ReviewFrontiers in oncology2023
EGFR alterations in glioblastoma play a role in antitumor immunity regulation.
Review in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed, 18 citations in OpenAlex.
- Breaking adaptive oncogenic resistance in glioblastoma via targeting the EGFR-STAT3 axis.Medical oncology (Northwood, London, England) · 2026Review
- Shifting AAV9 tropism by binding moiety insertion enhances transduction of tumor cell lines and human glioblastoma explants.Scientific reports · 2026Article
- Identification of hub mRNAs and long non-coding RNAs involved in temozolomide-resistant glioblastoma (brain cancer) cell lines.Discover oncology · 2026Article
- ErbB Receptor Feedback Inhibitor 1 Mutation in Biliary Tract Cancers: Turning Resistance Into Response.JCO precision oncology · 2026Article
- Dual Targeting of DNA and EGFR by ZYH005 Induces DNA Damage and Mitotic Catastrophe in Glioblastoma.MedComm · 2026Article
- Review
- NF-κB and STAT3 signaling uniquely stratify survival in female glioblastoma patients.iScience · 2026Article
- Construction of circadian clock signature for tumor microenvironment in predicting survival of esophageal squamous cell carcinoma.Frontiers in immunology · 2026Article
- EGFR gene amplification in IDH-wildtype glioblastomas: an integrative bioinformatic and histopathological analysis using immunohistochemistry and fluorescence in situ hybridization.Discover oncology · 2025Article
- EGFR Amplification in Diffuse Glioma and Its Correlation to Language Tract Integrity.Diagnostics (Basel, Switzerland) · 2025Article
- Article
- Integrative analysis of glioblastoma multiforme: the power of non-coding RNAs and hub genes in cancer research.Clinical and experimental medicine · 2025Article
- Immunotherapy in Glioblastoma: An Overview of Current Status.Clinical pharmacology : advances and applications · 2025Review
- Structural and dynamical insights revealed the anti-glioblastoma potential of withanolides from Withania coagulans against vascular endothelial growth factor receptor (VEGFR).Journal of molecular modeling · 2024Article
- Prospective Molecular Targets for Natural Killer Cell Immunotherapy against Glioblastoma Multiforme.Cells · 2024Review
- Tumor microenvironment and cancer metastasis: molecular mechanisms and therapeutic implications.Frontiers in pharmacology · 2024Review
- TACkling Cancer by Targeting Selective Protein Degradation.Pharmaceutics · 2023Review
- Imaging the effects of treatment with TERT and EGFR inhibitors on glioblastoma: An MR study.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epidermal growth factor receptor (EGFR) is the most frequently altered gene in glioblastoma (GBM), which plays an important role in tumor development and anti-tumor immune response. While current molecular targeted therapies against the EGFR signaling pathway and its downstream key molecules have not demonstrated favorable clinical outcomes in GBM. Whereas tumor immunotherapies, especially immune checkpoint inhibitors, have shown durable antitumor responses in many cancers. However, the clinical efficacy is limited in patients carrying EGFR alterations, indicating that EGFR signaling may involve tumor immune response. Recent studies reveal that EGFR alterations not only promote GBM cell proliferation but also influence immune components in the tumor microenvironment (TME), leading to the recruitment of immunosuppressive cells (e.g., M2-like TAMs, MDSCs, and Tregs), and inhibition of T and NK cell activation. Moreover, EGFR alterations upregulate the expression of immunosuppressive molecules or cytokines (such as PD-L1, CD73, TGF-β). This review explores the role of EGFR alterations in establishing an immunosuppressive TME and hopes to provide a theoretical basis for combining targeted EGFR inhibitors with immunotherapy for GBM.
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.