ArticleJournal of neuro-oncology2009
Genetically engineered T cells to target EGFRvIII expressing glioblastoma.
Article in Journal of neuro-oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of targeted therapies in the management of progressive glioblastoma : a systematic review and evidence-based clinical practice guideline.Journal of neuro-oncology · 2014Guideline
- Bispecific T-Cell Engagers and Chimeric Antigen Receptor T-Cell Therapies in Glioblastoma: An Update.Current oncology (Toronto, Ont.) · 2023Review
- Review
- Definition and Characterization of SOX11-Derived T Cell Epitopes towards Immunotherapy of Glioma.International journal of molecular sciences · 2023Article
- Review
- Challenges in the Treatment of Glioblastoma by Chimeric Antigen Receptor T-Cell Immunotherapy and Possible Solutions.Frontiers in immunology · 2022Review
- Exploring the role of epidermal growth factor receptor variant III in meningeal tumors.PloS one · 2021Article
- CAR T cells and checkpoint inhibition for the treatment of glioblastoma.Expert opinion on biological therapy · 2020Review
- Pilot Trial of Adoptive Transfer of Chimeric Antigen Receptor-transduced T Cells Targeting EGFRvIII in Patients With Glioblastoma.Journal of immunotherapy (Hagerstown, Md. : 1997) · 2019Article
- CAR T-cell therapy for glioblastoma: ready for the next round of clinical testing?Expert review of anticancer therapy · 2018Review
- Article
- The Potential of Cellular- and Viral-Based Immunotherapies for Malignant Glioma-Dendritic Cell Vaccines, Adoptive Cell Transfer, and Oncolytic Viruses.Current neurology and neuroscience reports · 2017Review
- Chimeric antigen receptors for treatment of glioblastoma: a practical review of challenges and ways to overcome them.Cancer gene therapy · 2017Review
- Targeting Malignant Brain Tumors with Antibodies.Frontiers in immunology · 2017Review
- Cellular immunotherapy for malignant gliomas.Expert opinion on biological therapy · 2016Review
- Improving vaccine efficacy against malignant glioma.Oncoimmunology · 2016Review
- Emerging immunotherapies for glioblastoma.Expert opinion on emerging drugs · 2016Review
- Recent advances in T-cell engineering for use in immunotherapy.F1000Research · 2016Review
- Immunotherapeutic advancements for glioblastoma.Frontiers in oncology · 2015Review
- T cells redirected to interleukin-13Rα2 with interleukin-13 mutein--chimeric antigen receptors have anti-glioma activity but also recognize interleukin-13Rα1.Cytotherapy · 2014Article
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Authors and funding
10 authors.
Funding
Abstract
Glioblastoma remains a significant therapeutic challenge, warranting further investigation of novel therapies. We describe an immunotherapeutic strategy to treat glioblastoma based on adoptive transfer of genetically modified T-lymphocytes (T cells) redirected to kill EGFRvIII expressing gliomas. We constructed a chimeric immune receptor (CIR) specific to EGFRvIII, (MR1-zeta). After in vitro selection and expansion, MR1-zeta genetically modified primary human T-cells specifically recognized EGFRvIII-positive tumor cells as demonstrated by IFN-gamma secretion and efficient tumor lysis compared to control CIRs defective in EGFRvIII binding (MRB-zeta) or signaling (MR1-delzeta). MR1-zeta expressing T cells also inhibited EGFRvIII-positive tumor growth in vivo in a xenografted mouse model. Successful targeting of EGFRvIII-positive tumors via adoptive transfer of genetically modified T cells may represent a new immunotherapy strategy with great potential for clinical applications.
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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.