Evidence map›Paper›PMID 40241149›Full record

ArticleActa neuropathologica communications2025

Characteristics and outcomes of diffuse non-midline gliomas with H3F3A gene mutation in the Kansai Molecular Diagnosis Network for CNS Tumors (Kansai Network): multicenter retrospective cohort study.

Hirokazu Nakatogawa, Junya Fukai, Hiroshi Kawaji, Nobuhide Hayashi, Ema Yoshioka, Yoshinori Kodama, Kosuke Nakajo, Takehiro Uda, Yoshiki Arakawa, Shigeki Takada and 21 more

Abstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

31 authors.

Hirokazu NakatogawaDepartment of Pediatric Neurosurgery, Seirei Hamamatsu General Hospital, Chuo-ku Sumiyoshi 2-12-12, Hamamatsu, Shizuoka, 430-8558, Japan. hiro-nakato@sis.seirei.or.jp.ORCID 0000-0002-4241-3028
Junya FukaiKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan. junfukai@wakayama-med.ac.jp.ORCID 0000-0001-7103-8493
Hiroshi KawajiDepartment of Neurosurgery, Seirei Hamamatsu General Hospital, Hamamatsu, Shizuoka, 430-8558, Japan.
Nobuhide HayashiKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Ema YoshiokaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Yoshinori KodamaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Kosuke NakajoKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Takehiro UdaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Yoshiki ArakawaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Shigeki TakadaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Noriyuki KijimaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Kenichi IshibashiKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Takeshi OkudaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Yukihiko SonodaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Shiro OhueKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Hideyuki AritaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Masahide MatsudaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Tadateru FukamiKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Takahiro TomitaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Akihiro InoueKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Takamune AchihaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Hideki KashiwagiKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Daisuke KanematsuKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Asako KatsumaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Miho SumidaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Tomoko ShofudaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Masayuki ManoKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Manabu KinoshitaKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Kanji MoriKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.
Chikanori InenagaDepartment of Neurosurgery, Seirei Hamamatsu General Hospital, Hamamatsu, Shizuoka, 430-8558, Japan.
Yonehiro KanemuraKansai Molecular Diagnosis Network for CNS Tumors, Osaka, 540-0006, Japan.

Funding

Japan Society for the Promotion of Science 23K08529
6 · The paper itself

Abstract

Diffuse gliomas with H3F3A gene mutation such as H3.3 K27M and G34R/V are infrequently found in the cerebral hemisphere. These tumors may be called histone H3 K27M-mutant diffuse non-midline gliomas (NDMG) or H3 G34-mutant diffuse hemispheric gliomas (DHG), respectively. We investigated the clinical, radiological and molecular characteristics and treatment outcomes of patients with H3 K27-mutant NDMG compared with those with H3 G34-mutant DHG. We collected cases of histone H3-mutant diffuse glioma at non-midline location that were enrolled in the Kansai Molecular Diagnosis Network for CNS Tumors. The clinical, radiological and pathological characteristics and DNA methylation were retrospectively analyzed and then compared between cases of NDMG and DHG. We evaluated various factors to examine their effects on overall survival. Included in this study were 16 patients with H3 K27M-mutant NDMG and nine patients with H3 G34R/V-mutant DHG. Patients with NDMG were older than those with DHG (median age: 45 vs. 25 years old). Overall survival times of patients with NDMG were comparable to those of DHG (median overall survival: 20.0 vs. 22.5 months). Female sex, preoperative Karnofsky performance status score ≥ 80 and extensive surgical resection tended be related to better prognoses in the patients with these tumors. H3 K27M-mutant NDMGs were shown to possess similar DNA methylation properties to H3 K27M-mutant DMGs. Diffuse gliomas harboring histone H3 K27M mutation can arise in the cerebral hemisphere in older adults. These findings suggest that H3 K27M-mutant NDMGs show different clinical manifestations to H3 K27M-mutant DMGs and H3 G34R/V-mutant DHGs, despite having similar molecular properties to H3 K27M-mutant DMGs.

Indexed as

Brain NeoplasmsGliomaHistonesAdolescentAdultAgedDNA MethylationFemaleHumansMaleMiddle AgedMutationRetrospective StudiesYoung AdultH3-3A protein, humanHistonesDiffuse hemispheric gliomaDiffuse non-midline gliomaDNA methylationH3F3A gene mutationH3G34-mutantH3K27-altered

Identifiers

PMID40241149
PMCPMC12001451

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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.