ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009
Release of HMGB1 in response to proapoptotic glioma killing strategies: efficacy and neurotoxicity.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed.
- Tumor-intrinsic TLR4 signaling as a context-dependent rheostat in glioblastoma.Journal of molecular medicine (Berlin, Germany) · 2026Review
- HMGB1 enhances the migratory and invasive abilities of A2780/DDP cells by facilitating epithelial to mesenchymal transition via GSK‑3β.Experimental and therapeutic medicine · 2024Article
- HMGB1/RAGE axis in tumor development: unraveling its significance.Frontiers in oncology · 2024Review
- Cell and gene therapy in neuro-oncology.Handbook of clinical neurology · 2024Review
- Therapeutic effects against high-grade glioblastoma mediated by engineered induced neural stem cells combined with GD2-specific CAR-NK.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Combined cytotoxic and immune-stimulatory gene therapy using Ad-TK and Ad-Flt3L: Translational developments from rodents to glioma patients.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Impact of epigenetic reprogramming on antitumor immune responses in glioma.The Journal of clinical investigation · 2023Review
- The tumor micro-environment in pediatric glioma: friend or foe?Frontiers in immunology · 2023Review
- Review
- Optimization of cancer immunotherapy through pyroptosis: A pyroptosis-related signature predicts survival benefit and potential synergy for immunotherapy in glioma.Frontiers in immunology · 2022Article
- Review
- CD200 Immune-Checkpoint Peptide Elicits an Anti-glioma Response Through the DAP10 Signaling Pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Targeting Neuroinflammation in Brain Cancer: Uncovering Mechanisms, Pharmacological Targets, and Neuropharmaceutical Developments.Frontiers in pharmacology · 2021Review
- Current Approaches for Glioma Gene Therapy and Virotherapy.Frontiers in molecular neuroscience · 2021Review
- Immune-stimulatory (TK/Flt3L) gene therapy opens the door to a promising new treatment strategy against brainstem gliomas.Oncotarget · 2020Article
- Detection of immunogenic cell death and its relevance for cancer therapy.Cell death & disease · 2020Review
- Therapeutic Efficacy of Immune Stimulatory Thymidine Kinase and fms-like Tyrosine Kinase 3 Ligand (TK/Flt3L) Gene Therapy in a Mouse Model of High-Grade Brainstem Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers.Cancers · 2020Review
- Prospects of biological and synthetic pharmacotherapies for glioblastoma.Expert opinion on biological therapy · 2020Review
- LINC00662 sponges miR-107 accelerating the invasiveness and proliferation of glioma cells.Journal of Cancer · 2020Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors.
Funding
Abstract
purposeIn preparation for a phase I clinical trial using a combined cytotoxic/immunotherapeutic strategy with adenoviruses (Ad) expressing Flt3L (Ad-Flt3L) and thymidine kinase (Ad-TK) to treat glioblastoma (GBM), we tested the hypothesis that Ad-TK+GCV would be the optimal tumor-killing agent in relation to efficacy and safety when compared with other proapoptotic approaches. EXPERIMENTAL
designThe efficacy and neurotoxicity of Ad-TK+GCV was compared with Ads encoding the proapoptotic cytokines [tumor necrosis factor-alpha, tumor necrosis factor-related apoptosis-inducing factor (TRAIL), and Fas ligand (FasL)], alone or in combination with Ad-Flt3L. In rats bearing small GBMs (day 4), only Ad-TK+GCV or Ad-FasL improved survival.
resultsIn rats bearing large GBMs (day 9), the combination of Ad-Flt3L with Ad-FasL did not improve survival over FasL alone, whereas Ad-Flt3L combined with Ad-TK+GCV led to 70% long-term survival. Expression of FasL and TRAIL caused severe neuropathology, which was not encountered when we used Ad-TK+/-Ad-Flt3L. In vitro, all treatments elicited release of high mobility group box 1 protein (HMGB1) from dying tumor cells. In vivo, the highest levels of circulating HMGB1 were observed after treatment with Ad-TK+GCV+Ad-Flt3L; HMGB1 was necessary for the therapeutic efficacy of AdTK+GCV+Ad-Flt3L because its blockade with glycyrrhizin completely blocked tumor regression. We also showed the killing efficacy of Ad-TK+GCV in human GBM cell lines and GBM primary cultures, which also elicited release of HMGB1.
conclusionsOur results indicate that Ad-TK+GCV+Ad-Flt3L exhibit the highest efficacy and safety profile among the several proapoptotic approaches tested. The results reported further support the implementation of this combined approach in a phase I clinical trial for GBM.
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