ArticleOncogene2008
Oncolytic herpes virus with defective ICP6 specifically replicates in quiescent cells with homozygous genetic mutations in p16.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
- Clinical Application of Oncolytic Viruses: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Cracking the shield: oncolytic viruses versus the tumor-immune fortress.Cancer cell international · 2026Review
- Enhancing antitumor immunity through oncolytic viruses: advances in genetic engineering.Discover oncology · 2026Review
- Oncolytic HSV and cancer drug interactions: Current clinical status and future directions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Engineering a novel HSV-1 strain for oncolytic therapy of solid tumors.Molecular therapy. Oncology · 2025Article
- Advances in the Drug Development and Quality Evaluation Principles of Oncolytic Herpes Simplex Virus.Viruses · 2025Review
- Targeting IGF2 to reprogram the tumor microenvironment for enhanced viro-immunotherapy.Neuro-oncology · 2024Article
- Review
- Revolutionizing cancer treatment: the power of bi- and tri-specific T-cell engagers in oncolytic virotherapy.Frontiers in immunology · 2024Review
- Tumor Tropism of DNA Viruses for Oncolytic Virotherapy.Viruses · 2023Review
- Article
- IDH1 mutation impairs antiviral response and potentiates oncolytic virotherapy in glioma.Nature communications · 2023Article
- CRISPR/Cas9 and next generation sequencing in the personalized treatment of Cancer.Molecular cancer · 2022Review
- Tumor-Associated Macrophages/Microglia in Glioblastoma Oncolytic Virotherapy: A Double-Edged Sword.International journal of molecular sciences · 2022Review
- Glioblastoma microenvironment and its reprogramming by oncolytic virotherapy.Frontiers in cellular neuroscience · 2022Review
- Therapeutic Efficacy of Oncolytic Viruses in Fighting Cancer: Recent Advances and Perspective.Oxidative medicine and cellular longevity · 2022Review
- Role of Adenoviruses in Cancer Therapy.Frontiers in oncology · 2022Review
- Biological basis for novel mesothelioma therapies.British journal of cancer · 2021Review
- Review
- Against the Resilience of High-Grade Gliomas: Gene Therapies (Part II).Brain sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Oncolytic herpes simplex viruses (HSVs), in clinical trials for the treatment of malignant gliomas, are assumed to be selective for tumor cells because their replication is strongly attenuated in quiescent cells, but not in cycling cells. Oncolytic selectivity is thought to occur because mutations in viral ICP6 (encoding a viral ribonucleotide reductase function) and/or gamma34.5 function are respectively complemented by mammalian ribonucleotide reductase and GADD34, whose genes are expressed in cycling cells. However, it is estimated that only 5-15% of malignant glioma cells are in mitosis at any one time. Therefore, effective replication of HSV oncolytic viruses might be limited to a subpopulation of tumor cells, since at any one time the majority of tumor cells would not be cycling. However, we report that an HSV with defective ICP6 function replicates in quiescent cultured murine embryonic fibroblasts obtained from mice with homozygous p16 deletions. Furthermore, intracranial inoculation of this virus into the brains of p16-/- mice provides evidence of viral replication that does not occur when the virus is injected into the brains of wild-type mice. These approaches provide in vitro and in vivo evidence that ICP6-negative HSVs are 'molecularly targeted,' because they replicate in quiescent tumor cells carrying specific oncogene deletions, independent of cell cycle status.
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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.