Evidence map›Paper›PMID 40775657›Full record

ArticleActa neuropathologica communications2025

Integrated molecular and detailed anatomical profiling identifies a prognostically adverse subtype of posterior fossa meningiomas: high-risk copy number alterations are associated with midline predilection and predict poor prognosis.

Yudai Hirano, Satoru Miyawaki, Yu Sakai, Yu Teranishi, Motoyuki Umekawa, Takeru Hirata, Shotaro Ogawa, Daisuke Komura, Hiroto Katoh, Masako Ikemura and 5 more

Abstract read
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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
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

15 authors.

Yudai HiranoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Satoru MiyawakiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. smiya-nsu@m.u-tokyo.ac.jp.
Yu SakaiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Yu TeranishiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Motoyuki UmekawaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Takeru HirataDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Shotaro OgawaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Daisuke KomuraDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Hiroto KatohDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Masako IkemuraDepartment of Pathology, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Satoshi KoizumiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Hideaki OnoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Tetsuo UshikuDepartment of Pathology, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Shumpei IshikawaDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Nobuhito SaitoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.

Funding

Japan Society for the Promotion of Science 21H03041Japan Society for the Promotion of Science 23H03018Japan Society for the Promotion of Science 23KJ0427Japan Society for the Promotion of Science 24KJ0852Japan Society for the Promotion of Science,Japan 23K08495
6 · The paper itself

Abstract

Anatomical localization of meningiomas has been increasingly linked to their genetic alterations. However, studies focusing specifically on the genomic landscape and clinical implications of posterior fossa meningiomas remain limited. In this study, we investigated the genetic, anatomical, and clinical characteristics of posterior fossa meningiomas, aiming to clarify the association between genetic alterations, precise tumor localization, and prognosis. Whole-exome sequencing was performed on 132 consecutive tumors to identify driver mutations and copy number alterations (CNAs). Tumor localization was carefully assessed based on dural attachment, arterial supply, and intraoperative findings. Based on driver mutations and CNAs, tumors were classified into three molecular groups: Group A (no Merlin pathway alterations, n = 71 (54%)), Group B (NF2 mutation/22q loss without high-risk CNAs, n = 45 (34%)), and Group C (high-risk CNAs, n = 16 (12%)). Notably, Group C showed a strong anatomical predilection, with 81% arising from midline structures, including the medial incisura and clivus. Group C tumors were significantly associated with poor progression-free survival following gross total resection (P = 0.023), and this remained significant even when the analysis was anatomically restricted to tumors located in the medial incisura and clivus (P = 0.0003). In multivariable analysis, Group C (P = 0.020, HR 6.60) and preoperative tumor volume > 10 cc (P = 0.044, HR 9.41) independently predicted poor prognosis. Overall, the results demonstrated that approximately 10% of posterior fossa meningiomas harbored high-risk CNAs, predominantly in midline locations, and were associated with worse clinical outcomes. CNA profiling in addition to the identification of driver mutations may provide a valuable tool for risk stratification and decision-making regarding adjuvant therapy in posterior fossa meningiomas.

Indexed as

Cranial Fossa, PosteriorDNA Copy Number VariationsInfratentorial NeoplasmsMeningiomaAdultAgedAged, 80 and overExome SequencingFemaleGenetic Predisposition to DiseaseHumansMagnetic Resonance ImagingMaleMiddle AgedMutationNeurofibromin 2Neurofibromin 2NF2 protein, humanAnatomical localizationCopy number alterationsGeneticNF2Posterior fossa meningiomaPrognosisRecurrence

Identifiers

PMID40775657
PMCPMC12329998

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.