ArticleMolecular cancer2024
Capmatinib is an effective treatment for MET-fusion driven pediatric high-grade glioma and synergizes with radiotherapy.
Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic study of molecular diagnosis, treatment, and prognosis in infant-type hemispheric glioma: An individual patient data meta-analysis of 164 patients.Neuro-oncology · 2026Pooled it
- Association of MUC3A P258S mutation with advanced phase CML structural and in silico insights.Functional & integrative genomics · 2026Article
- MET fusions and splicing variants in glioma: a landscape integrating clinical, pathological, and survival features.The journal of pathology. Clinical research · 2026Article
- Construction of an actin cytoskeleton-related gene signature for predicting prognosis and therapeutic response in glioblastoma: based on machine learning.Translational cancer research · 2026Article
- Efficacy of tepotinib in patients with high-grade glioma withNeuro-oncology practice · 2026Article
- CUX1::MET fusion defines an indolent subtype of diffuse low-grade glioma, MAPK pathway-altered.Acta neuropathologica communications · 2026Article
- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- From Classical to Emerging Biomarkers of Brain and Central Nervous System Tumors. An Evidence-Based Review with a Focus on Gliomas.Cellular and molecular neurobiology · 2026Review
- Investigation of a global mouse methylome atlas reveals subtype-specific copy number alterations in pediatric cancer models.Nature genetics · 2026Article
- Capmatinib targeted therapy in MET-fusion driven radiation induced glioma.Frontiers in oncology · 2026Article
- Illuminating radiogenomic signatures in pediatric-type diffuse gliomas: insights into molecular, clinical, and imaging correlations. Part I: high-grade group.La Radiologia medica · 2025Review
- MET promotes hepatocellular carcinoma development through the promotion of TRIB3-mediated FOXO1 degradation.Clinical and molecular hepatology · 2025Article
- Extra-central nervous system metastasis from high-grade glioma: a single-institution experience.Journal of neuro-oncology · 2025Article
- Pazopanib in patients with primary multi-metastatic bone Ewing sarcoma.Frontiers in oncology · 2025Article
- Rare Oncogenic Fusions in Pediatric Central Nervous System Tumors: A Case Series and Literature Review.Cancers · 2024Review
- Revisiting pediatric HGGs and PNETs according to the WHO CNS5 criteria: A clinical and genomic retrospective analysis.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
34 authors.
Funding
Abstract
backgroundPediatric-type diffuse high-grade glioma (pHGG) is the most frequent malignant brain tumor in children and can be subclassified into multiple entities. Fusion genes activating the MET receptor tyrosine kinase often occur in infant-type hemispheric glioma (IHG) but also in other pHGG and are associated with devastating morbidity and mortality.
methodsTo identify new treatment options, we established and characterized two novel orthotopic mouse models harboring distinct MET fusions. These included an immunocompetent, murine allograft model and patient-derived orthotopic xenografts (PDOX) from a MET-fusion IHG patient who failed conventional therapy and targeted therapy with cabozantinib. With these models, we analyzed the efficacy and pharmacokinetic properties of three MET inhibitors, capmatinib, crizotinib and cabozantinib, alone or combined with radiotherapy.
resultsCapmatinib showed superior brain pharmacokinetic properties and greater in vitro and in vivo efficacy than cabozantinib or crizotinib in both models. The PDOX models recapitulated the poor efficacy of cabozantinib experienced by the patient. In contrast, capmatinib extended survival and induced long-term progression-free survival when combined with radiotherapy in two complementary mouse models. Capmatinib treatment increased radiation-induced DNA double-strand breaks and delayed their repair.
conclusionsWe comprehensively investigated the combination of MET inhibition and radiotherapy as a novel treatment option for MET-driven pHGG. Our seminal preclinical data package includes pharmacokinetic characterization, recapitulation of clinical outcomes, coinciding results from multiple complementing in vivo studies, and insights into molecular mechanism underlying increased efficacy. Taken together, we demonstrate the groundbreaking efficacy of capmatinib and radiation as a highly promising concept for future clinical trials.
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.