Evidence map›Paper›PMID 41239509›Full record

ArticleActa neuropathologica communications2025

Molecular insights into prognostic model for meningiomas treated with stereotactic radiosurgery: negative impacts of 1q gain on tumor control and survival.

Motoyuki Umekawa, Yuki Shinya, Yudai Hirano, Satoru Miyawaki, Hirotaka Hasegawa, Yu Sakai, Yu Teranishi, Shotaro Ogawa, Atsuto Katano, Daisuke Komura and 6 more

Erratum issuedAbstract 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. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Motoyuki UmekawaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0002-7722-9861
Yuki ShinyaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0003-0097-5804
Yudai HiranoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0003-4043-0593
Satoru MiyawakiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan. smiya-nsu@m.u-tokyo.ac.jp.ORCID 0000-0001-6369-3391
Hirotaka HasegawaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0002-3585-2188
Yu SakaiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0001-7854-1462
Yu TeranishiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0001-7448-742X
Shotaro OgawaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0002-2919-2224
Atsuto KatanoDepartment of Radiology, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0003-4393-1828
Daisuke KomuraDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0002-0038-728X
Hiroto KatohDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0001-6550-6203
Masako IkemuraDepartment of Pathology, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0002-7148-778X
Hideaki OnoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0001-9615-0553
Tetsuo UshikuDepartment of Pathology, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0002-1763-8380
Shumpei IshikawaDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0003-4392-090X
Nobuhito SaitoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-8655, Japan.ORCID 0000-0001-9756-781X

Funding

Japan Society for the Promotion of Science 22K20815Japan Society for the Promotion of Science 23K27709Japan Society for the Promotion of Science 24K23523Japan Society for the Promotion of Science,Japan 21H03041Japan Society for the Promotion of Science,Japan 24KJ0852
6 · The paper itself

Abstract

Molecular classifications enhance prognostic accuracy in meningiomas; however, their predictive significance following stereotactic radiosurgery (SRS) remains unclear. This study aimed to assess whether molecular characteristics identified by whole-exome sequencing (WES), specifically driver mutations and copy number alterations (CNAs), are prognostic indicators of outcomes after SRS. This retrospective cohort study included 95 patients (median age 61; 66% female) with 97 surgically resected meningiomas treated with SRS between 1999 and 2023. Primary outcomes were progression-free survival (PFS) and disease-specific survival (DSS). Tumors were molecularly classified using WES into Group A (NF2-wildtype), Group B (NF2 mutation/22q loss without high-risk CNAs), and Group C (high-risk CNAs including 1p loss, 1q gain, 6p/6q loss, 10p/10q loss, 14q loss, 18p/18q loss, and CDKN2A/B homozygous deletion). Group C exhibited significantly inferior PFS at 5 years (49.7%) compared with Groups A (88.5%, p < 0.001) and B (100%, p = 0.002). DSS at 10 years was also significantly reduced in Group C (60.4%) relative to Groups A and B (100%, p < 0.001 and p = 0.016, respectively). Within Group C, 1q gain correlated strongly with poorer outcomes, with significantly lower 5-year PFS (15.9% vs. 64.3%, p < 0.001) and DSS (51.3% vs. 90.4%, p < 0.001). Furthermore, even WHO grade 1 tumors with 1q gain demonstrated significantly worse outcomes (5-year PFS: 33.3% vs. 76.5%, p = 0.023; DSS: 44.4% vs. 89.3%, p = 0.011). Molecular classification utilizing WES-derived CNAs substantially improves prognostic prediction after SRS for meningiomas. Chromosome 1q gain was a critical biomarker indicating elevated risk for tumor progression and mortality, even among WHO grade 1 tumors.

Indexed as

Chromosomes, Human, Pair 1Meningeal NeoplasmsMeningiomaRadiosurgeryAdultAgedAged, 80 and overDNA Copy Number VariationsExome SequencingFemaleHumansMaleMiddle AgedMutationPrognosisProgression-Free Survival1q gainCopy number alterationMeningiomaStereotactic radiosurgeryWhole-exome sequencing

Identifiers

PMID41239509
PMCPMC12619156

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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.