ArticleCancer gene therapy2012
Oncolytic poxvirus armed with Fas ligand leads to induction of cellular Fas receptor and selective viral replication in FasR-negative cancer.
Article in Cancer gene therapy, 2012. 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.
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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.
- Enhancing cancer therapy: the integration of oncolytic virus therapy with diverse treatments.Cancer cell international · 2024Review
- The emerging field of oncolytic virus-based cancer immunotherapy.Trends in cancer · 2023Review
- Immuno-Oncolytic Viruses: Emerging Options in the Treatment of Colorectal Cancer.Molecular diagnosis & therapy · 2021Review
- The evolution of poxvirus vaccines.Viruses · 2015Review
- Enhancing the bystander killing effect of an oncolytic HSV by arming it with a secretable apoptosis activator.Gene therapy · 2015Article
- Chemotherapy and Oncolytic Virotherapy: Advanced Tactics in the War against Cancer.Frontiers in oncology · 2014Review
- From scourge to cure: tumour-selective viral pathogenesis as a new strategy against cancer.PLoS pathogens · 2014Review
- A rationally designed A34R mutant oncolytic poxvirus: improved efficacy in peritoneal carcinomatosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor necrosis factor superfamily members, including Fas ligand and TRAIL, have been studied extensively for cancer therapy, including as components of gene therapy. We examined the use of FasL expression to achieve tumor-selective replication of an oncolytic poxvirus (vFasL), and explored its biology and therapeutic efficacy for FasR- and FasR+ cancers. Infection of FasR+ normal and MC38 cancer cells by vFasL led to abortive viral replication owing to acute apoptosis and subsequently showed both reduced pathogenicity in non-tumor-bearing mice and reduced efficacy in FasR+ tumor-bearing mice. Infection of FasR- B16 cancer cells by vFasL led to efficient viral replication, followed by late induction of FasR and subsequent apoptosis. Treatment with vFasL as compared with its parental virus (vJS6) led to increased tumor regression and prolonged survival of mice with FasR- cancer (B16) but not with FasR+ cancer (MC38). The delayed induction of FasR by viral infection in FasR- cells provides for potential increased efficacy beyond the limit of the direct oncolytic effect. FasR induction provides one mechanism for tumor-selective replication of oncolytic poxviruses in FasR- cancers with enhanced safety. The overall result is both a safer and more effective oncolytic virus for FasR- cancer.
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What OpenQuestion holds
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.