ArticleJournal of virology2006
Activated MEK suppresses activation of PKR and enables efficient replication and in vivo oncolysis by Deltagamma(1)34.5 mutants of herpes simplex virus 1.
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 70 papers.
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
70 citing papers in PubMed, 101 citations in OpenAlex.
- Clinical Progress in Virotherapy: Application and Future Prospects in Head and Neck Cancer.International journal of molecular sciences · 2026Review
- Engineering HSV-1 for oncolytic therapy: From molecular entry mechanisms to retargeting strategies.Genes & diseases · 2026Review
- Review
- Oncolytic Herpes Simplex Virus Therapy: Latest Advances, Core Challenges, and Future Outlook.Vaccines · 2025Review
- Oncolytic virus encoding 4-1BBL and IL15 enhances the efficacy of tumor-infiltrating lymphocyte adoptive therapy in HCC.Cancer gene therapy · 2025Article
- Review
- Article
- Immunomodulatory Arming Factors-The Current Paradigm for Oncolytic Vectors Relies on Immune Stimulating Molecules.International journal of molecular sciences · 2021Review
- Oncolytic HSV: Underpinnings of Tumor Susceptibility.Viruses · 2021Review
- Coxsackievirus B3-Its Potential as an Oncolytic Virus.Viruses · 2021Review
- Oncolytic Virotherapy: The Cancer Cell Side.Cancers · 2021Review
- Recent advances of oncolytic virus in cancer therapy.Human vaccines & immunotherapeutics · 2020Review
- VHS, US3 and UL13 viral tegument proteins are required for Herpes Simplex Virus-Induced modification of protein kinase R.Scientific reports · 2020Article
- Virotherapy as a Potential Therapeutic Approach for the Treatment of Aggressive Thyroid Cancer.Cancers · 2019Review
- Human DNA Virus Exploitation of the MAPK-ERK Cascade.International journal of molecular sciences · 2019Review
- Selective Editing of Herpes Simplex Virus 1 Enables Interferon Induction and Viral Replication That Destroy Malignant Cells.Journal of virology · 2019Article
- MEK inhibition enhances oncolytic virus immunotherapy through increased tumor cell killing and T cell activation.Science translational medicine · 2018Article
- Enhanced Sensitivity of Patient-Derived Pediatric High-Grade Brain Tumor Xenografts to Oncolytic HSV-1 Virotherapy Correlates with Nectin-1 Expression.Scientific reports · 2018Article
- Talimogene laherparepvec: First in class oncolytic virotherapy.Human vaccines & immunotherapeutics · 2018Review
- Fucoidan from Fucus vesiculosus suppresses hepatitis B virus replication by enhancing extracellular signal-regulated Kinase activation.Virology journal · 2017Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Herpes simplex virus mutants lacking the gamma(1)34.5 gene are not destructive to normal tissues but are potent cytolytic agents in human tumor cells in which the activation of double-stranded RNA-dependent protein kinase (PKR) is suppressed. Thus, replication of a Deltagamma(1)34.5 mutant (R3616) in 12 genetically defined cancer cell lines correlates with suppression of PKR but not with the genotype of RAS. Extensive analyses of two cell lines transduced with either dominant negative MEK (dnMEK) or constitutively active MEK (caMEK) indicated that in R3616 mutant-infected cells dnMEK enabled PKR activation and decreased virus yields, whereas caMEK suppressed PKR and enabled better viral replication and cell destruction in transduced cells in vitro or in mouse xenografts. The results indicate that activated MEK mediates the suppression of PKR and that the status of MEK predicts the ability of Deltagamma(1)34.5 mutant viruses to replicate in and destroy tumor cells.
Indexed as
Identifiers
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.