ArticleCell reports2026
A pontine-specific niche supports de novo gliomagenesis.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Update of
Authors and funding
4 authors.
Funding
Abstract
Pediatric high-grade gliomas (HGGs) exhibit genetic profiles accompanied by anatomical specificities. These features suggest that specific anatomical niches favor the onset and/or progression of these diseases. However, such niche identities remain elusive as existing genetically engineered mouse models fail to recapitulate these anatomical specificities. Herein, we investigate the anatomical specificities of histone H3.1 lysine 27-to-methionine (H3.1K27M) and activating ACVR1 mutations for diffuse intrinsic pontine gliomas (DIPGs)-a major pons-specific pediatric HGG. We describe a murine model where expression of H3.1K27M and activating Acvr1 and Pik3ca mutations (which co-occur with H3.1K27M in human DIPGs) induces rapid gliomagenesis specifically in the pons. We show that gliomagenesis occurs predominantly at the trigeminal root entry zone (TREZ) and requires hyaluronan receptor (HMMR) signaling. Our data demonstrate that anatomical specificities of human HGGs can be accurately recapitulated in mice and identify the TREZ as an anatomical niche that plays a key role in DIPG pathogenesis.
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.