ArticleCancer research2014
Targeting a glioblastoma cancer stem-cell population defined by EGF receptor variant III.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 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
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- EGFRvIII Reduces Neural Stem/Progenitor Marker Expression in GFAP-Negative iNSCs: Evidence for a Context-Dependent Cellular Response.International journal of molecular sciences · 2026Article
- Comparative efficacy and safety of therapeutic strategies for EGFRvIII positive recurrent glioblastoma.iScience · 2025Article
- Tissue mechanics in tumor heterogeneity and aggression.Trends in cancer · 2025Review
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
- In Silico Born Designed Anti-EGFR Aptamer Gol1 Has Anti-Proliferative Potential for Patient Glioblastoma Cells.International journal of molecular sciences · 2025Article
- In Vitro Functional Validation of an Anti-FREM2 Nanobody for Glioblastoma Cell Targeting.Antibodies (Basel, Switzerland) · 2025Article
- Expression features of targets for anti-glioma CAR-T cell immunotherapy.Journal of neuro-oncology · 2025Article
- Comprehensive insights into glioblastoma multiforme: drug delivery challenges and multimodal treatment strategies.Therapeutic delivery · 2025Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Review
- The hope, hype and obstacles surrounding cell therapy.Journal of cellular and molecular medicine · 2024Review
- A novel EGFR variant EGFRx maintains glioblastoma stem cells through STAT5.Neuro-oncology · 2024Article
- Recent advances in drug delivery systems for targeting brain tumors.Drug delivery · 2023Review
- Molecular Targeted Therapies in Glioblastoma Multiforme: A Systematic Overview of Global Trends and Findings.Brain sciences · 2023Review
- Identification of glioblastoma stem cell-associated lncRNAs using single-cell RNA sequencing datasets.Stem cell reports · 2023Article
- Review
- Shaping the brain vasculature in development and disease in the single-cell era.Nature reviews. Neuroscience · 2023Review
- CAR T Cell Therapy in Glioblastoma: Overcoming Challenges Related to Antigen Expression.Cancers · 2023Review
- Increased EGFRvIII Epitope Accessibility after Tyrosine Kinase Inhibitor Treatment of Glioblastoma Cells Creates More Opportunities for Immunotherapy.International journal of molecular sciences · 2023Article
34 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
12 authors at 7 institutions in 3 countries.
Funding
Abstract
The relationship between mutated proteins and the cancer stem-cell population is unclear. Glioblastoma tumors frequently express EGFRvIII, an EGF receptor (EGFR) variant that arises via gene rearrangement and amplification. However, expression of EGFRvIII is restricted despite the prevalence of the alteration. Here, we show that EGFRvIII is highly coexpressed with CD133 and that EGFRvIII(+)/CD133(+) defines the population of cancer stem cells (CSC) with the highest degree of self-renewal and tumor-initiating ability. EGFRvIII(+) cells are associated with other stem/progenitor markers, whereas markers of differentiation are found in EGFRvIII(-) cells. EGFRvIII expression is lost in standard cell culture, but its expression is maintained in tumor sphere culture, and cultured cells also retain the EGFRvIII(+)/CD133(+) coexpression, self-renewal, and tumor initiating abilities. Elimination of the EGFRvIII(+)/CD133(+) population using a bispecific antibody reduced tumorigenicity of implanted tumor cells better than any reagent directed against a single epitope. This work demonstrates that a mutated oncogene can have CSC-specific expression and be used to specifically target this population.
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.