ReviewCurrent cancer drug targets2017
A Rational Approach to Target the Epidermal Growth Factor Receptor in Glioblastoma.
Review in Current cancer drug targets, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Activation of PI3K/AKT/mTOR and RAF/MEK/ERK Pathways in Aggressive Pituitary Adenomas-New Potential Therapeutic Approach-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Use of Gefitinib in EGFR-Amplified Refractory Solid Tumors: An Open-Label, Single-Arm, Single-Center Prospective Pilot Study.Targeted oncology · 2020Trial
- Ethanol extract of Vanilla planifolia stems reduces PAK6 expression and induces cell death in glioblastoma cells.Journal of cellular and molecular medicine · 2024Article
- Dual blockade of EGFR and PI3K signaling pathways offers a therapeutic strategy for glioblastoma.Cell communication and signaling : CCS · 2023Article
- Personalized Medicine in Brain Gliomas: Targeted Therapy, Patient-Derived Tumor Models (Review).Sovremennye tekhnologii v meditsine · 2023Review
- Molecular dynamics simulations of a central nervous system-penetrant drug AZD3759 with lipid bilayer.Journal of molecular modeling · 2022Article
- GZ17-6.02 Inhibits the Growth of EGFRvIII+ Glioblastoma.International journal of molecular sciences · 2022Article
- Review
- 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
- Phosphorous Magnetic Resonance Spectroscopy and Molecular Markers in IDH1 Wild Type Glioblastoma.Cancers · 2021Article
- Generation of T-cell-redirecting bispecific antibodies with differentiated profiles of cytokine release and biodistribution by CD3 affinity tuning.Scientific reports · 2021Article
- Epidermal growth factor receptor as a molecular determinant of glioblastoma response to dopamine receptor D2 inhibitors.Neuro-oncology · 2021Article
- Against the Resilience of High-Grade Gliomas: The Immunotherapeutic Approach (Part I).Brain sciences · 2021Review
- Review
- Updated Insights on EGFR Signaling Pathways in Glioma.International journal of molecular sciences · 2021Review
- A pentapeptide enabled AL3810 liposome-based glioma-targeted therapy with immune opsonic effect attenuated.Acta pharmaceutica Sinica. B · 2021Article
- EGFRvIII expression and isocitrate dehydrogenase mutations in patients with glioma.Oncology letters · 2020Article
- Innovative therapies for malignant brain tumors: the road to a tailored cure.Acta bio-medica : Atenei Parmensis · 2020Article
- Adoptive immunotherapies in neuro-oncology: classification, recent advances, and translational challenges.Acta bio-medica : Atenei Parmensis · 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
1 author.
Funding
Abstract
Glioblastoma (GBM) is a deadly brain cancer, and all attempts to control it have failed so far. However, the future looks bright, as we now know the molecular landscape of GBM through the work of The Cancer Genome Atlas (TCGA) program. GBMs exhibit significant inter- and intratumoral heterogeneity, and to control this type of tumor, a personalized approach is required. One target, whose gene is amplified and mutated in a large number of GBMs, is the epidermal growth factor receptor (EGFR). But all attempts to target it have been unsuccessful. We attribute the reason for this failure to the molecular heterogeneity of EGFR in GBM, as well as to the poor brain penetration of previously tested EGFR-Tyrosine Kinase Inhibitors (EGFR-TKIs). In this review, we discuss the molecular heterogeneity of EGFR and provide rational preclinical and clinical guidelines for testing AZD9291, a third generation, irreversible EGFR-TKI with both a high affinity for EGFRvIII and excellent brain penetration.
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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.