ArticleThe Journal of clinical investigation2020
Everolimus improves the efficacy of dasatinib in PDGFRα-driven glioma.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03352427 (A Phase 2 Study of Dasatinib in Combination With Everolimus for Children With Gliomas Harboring PDGFR Alterations), which is not on this map. Cited by 52 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.
A Phase 2 Study of Dasatinib in Combination With Everolimus for Children With Gliomas Harboring PDGFR Alterations
Who cites it
52 citing papers in PubMed, 70 citations in OpenAlex.
- Oncohistone inhibition reshapes tumor-microenvironment communication in Diffuse Midline Glioma (DMG).bioRxiv : the preprint server for biology · 2026Article
- Combinatorial Targeting of Avapritinib-Driven MAP Kinase Activation in High-Grade Glioma.Research square · 2026Article
- Disrupting MED8-dependent epigenetic reprogramming augments avapritinib sensitivity in PDGFRA-driven glioma.Journal of experimental & clinical cancer research : CR · 2026Article
- A new hope: Clinical advances in targeted therapies for pediatric diffuse midline glioma.Neuro-oncology advances · 2026Review
- Article
- Beyond synapses non-synaptic neural microenvironment interactions remodel circuits and drive glioma progression.Frontiers in oncology · 2026Review
- AI-derived prognostic model identifies high-risk gene signatures in pediatric gliomas.Frontiers in immunology · 2026Article
- Disrupting PDGFRA-driven immune evasion in glioma: vaccine-based strategies on the horizon.Frontiers in oncology · 2026Review
- Modeling diffuse midline glioma through triple-electrode in utero electroporation of the developing mouse pons.PloS one · 2026Article
- Non-canonical splice variant of PFKFB4 in hepatocellular carcinoma activates AKT through direct interaction.JHEP reports : innovation in hepatology · 2025Article
- RBM39 degrader invigorates innate immunity to eradicate neuroblastoma despite cancer cell plasticity.Nature communications · 2025Article
- H3K27M diffuse midline glioma is homologous recombination defective and sensitized to radiotherapy and NK cell-mediated antitumor immunity by PARP inhibition.Neuro-oncology · 2025Article
- Current Landscape of Preclinical Models for Pediatric Gliomas: Clinical Implications and Future Directions.Cancers · 2025Review
- Article
- Navigating Glioma Complexity: The Role of Abnormal Signaling Pathways in Shaping Future Therapies.Biomedicines · 2025Review
- Advances in the Repurposing and Blood-Brain Barrier Penetrance of Drugs in Pediatric Brain Tumors.Cancers · 2025Review
- Spermine Synthase : A Potential Prognostic Marker for Lower-Grade Gliomas.Journal of Korean Neurosurgical Society · 2025Article
- Overcoming immunotherapy resistance in glioblastoma: challenges and emerging strategies.Frontiers in pharmacology · 2025Review
- Involvement of everolimus‑induced ABCB1 downregulation in drug‑drug interactions.Biomedical reports · 2024Article
- Therapeutic targeting of differentiation-state dependent metabolic vulnerabilities in diffuse midline glioma.Nature communications · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors at 8 institutions in 1 country.
Funding
Abstract
Pediatric and adult high-grade gliomas (HGGs) frequently harbor PDGFRA alterations. We hypothesized that cotreatment with everolimus may improve the efficacy of dasatinib in PDGFRα-driven glioma through combinatorial synergism and increased tumor accumulation of dasatinib. We performed dose-response, synergism, P-glycoprotein inhibition, and pharmacokinetic studies in in vitro and in vivo human and mouse models of HGG. Six patients with recurrent PDGFRα-driven glioma were treated with dasatinib and everolimus. We found that dasatinib effectively inhibited the proliferation of mouse and human primary HGG cells with a variety of PDGFRA alterations. Dasatinib exhibited synergy with everolimus in the treatment of HGG cells at low nanomolar concentrations of both agents, with a reduction in mTOR signaling that persisted after dasatinib treatment alone. Prolonged exposure to everolimus significantly improved the CNS retention of dasatinib and extended the survival of PPK tumor-bearing mice (mutant TP53, mutant PDGFRA, H3K27M). Six pediatric patients with glioma tolerated this combination without significant adverse events, and 4 patients with recurrent disease (n = 4) had a median overall survival of 8.5 months. Our results show that the efficacy of dasatinib treatment of PDGFRα-driven HGG was enhanced with everolimus and suggest a promising route for improving targeted therapy for this patient population.
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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.