ReviewOncogene2023
Biological and clinical implications of FGFR aberrations in paediatric and young adult cancers.
Review in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 28 citations in OpenAlex.
- Dual PI3K/AKT and CDK4/6 inhibition reveals selective sensitivity in an SHH medulloblastoma stem cell model.Molecular oncology · 2026Article
- Identification and validation of exosome-related biomarkers in pediatric glioblastoma.Discover oncology · 2026Article
- Review
- FGFR alterations and potential role of FGFR inhibitors in pediatric brain tumors.Neuro-oncology advances · 2026Review
- Mutated FGFR1 is an oncogenic driver and therapeutic target in high-risk neuroblastoma.The Journal of clinical investigation · 2026Article
- Comprehensive Multiplatform Tyrosine Kinase Profiling Reveals Novel Actionable FGFR Aberrations across Sarcomas Affecting the Young.Molecular cancer therapeutics · 2026Article
- Postmarketing Cases of Erdafitinib-Associated Skeletal Growth Toxicity Events in Pediatric Patients.Pediatric blood & cancer · 2026Article
- Antagonists of the N-cadherin/Fibroblast growth factor receptor tyrosine kinase complex.Tissue barriers · 2026Review
- FGFR Aberrations in Solid Tumors: Mechanistic Insights and Clinical Translation of Targeted Therapies.Cancers · 2025Review
- Molecular Landscape of Pediatric Low-Grade Gliomas: Insights From RNA-NGS and Bioinformatic Analysis.Genes, chromosomes & cancer · 2025Article
- Genetic profiling of osteosarcoma in an adolescent using a next‑generation sequencing panel and Sanger sequencing: A case report and review of the literature.Biomedical reports · 2025Article
- Targeting the BAG2/CHIP axis promotes gastric cancer apoptosis by blocking apoptosome assembly.Frontiers in immunology · 2025Article
- Integration of single-nuclei and spatial transcriptomics to decipher tumor phenotype predictive of relapse-free survival in Wilms tumor.Frontiers in immunology · 2025Article
- A structure-based tool to interpret the significance of kinase mutations in clinical next generation sequencing in cancer.Frontiers in oncology · 2025Article
- Exploring Shootin1's oncogenic role withinTurkish journal of biology = Turk biyoloji dergisi · 2025Article
- Signaling of Mitogenic and Metabolic Activities by Fibroblast Growth Factors.Journal of cellular signaling · 2025Article
- Sex Differences in Ependymoma Methylation by Methylation-Defined Subgroup.Journal of cellular and molecular medicine · 2024Article
- Review
- Elucidating the Role of Wildtype and Variant FGFR2 Structural Dynamics in (Dys)Function and Disorder.International journal of molecular sciences · 2024Article
- FGFR1 fusions as a novel molecular driver in rhabdomyosarcoma.Genes, chromosomes & cancer · 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rare but recurrent mutations in the fibroblast growth factor receptor (FGFR) pathways, most commonly in one of the four FGFR receptor tyrosine kinase genes, can potentially be targeted with broad-spectrum multi-kinase or FGFR selective inhibitors. The complete spectrum of these mutations in paediatric cancers is emerging as precision medicine programs perform comprehensive sequencing of individual tumours. Identification of patients most likely to benefit from FGFR inhibition currently rests on identifying activating FGFR mutations, gene fusions, or gene amplification events. However, the expanding use of transcriptome sequencing (RNAseq) has identified that many tumours overexpress FGFRs, in the absence of any genomic aberration. The challenge now presented is to determine when this indicates true FGFR oncogenic activity. Under-appreciated mechanisms of FGFR pathway activation, including alternate FGFR transcript expression and concomitant FGFR and FGF ligand expression, may mark those tumours where FGFR overexpression is indicative of a dependence on FGFR signalling. In this review, we provide a comprehensive and mechanistic overview of FGFR pathway aberrations and their functional consequences in paediatric cancer. We explore how FGFR over expression might be associated with true receptor activation. Further, we discuss the therapeutic implications of these aberrations in the paediatric setting and outline current and emerging therapeutic strategies to treat paediatric patients with FGFR-driven cancers.
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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.