Cancer Cells.Journal of virology · 2020Article
- Bioprofiling TS/A Murine Mammary Cancer for a Functional Precision Experimental Model.Cancers · 2019Review
- M51R and Delta-M51 matrix protein of the vesicular stomatitis virus induce apoptosis in colorectal cancer cells.Molecular biology reports · 2019Article
- Oncolytic Virotherapy versus Cancer Stem Cells: A Review of Approaches and Mechanisms.Cancers · 2018Review
- Review
- Recent advances in vesicular stomatitis virus-based oncolytic virotherapy: a 5-year update.The Journal of general virology · 2017Article
- Combining Oncolytic Virotherapy with p53 Tumor Suppressor Gene Therapy.Molecular therapy oncolytics · 2017Review
- Viroimmunotherapy for Colorectal Cancer: Clinical Studies.Biomedicines · 2017Review
- Oncolytic Immunotherapy: Conceptual Evolution, Current Strategies, and Future Perspectives.Frontiers in immunology · 2017Review
- Murine Tumor Models for Oncolytic Rhabdo-Virotherapy.ILAR journal · 2016Article
- An unexpected inhibition of antiviral signaling by virus-encoded tumor suppressor p53 in pancreatic cancer cells.Virology · 2015Article
- Interferon Beta and Interferon Alpha 2a Differentially Protect Head and Neck Cancer Cells from Vesicular Stomatitis Virus-Induced Oncolysis.Journal of virology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Vesicular stomatitis virus (VSV), a negative-strand RNA rhabdovirus, preferentially replicates in and eradicates transformed versus nontransformed cells and is thus being considered for use as a potential anticancer treatment. The genetic malleability of VSV also affords an opportunity to develop more potent agents that exhibit increased therapeutic activity. The tumor suppressor p53 has been shown to exert potent antitumor properties, which may in part involve stimulating host innate immune responses to malignancies. To evaluate whether VSV expressing p53 exhibited enhanced oncolytic action, the murine p53 (mp53) gene was incorporated into recombinant VSVs with or without a functional viral M gene-encoded protein that could either block (VSV-mp53) or enable [VSV-M(mut)-mp53] host mRNA export following infection of susceptible cells. Our results indicated that VSV-mp53 and VSV-M(mut)-mp53 expressed high levels of functional p53 and retained the ability to lyse transformed versus normal cells. In addition, we observed that VSV-ΔM-mp53 was extremely attenuated in vivo due to p53 activating innate immune genes, such as type I interferon (IFN). Significantly, immunocompetent animals with metastatic mammary adenocarcinoma exhibited increased survival following treatment with a single inoculation of VSV-ΔM-mp53, the mechanisms of which involved enhanced CD49b+ NK and tumor-specific CD8+ T cell responses. Our data indicate that VSV incorporating p53 could provide a safe, effective strategy for the design of VSV oncolytic therapeutics and VSV-based vaccines.
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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.