ReviewNeuromolecular medicine2013
Epidermal growth factor receptor as a therapeutic target in glioblastoma.
Review in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 48 citations in OpenAlex.
- Auger electron-emitting EGFR-targeted and non-targeted [EJNMMI radiopharmacy and chemistry · 2025Article
- A Pharmacologic Approach Against Glioblastoma-A Synergistic Combination of a Quinoxaline-Based and a PI3K/mTOR Dual Inhibitor.International journal of molecular sciences · 2025Article
- Article
- Anti-Gene IGF-I Vaccines in Cancer Gene Therapy: A Review of a Case of Glioblastoma.Current medicinal chemistry · 2024Review
- Highly Sensitive EGFRvIII Detection in Circulating Extracellular Vesicle RNA of Glioma Patients.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Glioma-Targeted Therapeutics: Computer-Aided Drug Design Prospective.The protein journal · 2021Review
- Multi-institutional noninvasive in vivo characterization ofNeuro-oncology advances · 2020Article
- MiRNA-7 Replacement Effect on Proliferation and Tarceva-Sensitivity in U373-MG Cell Line.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Neuropathology, my friend - on the paths of being and non-being.Free neuropathology · 2020Article
- Precision diagnostics based on machine learning-derived imaging signatures.Magnetic resonance imaging · 2019Review
- Improved characterization of the relationship between long intergenic non-coding RNA Linc00152 and the occurrence and development of malignancies.Cancer medicine · 2019Review
- The protean world of non-coding RNAs in glioblastoma.Journal of molecular medicine (Berlin, Germany) · 2019Review
- Molecular Subgroups of Glioblastoma- an Assessment by Immunohistochemical Markers.Pathology oncology research : POR · 2019Article
- A network pharmacology-based study on the anti-hepatoma effect of RadixChinese medicine · 2019Article
- A novel matrine derivative WM622 inhibits hepatocellular carcinoma by inhibiting PI3K/AKT signaling pathways.Molecular and cellular biochemistry · 2018Article
- Review
- Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Exploration of Dynamic Elastic Modulus Changes on Glioblastoma Cell Populations with Aberrant EGFR Expression as a Potential Therapeutic Intervention Using a Tunable Hyaluronic Acid Hydrogel Platform.Gels (Basel, Switzerland) · 2017Article
- Therapeutic Potential for Bone Morphogenetic Protein 4 in Human Malignant Glioma.Neoplasia (New York, N.Y.) · 2017Review
- The EGFR-HER2 module: a stem cell approach to understanding a prime target and driver of solid tumors.Oncogene · 2016Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma represents one of the most challenging problems in neurooncology. Among key elements driving its behavior is the transmembrane epidermal growth factor receptor family, with the first member epidermal growth factor receptor (EGFR) centered in most studies. Engagement of the extracellular domain with a ligand activates the intracellular tyrosine kinase (TK) domain of EGFR, leading to autophosphorylation and signal transduction that controls proliferation, gene transcription, and apoptosis. Oncogenic missense mutations, deletions, and insertions in the EGFR gene are preferentially located in the extracellular domain in glioblastoma and cause constitutive activation of the receptor. The mutant EGFR may also transactivate other cell surface molecules, such as additional members of the EGFR family and the platelet-derived growth factor receptor, which ignite signaling cascades that synergize with the EGFR-initiated cascade. Because of the cell surface location and increased expression of the receptor along with its important biological function, EGFR has triggered much effort for designing targeted therapy. These approaches include TK inhibition, monoclonal antibody, vaccine, and RNA-based downregulation of the receptor. Treatment success requires that the drug penetrates the blood-brain barrier and has low systemic toxicity but high selectivity for the tumor. While the blockade of EGFR-dependent processes resulted in experimental and clinical treatment success, cells capable of using alternative signaling ultimately escape this strategy. A combination of interventions targeting tumor-specific cell surface regulators along with convergent downstream signaling pathways will likely enhance efficacy. Studies on EGFR in glioblastoma have revealed much information about the complexity of gliomagenesis and also facilitated the development of strategies for targeting drivers of tumor growth and combination therapies with increasing complexity.
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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.