ArticleNeuro-oncology2015
Changes in the EGFR amplification and EGFRvIII expression between paired primary and recurrent glioblastomas.
Article in Neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.
- Receptor tyrosine kinase targeted therapies in glioblastoma: a systematic review.Frontiers in medicine · 2026Pooled it
- Congress of neurological surgeons systematic review and evidence-based guidelines update on the role of neuropathology in the management of progressive glioblastoma in adults.Journal of neuro-oncology · 2022Pooled it
- INTELLANCE 2/EORTC 1410 randomized phase II study of Depatux-M alone and with temozolomide vs temozolomide or lomustine in recurrent EGFR amplified glioblastoma.Neuro-oncology · 2020Trial
- Epidermal growth factor receptor (EGFR) amplification rates observed in screening patients for randomized trials in glioblastoma.Journal of neuro-oncology · 2019Trial
- Phase II trial of dacomitinib, a pan-human EGFR tyrosine kinase inhibitor, in recurrent glioblastoma patients with EGFR amplification.Neuro-oncology · 2017Trial
- The intersection of chemokine signaling with the hallmarks of cancer in glioblastoma.Journal of neuro-oncology · 2026Review
- Uncovering the signaling networks of disseminated glioblastoma cells in vivo with INSIGHT.Nature communications · 2026Article
- Mechanisms of Therapeutic Resistance and Recent Advances in Glioblastoma Treatment.Immunology and cell biology · 2026Review
- Review
- The functional imperative in high-grade glioma.Experimental & molecular medicine · 2026Review
- Diversity and function of tumor-associated macrophages in brain metastases: mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Utilization of universal-targeting mSA2 CAR-T cells for the treatment of glioblastoma.Oncoimmunology · 2025Article
- Glioblastoma in adults: A Society for Neuro-Oncology (SNO) and European Society of Neuro-Oncology (EANO) consensus review on current management and future directions.Neuro-oncology · 2025Review
- Illuminating radiogenomic signatures in pediatric-type diffuse gliomas: insights into molecular, clinical, and imaging correlations. Part I: high-grade group.La Radiologia medica · 2025Review
- Immunologic specificity in glioblastoma: Antigen discovery and translational implications.Neuro-oncology advances · 2025Review
- Imaging-Based Molecular Characterization of Adult-Type Diffuse Glioma Using Diffusion and Perfusion MRI in Pre- and Post-Treatment Stage Considering Spatial and Temporal Heterogeneity.Journal of magnetic resonance imaging : JMRI · 2025Article
- CAR T cell therapy for glioblastoma: A review of the first decade of clinical trials.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- CAR-NK cell therapy combined with checkpoint inhibition induces an NKT cell response in glioblastoma.British journal of cancer · 2025Article
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Study on the anti-tumor effect of PDL1-CAR-γδT cells constructed with nanobody sequences on glioblastoma.American journal of cancer research · 2025Article
67 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe efficacy of novel targeted therapies is often tested at the time of tumor recurrence. However, for glioblastoma (GBM) patients, surgical resections at recurrence are performed only in a minority of patients; therefore, molecular data are predominantly derived from the initial tumor. Molecular data of the initial tumor for patient selection into personalized medicine trials can therefore be used only when the specific genetic change is retained in the recurrent tumor.
methodsIn this study we determined whether EGFR amplification and expression of the most common mutation in GBMs (EGFRvIII) is retained at tumor recurrence. Because retention of genetic changes may be dependent on the initial treatment, we only used a cohort of GBM samples that were uniformly treated according to the current standard of care (ie, chemo-irradiation with temozolomide).
resultsOur data show that, in spite of some quantitative differences, the EGFR amplification status remains stable in the majority (84%) of tumors evaluated. EGFRvIII expression remained similar in 79% of GBMs. However, within the tumors expressing EGFRvIII at initial diagnosis, approximately one-half lose their EGFRvIII expression at tumor recurrence.
conclusionsThe relative stability of EGFR amplification indicates that molecular data obtained in the primary tumor can be used to predict the EGFR status of the recurrent tumor, but care should be taken in extrapolating EGFRvIII expression from the primary tumor, particularly when expressed at first diagnosis.
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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.