ArticleJournal of virology2006
Prostate tumor cells infected with a recombinant influenza virus expressing a truncated NS1 protein activate cytolytic CD8+ cells to recognize noninfected tumor cells.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- The applications of live attenuated influenza a virus with modified NS1 gene.Molecular therapy. Nucleic acids · 2025Review
- Molecular Circuits of Immune Sensing and Response to Oncolytic Virotherapy.International journal of molecular sciences · 2024Review
- Review
- Oncolyic Virotherapy for Prostate Cancer: Lighting a Fire in Winter.International journal of molecular sciences · 2022Review
- Development and application of reverse genetic technology for the influenza virus.Virus genes · 2021Review
- From threat to cure: understanding of virus-induced cell death leads to highly immunogenic oncolytic influenza viruses.Cell death discovery · 2020Review
- Colonization of xenograft tumors by oncolytic vaccinia virus (VACV) results in enhanced tumor killing due to the involvement of myeloid cells.Journal of translational medicine · 2016Article
- Attenuated Recombinant Influenza A Virus Expressing HPV16 E6 and E7 as a Novel Therapeutic Vaccine Approach.PloS one · 2015Article
- Oncolytic activity of avian influenza virus in human pancreatic ductal adenocarcinoma cell lines.Journal of virology · 2014Article
- Oncolytic effects of a novel influenza A virus expressing interleukin-15 from the NS reading frame.PloS one · 2012Article
- Serum-free microcarrier based production of replication deficient influenza vaccine candidate virus lacking NS1 using Vero cells.BMC biotechnology · 2011Article
- A peptidoglycan monomer with the glutamine to serine change and basic peptides bind in silico to TLR-2 (403-455).Cancer immunology, immunotherapy : CII · 2011Article
- Tumor cells infected with oncolytic influenza A virus prime natural killer cells for lysis of resistant tumor cells.Medical microbiology and immunology · 2010Article
- Breast cancer cells expressing stem cell markers CD44+ CD24 lo are eliminated by Numb-1 peptide-activated T cells.Cancer immunology, immunotherapy : CII · 2009Article
- Influenza a virus induces an immediate cytotoxic activity in all major subsets of peripheral blood mononuclear cells.PloS one · 2009Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Many viral oncolytic approaches against cancer are based on the ability of specific viruses to replicate in tumors expressing components of the constitutively activated Ras/mitogen-activated protein kinase (MAPK) pathways and/or inhibited or dysregulated alpha/beta interferon (IFN-alpha/beta) response pathways. A major issue when considering these approaches is their applicability to tumors that lack activated Ras. To identify the effector mechanisms activated by oncolytic viruses, we investigated inhibition of proliferation of the prostate cancer line LNCap by the recombinant TR-NS1 influenza A virus, a genetically attenuated influenza A/PR8/34 virus expressing a truncated nonstructural protein (NS1) of 126 amino acids. LNCap cells lack constitutively activated MAPK, extracellular signal-regulated kinase (ERK), and p38 and are resistant to death by IFN-alpha. Truncation of the NS1 protein of influenza viruses is known to result in viral attenuation due to a reduced ability of the NS1 to inhibit the IFN-alpha/beta response. Infection with TR-NS1 virus rapidly activated ERK-1 more than ERK-2 in LNCap cells. Importantly, TR-NS1 virus infection transiently inhibited cell proliferation and induced apoptosis in LNCap cells. Addition of peripheral blood mononuclear cells (PBMC) and interleukin 12 (IL-12) to TR-NS1 virus-infected LNCap cells (TR-NS1-LNCap) resulted in faster elimination of TR-NS1-LNCap cells compared with LNCap cells. Moreover, TR-NS1-LNCap cells induced IFN-gamma in PBMC. The levels of IFN-gamma were amplified by IL-12. TR-NS1-LNCap cells also induced tumor-lytic cytotoxic T lymphocytes (CTL). These CTL lysed noninfected LNCap cells in a CD8-dependent manner. Activation of cellular immunity to tumor cells by viruses is an intriguing effector pathway, which should be especially significant for elimination of human tumors that lack activated Ras.
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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.