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Updated: Aug 9, 2026

Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures
Published on: January 9, 2019
Aberrant receptor signaling in human malignant gliomas: mechanisms and therapeutic implications
1Ludwig Institute for Cancer Research, San Diego Branch, 3080 CMM-East, 9500 Gilman Drive, La Jolla, CA 92093-0660, USA.
Abstract:
Alterations of the epidermal growth factor receptor (EGFR) occur frequently in malignant gliomas through gene amplification or rearrangement, especially in a large fraction of de novo type glioblastomas. The most common of these mutant EGFRs (variously named de2-7 EGFR, deltaEGFR or EGFRvIII) lacks a portion of the extracellular ligand-binding domain. Here, we review the evidence that shows that expression of deltaEGFR bestows in vivo growth advantages to human glioma cells through its constitutively active tyrosine kinase activity. Thus, deltaEGFR may provide a novel therapeutic target for the most aggressive type of glioblastoma.
Insights
Mutant epidermal growth factor receptor (EGFR) variants, particularly EGFRvIII, are common in glioblastomas. This constitutively active receptor drives tumor growth, presenting EGFRvIII as a potential therapeutic target for aggressive brain tumors.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epidermal growth factor receptor (EGFR) alterations, including gene amplification and rearrangement, are prevalent in malignant gliomas.
- A common EGFR variant, EGFRvIII (also known as de2-7 EGFR or deltaEGFR), lacks part of the extracellular ligand-binding domain.
- EGFRvIII is frequently observed in de novo glioblastomas, the most aggressive form of brain cancer.
Purpose of the Study:
- To review the evidence supporting the role of EGFRvIII in promoting glioma cell growth.
- To highlight the therapeutic potential of targeting EGFRvIII in glioblastoma.
Main Methods:
- Review of existing scientific literature and research findings.
- Analysis of data on EGFR alterations in malignant gliomas.
- Examination of the functional consequences of EGFRvIII expression in vivo.
Main Results:
- Expression of deltaEGFR (EGFRvIII) confers a growth advantage to human glioma cells in vivo.
- This growth advantage is attributed to the constitutively active tyrosine kinase activity of EGFRvIII.
- EGFRvIII is a key driver of tumor progression in a significant subset of glioblastomas.
Conclusions:
- EGFRvIII plays a critical role in the pathogenesis of aggressive glioblastomas.
- The unique characteristics of EGFRvIII make it a promising and specific therapeutic target.
- Targeting EGFRvIII could offer a novel treatment strategy for patients with glioblastoma.
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