ArticleActa neuropathologica2013
EGFR wild-type amplification and activation promote invasion and development of glioblastoma independent of angiogenesis.
Article in Acta neuropathologica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.
- Glioblastoma cells potentiate the induction of the Th1-like profile in phosphoantigen-stimulated γδ T lymphocytes.Journal of neuro-oncology · 2021Pooled it
- Phase II trial of dacomitinib, a pan-human EGFR tyrosine kinase inhibitor, in recurrent glioblastoma patients with EGFR amplification.Neuro-oncology · 2017Trial
- Interpretable prototype learning for EGFR amplification prediction from whole-slide images in glioblastoma.Journal of pathology informatics · 2026Article
- Improving T-cell engager efficacy in glioblastoma with multi-antigen targeting and novel delivery approaches.Acta neuropathologica · 2026Review
- Review
- COL6A2: A Key Survival-Related Gene and Restricting Antitumor Immunity in Glioblastoma.Cancer science · 2025Article
- Spatial Multiomics Defines a Shared Tumor Infiltrative Signature at the Resection Margin in High-Grade Gliomas.Cancer research · 2025Article
- CLOCK promotes proliferation of glioblastoma cells through acetylating PRPS1/2.Journal of neuro-oncology · 2025Article
- Evolving therapeutic strategies in glioblastoma: traditional approaches and novel interventions.3 Biotech · 2025Review
- Targeting oncofetal fibronectin and neuropilin-1 in solid tumors with PL2 peptide.Scientific reports · 2025Article
- Fused exosomal targeted therapy in periprosthetic osteolysis through regulation of bone metabolic homeostasis.Bioactive materials · 2025Article
- Sex-Related Differences in Glioblastoma: A Single-Center Retrospective Cohort Study.Biomedicines · 2025Article
- Gasdermin E in glioblastoma -pyroptosis resistance and tumor-promoting functions.Cell death discovery · 2025Article
- Single-cell transcriptome sequencing reveals new epithelial-stromal associated mesenchymal-like subsets in recurrent gliomas.Acta neuropathologica communications · 2025Article
- Predictive modeling of glioblastoma recurrence for therapeutic target identification.EMBO molecular medicine · 2025Article
- Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025Review
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Identification of Brain Cell Type-Specific Therapeutic Targets for Glioma From Genetics.CNS neuroscience & therapeutics · 2024Article
- Immunomodulatory signalling networks in glioblastoma multiforme: a comprehensive review of therapeutic approaches.Human cell · 2024Review
- EGFR mutations and abnormal trafficking in cancers.Molecular biology reports · 2024Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis is regarded as a hallmark of cancer progression and it has been postulated that solid tumor growth depends on angiogenesis. At present, however, it is clear that tumor cell invasion can occur without angiogenesis, a phenomenon that is particularly evident by the infiltrative growth of malignant brain tumors, such as glioblastomas (GBMs). In these tumors, amplification or overexpression of wild-type (wt) or truncated and constitutively activated epidermal growth factor receptor (EGFR) are regarded as important events in GBM development, where the complex downstream signaling events have been implicated in tumor cell invasion, angiogenesis and proliferation. Here, we show that amplification and in particular activation of wild-type EGFR represents an underlying mechanism for non-angiogenic, invasive tumor growth. Using a clinically relevant human GBM xenograft model, we show that tumor cells with EGFR gene amplification and activation diffusely infiltrate normal brain tissue independent of angiogenesis and that transient inhibition of EGFR activity by cetuximab inhibits the invasive tumor growth. Moreover, stable, long-term expression of a dominant-negative EGFR leads to a mesenchymal to epithelial-like transition and induction of angiogenic tumor growth. Analysis of human GBM biopsies confirmed that EGFR activation correlated with invasive/non-angiogenic tumor growth. In conclusion, our results indicate that activation of wild-type EGFR promotes invasion and glioblastoma development independent of angiogenesis, whereas loss of its activity results in angiogenic tumor growth.
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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.