ArticleCancer gene therapy2005
Enhanced inhibition of syngeneic murine tumors by combinatorial therapy with genetically engineered HSV-1 expressing CCL2 and IL-12.
Article in Cancer gene therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
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
44 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Review
- Unmasking the potential: mechanisms of neuroinflammatory modulation by oncolytic viruses in glioblastoma.Exploration of targeted anti-tumor therapy · 2025Review
- Interleukin-12 Delivery Strategies and Advances in Tumor Immunotherapy.Current issues in molecular biology · 2024Review
- Oncolytic Tanapoxvirus Variants Expressing mIL-2 and mCCL-2 Regress Human Pancreatic Cancer Xenografts in Nude Mice.Biomedicines · 2024Article
- Cytokine-armed oncolytic herpes simplex viruses: a game-changer in cancer immunotherapy?Journal for immunotherapy of cancer · 2024Review
- Advanced progress in the genetic modification of the oncolytic HSV-1 virus.Frontiers in oncology · 2024Review
- Kinetic analysis of oncolytic OrfV-induced innate and adaptive immune responses in a murine model of late-stage ovarian cancer.Molecular therapy oncolytics · 2023Article
- Review
- Recombinant Virus Quantification Using Single-Cell Droplet Digital PCR: A Method for Infectious Titer Quantification.Viruses · 2023Article
- Integrated re-analysis of transcriptomic and proteomic datasets reveals potential mechanisms for Zika viral-based oncolytic therapy in neuroblastoma.F1000Research · 2023Article
- Immunosuppressive cells in oncolytic virotherapy for glioma: challenges and solutions.Frontiers in cellular and infection microbiology · 2023Review
- Recombinant Viral Vectors for Therapeutic Programming of Tumour Microenvironment: Advantages and Limitations.Biomedicines · 2022Review
- Immunotherapy by mesenchymal stromal cell delivery of oncolytic viruses for treating metastatic tumors.Molecular therapy oncolytics · 2022Review
- Engineering strategies to enhance oncolytic viruses in cancer immunotherapy.Signal transduction and targeted therapy · 2022Review
- Current clinical landscape of oncolytic viruses as novel cancer immunotherapeutic and recent preclinical advancements.Frontiers in immunology · 2022Review
- Current strategies in engaging oncolytic viruses with antitumor immunity.Molecular therapy oncolytics · 2021Review
- Combining vanadyl sulfate with Newcastle disease virus potentiates rapid innate immune-mediated regression with curative potential in murine cancer models.Molecular therapy oncolytics · 2021Article
- Targeted Delivery of IL-12 Adjuvants Immunotherapy by Oncolytic Viruses.Advances in experimental medicine and biology · 2021Article
- The Current State of Oncolytic Herpes Simplex Virus for Glioblastoma Treatment.Oncolytic virotherapy · 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex viruses type 1 (HSV-1) that lack the gamma(1)34.5 gene are unable to replicate in the central nervous system (CNS), but maintain replication competence in actively dividing tumors. To determine if antitumor therapy by M002, a gamma(1)34.5(-) HSV that expresses interleukin-12 (IL-12), could be augmented by combinatorial therapy with another gamma(1)34.5-deleted HSV-1 engineered to express the chemokine CCL2, Neuro-2a tumors were established subcutaneously in the syngeneic A/J mouse strain. Tumors received multiple injections intratumorally either of saline, the parent, non-cytokine-expressing virus R3659, M002, M010 (gamma(1)34.5(-) HSV expressing CCL2), or a combination of M002 and M010. Efficacies were evaluated by monitoring inhibition of tumor growth over time. Results demonstrated the following: (1) inhibition of tumor growth was most pronounced in tumors treated with a combination of M002 and M010; (2) enhanced tumor growth inhibition for the combinatorial treatment group was statistically significant compared to either M002 or M010 alone; and (3) the variability between slopes of the tumor growth rates within an individual treatment group appeared to be virus-dependent, and was reproducible between experiments. Our results demonstrate that combinatorial cytokine/chemokine gamma(1)34.5(-) HSV therapies can provide superior antitumor effects in experimental tumors as a model for malignancies arising in the brain.
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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.