VSV strains with defects in their ability to shutdown innate immunity are potent systemic anti-cancer agents.

By D. Stojdl, B. Lichty, B. tenOever, J. Paterson, A. Power, Shane Knowles, R. Marius, J. Reynard, L. Poliquin, H. Atkins and 5 more. Cancer Cell, 2003

885 citations recorded by the source corpus.

Subfields: Animal Science and Zoology, Epidemiology, Genetics

View Paper: https://www.semanticscholar.org/paper/d542b11c012266e09085da2681fed5ea935bf1bd

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In Epidemiology

1. M. Gale
2. R. Randall
3. S. Goodbourn

Citations in the corpus

• Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “Mice lacking PKR are especially sensitive to VSV (Takaoka et al., 2003), whereas mice expressing an extra copy of p53 show increased resistance to VSV, due to enhanced apoptosis (MunozFontela et al., 2005).”
• SARS-CoV-2 ORF6 Disrupts Bidirectional Nucleocytoplasmic Transport through Interactions with Rae1 and Nup98 (2021, background): “Furthermore, VSV strains containing a mutation at the residue responsible for the VSV M-Rae1-Nup98 interactions induce significantly higher interferon-a protein levels than strains containing wild-type alleles of the M protein (22).”
• SARS-CoV-2 ORF6 disrupts nucleocytoplasmic transport through interactions with Rae1 and Nup98 (2020, background): “higher interferon-α protein levels than strains containing wild-type alleles of the M 244 protein (23).”
• Complexes of Vesicular Stomatitis Virus Matrix Protein with Host Rae1 and Nup98 Involved in Inhibition of Host Transcription (2012, background): “tion of antiviral cytokines such as interferons [3,8,9].”
• The interferon response circuit: Induction and suppression by pathogenic viruses (2005, neutral): “A VSV variant with mutations in the M gene inactivating its IFN-antagonistic capacity was shown to specifically lyse tumors in immunocompetent mice (Stojdl et al., 2003).”