ArticleNeoplasia (New York, N.Y.)2020
Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.
Article in Neoplasia (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Molecular Biomarkers in Glioblastoma: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2022Pooled it
- Glioblastoma Multiforme: Current Developments in Molecular Pathways, Magnetic Field-Based Interventions, and Personalized Therapy.Journal of clinical practice and research · 2026Review
- Management and survival trends for diffuse gliomas diagnosed at a single neurooncology center in China during 2000 to 2020.Scientific reports · 2025Article
- Targeting drug resistance in glioblastoma (Review).International journal of oncology · 2024Review
- Article
- EGFR/CEP7 high polysomy is separate and distinct from EGFR amplification in glioblastoma as determined by fluorescence in situ hybridization.Journal of neuropathology and experimental neurology · 2024Article
- Potential Diagnostic and Clinical Significance of Selected Genetic Alterations in Glioblastoma.International journal of molecular sciences · 2024Review
- Discrete Mechanistic Target of Rapamycin Signaling Pathways, Stem Cells, and Therapeutic Targets.Cells · 2024Review
- Clinical roles ofFrontiers in neuroscience · 2024Article
- Article
- Integrated molecular and multiparametric MRI mapping of high-grade glioma identifies regional biologic signatures.Nature communications · 2023Article
- Insights into the Role of LncRNAs and miRNAs in Glioma Progression and Their Potential as Novel Therapeutic Targets.Cancers · 2023Review
- Radiotherapy Plus Temozolomide With or Without Nimotuzumab Against the Newly Diagnosed EGFR-Positive Glioblastoma: A Retrospective Cohort Study.The oncologist · 2023Article
- Involvement of abnormal dystroglycan expression and matriglycan levels in cancer pathogenesis.Cancer cell international · 2022Review
- Article
- Leveraging Allele-Specific Expression for Therapeutic Response Gene Discovery in Glioblastoma.Cancer research · 2022Article
- Effectiveness and safety of tumor-treating fields therapy for glioblastoma: A single-center study in a Chinese cohort.Frontiers in neurology · 2022Article
- Alterations in 3D chromatin organization contribute to tumorigenesis ofComputational and structural biotechnology journal · 2022Article
- Novel Receptor Tyrosine Kinase Pathway Inhibitors for Targeted Radionuclide Therapy of Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Copy Number Variation and Rearrangements Assessment in Cancer: Comparison of Droplet Digital PCR with the Current Approaches.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of aggressiveness. Interestingly, accumulation of CNAs, as a measure of tumor mutational burden, was frequent and significantly associated to shortened survival. EGFR-amplified GBMs displayed both a higher number of concrete CNAs and a higher global tumor mutational burden than their no EGFR-amplified counterparts. In addition to genetic changes previously described in GBM, we found PARK2 and LARGE1 CNAs associated to EGFR amplification. The set of genes analyzed allowed us to explore relevant signaling pathways on GBM. Both PARK2 and LARGE1 are related to receptor tyrosine kinase/PI3K/PTEN/AKT/mTOR-signaling pathway. Finally, we found an association between the molecular pathways altered, EGFR amplification and a poor outcome. Our results underline the potential interest of categorizing GBM according to their EGFR amplification level and the usefulness of assessing the tumor mutational burden. These approaches would open new knowledge possibilities related to GBM biology and therapy.
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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 Socratic graph.