ArticleSurgery2013
Oncolytic vesicular stomatitis virus as a treatment for neuroendocrine tumors.
Article in Surgery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Employing the Oncolytic Vesicular Stomatitis Virus in Cancer Virotherapy: Resistance and Clinical Considerations.Viruses · 2024Review
- The Role of Vesicular Stomatitis Virus Matrix Protein in Autophagy in the Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Preclinical Development of Oncolytic Immunovirotherapy for Treatment of HPVMolecular therapy oncolytics · 2018Article
- Recent advances in vesicular stomatitis virus-based oncolytic virotherapy: a 5-year update.The Journal of general virology · 2017Article
- Molecular determinants of susceptibility to oncolytic vesicular stomatitis virus in pancreatic adenocarcinoma.The Journal of surgical research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTherapeutic goals for neuroendocrine tumors (NETs) not amenable to operative cure are limited to relieving symptoms and slowing progression. Many malignancies acquire defective antiviral responses as they undergo unregulated proliferation. Therefore, we explored the abilities of recombinant wild-type vesicular stomatitis virus and an attenuated matrix protein mutant (M51R-VSV) to exploit defective antiviral pathways in NETs.
methodsViral infectivity and lethality were evaluated in a panel of human NET cell lines H727, UMC-11, and CNDT2.5. We evaluated β-interferon pathways in these cells to define the acquired defect. Murine xenografts were treated with a single intratumoral injection of M51R-VSV to study viral efficacy in vivo.
resultsVSV infected >99% of cells within 24 hours and killed >95% within 72 hours. NET cells did not produce relevant amounts of β-interferon after infection, but exogenous β-interferon protected cells from oncolysis. Treatment with M51R-VSV resulted in suppressed tumor growth (mean value ± standard error of the mean) compared with mock-infected xenografts for H727 (87 ± 72% vs. 2,197 ± 335%; P < .001), UMC-11 (13 ± 59% vs. 1,471 ± 324%; P < .001), and CNDT2.5 (81 ± 121% vs. 1,576 ± 349%; P = .001).
conclusionVSV infects and kills human NETs by exploiting their inability to produce a type I antiviral response. Therefore, M51R-VSV is an excellent candidate for the treatment of advanced NETs.
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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.