ArticleNature genetics2014
Recurrent activating ACVR1 mutations in diffuse intrinsic pontine glioma.
Article in Nature genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 papers, 4 of them syntheses that pooled it.
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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
298 citing papers in PubMed, 4 syntheses or guidelines pooled it, 519 citations in OpenAlex.
- Prognostic Implication of Patient Age in H3K27M-Mutant Midline Gliomas.Frontiers in oncology · 2022Pooled it
- The clinicopathological and prognostic significance of TP53 alteration in K27M mutated gliomas: an individual-participant data meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2018Pooled it
- Reconstructing the molecular life history of gliomas.Acta neuropathologica · 2018Pooled it
- Integrated Molecular Meta-Analysis of 1,000 Pediatric High-Grade and Diffuse Intrinsic Pontine Glioma.Cancer cell · 2017Pooled it
- Pharmacokinetics of Zilurgisertib With and Without Food from Single and Multiple Ascending Dose Phase 1 Studies in Healthy Adults.European journal of drug metabolism and pharmacokinetics · 2025Trial
- A phase I/II study of ribociclib following radiation therapy in children with newly diagnosed diffuse intrinsic pontine glioma (DIPG).Journal of neuro-oncology · 2020Trial
- High-throughput spheroid profiling reveals BMP-driven rewiring of glioma cell death responses.bioRxiv : the preprint server for biology · 2026Article
- Single-cell multi-omic atlas and morphogen screening informs midbrain and hindbrain organoid engineering.Nature neuroscience · 2026Article
- Survival analysis of adult midline-located gliomas and diffuse midline gliomas: beyond the H3K27 mutation paradigm.Journal of neuro-oncology · 2026Article
- Targeting Activin Receptor-like Kinase 2 Using Heterobifunctional Protein Degraders.Journal of medicinal chemistry · 2026Article
- A perfused, parallelized blood brain barrier-tumor platform for compound permeation and efficacy investigations.Microsystems & nanoengineering · 2026Article
- RNA N6-methyladenosine (m6A) regulates cell cycle progression in diffuse midline glioma (DMG) and confers sensitivity to FTO inhibition.Cell death & disease · 2026Article
- Bone morphogenetic protein receptor 2 signaling mediates mitochondrial CaCell communication and signaling : CCS · 2026Article
- Dysregulated Microglial Synaptic Engulfment in Diffuse Midline Glioma.bioRxiv : the preprint server for biology · 2025Article
- Small Extracellular Vesicles From Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response.Journal of extracellular vesicles · 2025Article
- Molecular characterization and clinical features of diffuse midline glioma in the pediatric precision oncology registry INFORM.Acta neuropathologica · 2025Article
- Germline analysis of an international cohort of pediatric diffuse midline glioma patients.Neuro-oncology · 2025Article
- Establishment of xenografts and methods to evaluate tumor burden for the three most frequent subclasses of pediatric-type diffuse high grade gliomas.Journal of neuro-oncology · 2025Article
- An oncohistone-driven H3.3K27M/CREB5/ID1 axis maintains the stemness and malignancy of diffuse intrinsic pontine glioma.Nature communications · 2025Article
- Opportunities and challenges for patient-derived models of brain tumors in functional precision medicine.NPJ precision oncology · 2025Review
238 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 11 institutions in 6 countries.
Funding
Abstract
Diffuse intrinsic pontine gliomas (DIPGs) are highly infiltrative malignant glial neoplasms of the ventral pons that, due to their location within the brain, are unsuitable for surgical resection and consequently have a universally dismal clinical outcome. The median survival time is 9-12 months, with neither chemotherapeutic nor targeted agents showing substantial survival benefit in clinical trials in children with these tumors. We report the identification of recurrent activating mutations in the ACVR1 gene, which encodes a type I activin receptor serine/threonine kinase, in 21% of DIPG samples. Strikingly, these somatic mutations (encoding p.Arg206His, p.Arg258Gly, p.Gly328Glu, p.Gly328Val, p.Gly328Trp and p.Gly356Asp substitutions) have not been reported previously in cancer but are identical to mutations found in the germ line of individuals with the congenital childhood developmental disorder fibrodysplasia ossificans progressiva (FOP) and have been shown to constitutively activate the BMP-TGF-β signaling pathway. These mutations represent new targets for therapeutic intervention in this otherwise incurable disease.
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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.