ArticleCancer gene therapy2013
Overcoming cancer cell resistance to VSV oncolysis with JAK1/2 inhibitors.
Article in Cancer gene therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 66 citations in OpenAlex.
- Constitutive Interferon Pathway Activation in Tumors as an Efficacy Determinant Following Oncolytic Virotherapy.Journal of the National Cancer Institute · 2018Trial
- Comparative evaluation of oncolytic viruses reveals opposing preferences for glioblastoma subtypes.Molecular therapy. Oncology · 2026Article
- Beyond suppression: the paradox of JAK inhibitors as amplifiers of cancer immunotherapy.Nature reviews. Immunology · 2026Review
- Oncolytic viruses in head and neck cancer: therapeutic promise and translational challenges.Frontiers in immunology · 2026Review
- Constitutive NF-kB Activation Is Amplified by VSV in Aggressive PC3 Prostate Cancer Cells That Resist Viral Oncolysis.Viruses · 2026Article
- Fostamatinib (R788), a spleen tyrosine kinase inhibitor, sensitizes pancreatic cancer cells to oncolytic vesicular stomatitis virus.Molecular therapy. Oncology · 2025Article
- Constitutive NF-κB Activation is Amplified by VSV in Aggressive PC3 Prostate Cancer Cells that Resist Viral Oncolysis.bioRxiv : the preprint server for biology · 2025Article
- Oncolytic viruses as cancer therapeutics: From mechanistic insights to clinical translation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Employing the Oncolytic Vesicular Stomatitis Virus in Cancer Virotherapy: Resistance and Clinical Considerations.Viruses · 2024Review
- Murine colon cancer derived cells exhibit heterogeneous resistance profiles against an oncolytic virus.Scientific reports · 2024Article
- Oncolytic Coxsackievirus B3 Strain PD-H Is Effective Against a Broad Spectrum of Pancreatic Cancer Cell Lines and Induces a Growth Delay in Pancreatic KPC Cell Tumors In Vivo.International journal of molecular sciences · 2024Article
- Oclacitinib and Myxoma Virus Therapy in Dogs with High-Grade Soft Tissue Sarcoma.Biomedicines · 2023Article
- Cellular resistance to an oncolytic virus is driven by chronic activation of innate immunity.iScience · 2023Article
- Unlocking the potential of dimethyl fumarate: enhancing oncolytic HSV-1 efficacy for wider cancer applications.Frontiers in immunology · 2023Article
- Direct and indirect effects of IFN-α2b in malignancy treatment: not only an archer but also an arrow.Biomarker research · 2022Review
- The gamble between oncolytic virus therapy and IFN.Frontiers in immunology · 2022Review
- Computational prediction of intracellular targets of wild-type or mutant vesicular stomatitis matrix protein.PloS one · 2022Article
- Review
- Coxsackievirus B3-Its Potential as an Oncolytic Virus.Viruses · 2021Review
- Experimental virus evolution in cancer cell monolayers, spheroids, and tissue explants.Virus evolution · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Oncolytic vesicular stomatitis virus (VSV) has potent antitumor activity but some cancer cells are resistant to VSV killing, either constitutively or due to type I interferon (IFN) inducing an antiviral state in the cells. Here, we evaluated VSV oncolysis of a panel of human head and neck cancer cells and showed that VSV resistance in SCC25 and SCC15 cells could be reversed with Janus kinase (JAK) 1/2 inhibitors (JAK inhibitor I and ruxolitinib). Pre-treatment of cells with JAK1/2 inhibitors before or in conjunction with VSV enhanced viral infection, spread and progeny yield (100- to 1000-fold increase). In contrast, inhibitors of histone deacetylase (LBH589), phosphatidylinositol 3-kinase (GDC-0941, LY294002), mammalian target of rapamycin (rapamycin) or signal transducer and activator of transcription 3 (STAT3 inhibitor VII) were ineffective. Compared with VSV-sensitive SW579 cells, IFNα/β responsive antiviral genes (IRF-9, IRF-7, OAS1 but not MxA) are constitutively expressed in SCC25 cells. Pretreatment with JAK inhibitors reduced mRNA levels of these genes, increasing VSV expression in the cells. Interestingly, 1 h of drug exposure was sufficient to reverse SCC25 resistance to VSV and was still effective if virus was added 24 h later. Overall, we show here that JAK inhibitor I and ruxolitinib (Jakafi) can reverse resistance to VSV, supporting the rationale to incorporate JAK1/2 inhibitors in future VSV virotherapy trials.
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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.