ReviewNeuro-oncology advances
Receptor tyrosine kinases as druggable targets in glioblastoma: Do signaling pathways matter?
Review in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 52 citations in OpenAlex.
- Nerve growth factor receptor (NGFR): A key player in glioblastoma progression.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- AMPK Pathway Activation Markers in GBM: Expression Patterns and Clinical Associations in a Real-World Study.International journal of molecular sciences · 2026Article
- Targeting Kinase Signaling in Glioblastoma: Structural Optimization, Blood-Brain Barrier Dynamics and Combinatorial Translational Strategies.International journal of molecular sciences · 2026Review
- Glioma-intrinsic MAPK/ERK signaling promotes immunotherapy efficacy through T cell infiltration and interferon responses.Nature communications · 2026Article
- Lipocalin 2 orchestrates resistance to ferroptosis via AXL.Cell reports · 2026Article
- The development of CAR T cells for patients with CNS malignancies.Nature reviews. Clinical oncology · 2026Review
- Review
- The significance of epithelial-mesenchymal transition (EMT) in the initiation, plasticity, and treatment of glioblastoma.Genes & diseases · 2026Review
- Decoding EGFR A289 Mutation in Glioblastoma: A Predictive Biomarker Framework and Targeted Therapeutic Insights.Journal of molecular neuroscience : MN · 2025Article
- Genome-wide CRISPR-Cas9 screens identify BCL family members as modulators of response to regorafenib in experimental glioma.Neuro-oncology · 2025Article
- Efficacy of MET-targeting CAR T cells against glioblastoma patient-derived xenograft models.Journal of translational medicine · 2025Article
- Targeted therapy in pediatric central nervous system tumors: a review from the National Pediatric Cancer Foundation.Frontiers in oncology · 2025Review
- MAPK/ERK signaling in gliomas modulates interferon responses, T cell recruitment, microglia phenotype, and immune checkpoint blockade efficacy.bioRxiv : the preprint server for biology · 2024Article
- Epithelial UNC-23 limits mechanical stress to maintain glia-neuron architecture in C. elegans.Developmental cell · 2024Article
- A systematic computational analysis of the endosomal recycling pathway in glioblastoma.Biochemistry and biophysics reports · 2024Article
- Capmatinib is an effective treatment for MET-fusion driven pediatric high-grade glioma and synergizes with radiotherapy.Molecular cancer · 2024Article
- Glioblastoma: An Update in Pathology, Molecular Mechanisms and Biomarkers.International journal of molecular sciences · 2024Review
- Lactate dehydrogenase A regulates tumor-macrophage symbiosis to promote glioblastoma progression.Nature communications · 2024Article
- Targeted Glioma Therapy-Clinical Trials and Future Directions.Pharmaceutics · 2024Review
- Current and future therapeutic strategies for high-grade gliomas leveraging the interplay between epigenetic regulators and kinase signaling networks.Journal of experimental & clinical cancer research : CR · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most malignant primary brain tumor without effective therapies. Since bevacizumab was FDA approved for targeting vascular endothelial growth factor receptor 2 (VEGFR2) in adult patients with recurrent GBM, targeted therapy against receptor tyrosine kinases (RTKs) has become a new avenue for GBM therapeutics. In addition to VEGFR, the epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), hepatocyte growth factor receptor (HGFR/MET), and fibroblast growth factor receptor (FGFR) are major RTK targets. However, results from clinical Phase II/III trials indicate that most RTK-targeting therapeutics including tyrosine kinase inhibitors (TKIs) and neutralizing antibodies lack clinical efficacy, either alone or in combination. The major challenge is to uncover the genetic RTK alterations driving GBM initiation and progression, as well as to elucidate the mechanisms toward therapeutic resistance. In this review, we will discuss the genetic alterations in these 5 commonly targeted RTKs, the clinical trial outcomes of the associated RTK-targeting therapeutics, and the potential mechanisms toward the resistance. We anticipate that future design of new clinical trials with combination strategies, based on the genetic alterations within an individual patient's tumor and mechanisms contributing to therapeutic resistance after treatment, will achieve durable remissions and improve outcomes in GBM patients.
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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.