ArticleStem cells translational medicine2012
Oncolytic herpes simplex virus counteracts the hypoxia-induced modulation of glioblastoma stem-like cells.
Article in Stem cells translational medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- A phase I/II study of triple-mutated oncolytic herpes virus G47∆ in patients with progressive glioblastoma.Nature communications · 2022Trial
- Review
- Going viral: targeting glioblastoma using oncolytic viruses.Immunotherapy advances · 2025Review
- Personalizing Oncolytic Immunovirotherapy Approaches.Molecular diagnosis & therapy · 2024Article
- Effects of HSV-G47Δ Oncolytic Virus on Telomerase and Telomere Length Alterations in Glioblastoma Multiforme Cancer Stem Cells Under Hypoxia and Normoxia Conditions.Current cancer drug targets · 2024Article
- Photodynamic augmentation of oncolytic virus therapy for central nervous system malignancies.Cancer letters · 2023Article
- Modifying oncolytic virotherapy to overcome the barrier of the hypoxic tumor microenvironment. Where do we stand?Cancer cell international · 2022Review
- Histone deacetylase inhibitors enhance oncolytic herpes simplex virus therapy for malignant meningioma.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Oncolytic Herpes Simplex Virus and PI3K Inhibitor BKM120 Synergize to Promote Killing of Prostate Cancer Stem-like Cells.Molecular therapy oncolytics · 2019Article
- Transcriptional Repression of p53 by PAX3 Contributes to Gliomagenesis and Differentiation of Glioma Stem Cells.Frontiers in molecular neuroscience · 2018Article
- Blockade of transforming growth factor-β signaling enhances oncolytic herpes simplex virus efficacy in patient-derived recurrent glioblastoma models.International journal of cancer · 2017Article
- HIF1α regulates single differentiated glioma cell dedifferentiation to stem-like cell phenotypes with high tumorigenic potential under hypoxia.Oncotarget · 2017Article
- A new patient-derived orthotopic malignant meningioma model treated with oncolytic herpes simplex virus.Neuro-oncology · 2016Article
- Transient fasting enhances replication of oncolytic herpes simplex virus in glioblastoma.American journal of cancer research · 2016Article
- Targeting Hypoxia-Inducible Factor 1α in a New Orthotopic Model of Glioblastoma Recapitulating the Hypoxic Tumor Microenvironment.Journal of neuropathology and experimental neurology · 2015Article
- Single agent efficacy of the VEGFR kinase inhibitor axitinib in preclinical models of glioblastoma.Journal of neuro-oncology · 2015Article
- Oncolytic adenoviruses: A thorny path to glioma cure.Genes & diseases · 2014Article
- Oncolytic viral therapy: targeting cancer stem cells.Oncolytic virotherapy · 2014Article
- Oncolytic herpes simplex virus-based strategies: toward a breakthrough in glioblastoma therapy.Frontiers in microbiology · 2014Review
- ASYMMETRIC CELL DIVISION: IMPLICATIONS FOR GLIOMA DEVELOPMENT AND TREATMENT.Translational neuroscience · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM), a fatal malignant brain tumor, contains abundant hypoxic regions that provide a "niche" to promote both the maintenance and enrichment of glioblastoma stem-like cells (GSCs) and confer resistance to chemo- and radiotherapy. Since GSCs, with an ability to resist conventional therapies, may be responsible for tumor recurrence, targeting GSCs located in such a hypoxic environment may be critical to improving the therapeutic outcome for GBM patients. Oncolytic viral therapies have been tested in the clinic as a promising therapeutic approach for GBM. In this study, we analyzed and compared the therapeutic effects of oncolytic herpes simplex virus (oHSV) type 1 G47Δ (γ34.5(-)ICP6(-)LacZ(+)α47(-)) in patient-derived GSCs under normoxia (21% oxygen) and hypoxia (1% oxygen). GSCs cultured in hypoxia showed an increased ability to form neurospheres and expressed higher levels of the putative stem cell marker CD133 compared with GSCs cultured in normoxia. G47Δ exhibited a comparable ability to infect, replicate, and kill GSCs in normoxia and hypoxia in vitro. Importantly, G47Δ could counteract hypoxia-mediated enhancement of the stem-like properties of GSCs, inhibiting their self-renewal and stem cell marker expression. Using orthotopic human GSC xenografts in mice, we demonstrated that intratumoral injection of G47ΔUs11fluc, a newly developed G47Δ derivative that expresses firefly luciferase driven by a true late viral promoter, led to an equivalent frequency of viral infection and replication in hypoxic and nonhypoxic tumor areas. These findings suggest that oHSV G47Δ represents a promising therapeutic strategy to target and kill GSCs, not only in normoxic areas of GBM but also within the hypoxic niche.
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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.