Exploiting tumor-specific defects in the interferon pathway with a previously unknown oncolytic virus
By D. Stojdl, B. Lichty, Shane Knowles, R. Marius, H. Atkins, Nahum Sonenberg, J. Bell. Nature Medicine, 2000
877 citations recorded by the source corpus.
Subfields: Animal Science and Zoology, Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/336ee9f8b3b386325339803f037bcbd082ffa2bf
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
Citations in the corpus
- Double-Stranded RNA Is Produced by Positive-Strand RNA Viruses and DNA Viruses but Not in Detectable Amounts by Negative-Strand RNA Viruses (2006, background): “Nevertheless, it is well known that negative-strand RNA viruses can strongly induce IFN synthesis (18, 68), activate PKR or be sensitive to it (7, 56, 58), or express a dsRNA-binding protein, such as FLUAV NS1 (22, 36).”
- The interferon response circuit: Induction and suppression by pathogenic viruses (2005, neutral): “Mutations in tumor cells often cripple the IFN system, favoring unhindered proliferation and protection from apoptosis (Stojdl et al., 2000).”
- Oncolytic viruses: a new class of immunotherapy drugs (2015, background): “These include vaccinia virus 54 , NDV 58 , rabbit myxoma virus 59 , mumps 60 , alphaviruses 60 , and vesicular stomatitis virus (VSV) variants 61 .”
- From chemotherapy to biological therapy: A review of novel concepts to reduce the side effects of systemic cancer treatment (Review) (2018, neutral): “Tumor cells often have defects in the IFN pathway (94); this is why they are susceptible to infection by certain OVs, including the avian virus NDV (95).”
- 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).”