ArticleCancer gene therapy2015
STAT3 inhibition reduces toxicity of oncolytic VSV and provides a potentially synergistic combination therapy for hepatocellular carcinoma.
Article in Cancer gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Therapeutic Efficacy of Oncolytic Viruses in Fighting Cancer: Recent Advances and Perspective.Oxidative medicine and cellular longevity · 2022Review
- Improving antitumor efficacy via combinatorial regimens of oncolytic virotherapy.Molecular cancer · 2020Review
- The mechanisms of sorafenib resistance in hepatocellular carcinoma: theoretical basis and therapeutic aspects.Signal transduction and targeted therapy · 2020Review
- Oncolytic Viruses and Immune Checkpoint Inhibition: The Best of Both Worlds.Molecular therapy oncolytics · 2019Review
- Enhanced Safety and Efficacy of Oncolytic VSV Therapy by Combination with T Cell Receptor Transgenic T Cells as Carriers.Molecular therapy oncolytics · 2019Article
- Fine-Tuning of Type I Interferon Response by STAT3.Frontiers in immunology · 2019Review
- Cellular and molecular targets for the immunotherapy of hepatocellular carcinoma.Molecular and cellular biochemistry · 2018Review
- Recent advances in vesicular stomatitis virus-based oncolytic virotherapy: a 5-year update.The Journal of general virology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a refractory malignancy with a high mortality and increasing worldwide incidence rates, including the United States and central Europe. In this study, we demonstrate that a specific inhibitor of signal transducer and activator of transcription 3 (STAT3), NSC74859, efficiently reduces HCC cell proliferation and can be successfully combined with oncolytic virotherapy using vesicular stomatitis virus (VSV). The potential benefits of this combination treatment are strengthened by the ability of NSC74859 to protect primary hepatocytes and nervous system cells against virus-induced cytotoxicity, with an elevation of the VSV maximum tolerated dose in mice. Hereby we propose a strategy for improving the current regimen for HCC treatment and seek to further explore the molecular mechanisms underlying selective oncolytic specificity of VSV.
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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.