ReviewNeuro-oncology2014
Challenges to targeting epidermal growth factor receptor in glioblastoma: escape mechanisms and combinatorial treatment strategies.
Review in Neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Connexin 43 C-terminus directly inhibits the hyperphosphorylation of Akt/ERK through protein-protein interactions in glioblastoma.Cancer science · 2018Pooled it
- A multicenter, phase II trial of GC1118, a novel anti-EGFR antibody, for recurrent glioblastoma patients with EGFR amplification.Cancer medicine · 2023Trial
- Disrupted Signalling Landscapes in Glioblastoma: Mechanistic Insights and Therapeutic Frontiers.Biology · 2026Review
- Radiology-based artificial intelligence for predicting targeted therapy response in pan-cancer: a comprehensive review.Journal of translational medicine · 2025Review
- Signaling Pathways in Gliomas.Genes · 2025Review
- The m6A demethylase FTO suppresses glioma proliferation by regulating the EREG/PI3K/Akt signaling pathway.Frontiers in cell and developmental biology · 2025Article
- Revolutionizing Glioblastoma Treatment: A Comprehensive Overview of Modern Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Lactate dehydrogenase A regulates tumor-macrophage symbiosis to promote glioblastoma progression.Nature communications · 2024Article
- Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024Review
- Understanding Glioblastoma Signaling, Heterogeneity, Invasiveness, and Drug Delivery Barriers.International journal of molecular sciences · 2023Review
- Exosomes as Novel Diagnostic Biomarkers and Therapeutic Tools in Gliomas.International journal of molecular sciences · 2023Review
- EGFR, the Lazarus target for precision oncology in glioblastoma.Neuro-oncology · 2022Review
- CBX3 accelerates the malignant progression of glioblastoma multiforme by stabilizing EGFR expression.Oncogene · 2022Article
- AZD3759 inhibits glioma through the blockade of the epidermal growth factor receptor and Janus kinase pathways.Bioengineered · 2021Article
- Glioma-Targeted Therapeutics: Computer-Aided Drug Design Prospective.The protein journal · 2021Review
- A circuitous route to GBM stem cell signalling.Nature cell biology · 2021Article
- Review
- Article
- The Involvement of Exosomes in Glioblastoma Development, Diagnosis, Prognosis, and Treatment.Brain sciences · 2020Review
- The Bradykinin-BDKRB1 Axis RegulatesCancers · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor (EGFR) gene amplification and activating mutations are common findings in glioblastomas. EGFR is at the top of a downstream signaling cascade that regulates important characteristics of glioblastoma cells, including cellular proliferation, migration, and survival. Targeting EGFR has therefore been regarded as a promising therapeutic strategy in glioblastoma for decades. However, although various pharmacological inhibitors and anti-EGFR antibodies are available, the antiglioma activity of these agents has been largely limited to preclinical models, whereas their administration to glioblastoma patients was characterized by lack of clinical benefit. Comprehensive efforts have been made within the last years to understand the underlying mechanisms that confer resistance to EGFR inhibition in glioma cells. The absence of well-known mutations that predict response to EGFR tyrosine kinase inhibitors (TKIs) in gliomas as well as the presence of redundant and alternative compensatory pathways are among the most important escape mechanisms that prevent potent antiglioma effects of EGFR-targeting drugs. Accordingly, an increasing number of in vitro and in vivo studies are aimed at overcoming this resistance by combinatorial approaches using anti-EGFR treatment together with one or more additional drugs. Novel insights into the molecular mechanisms mediating resistance to anti-EGFR treatment and promising combinatorial approaches may help to better define a future role for EGFR inhibition in the treatment of glioblastoma.
Indexed as
Identifiers
What OpenQuestion holds
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.