Evidence map›Paper›PMID 40478424›Full record

ArticleTranslational stroke research2025

Clinical Significance of Somatic PIK3CA and MAP3K3 Mutations in Cerebral and Spinal Cavernous Malformations.

Hiroki Hongo, Satoru Miyawaki, Keisuke Takai, Hideaki Ono, Masahiro Shimizu, Takashi Matsukawa, Shotaro Ogawa, Yu Teranishi, Satoshi Kiyofuji, Kenta Ohara and 13 more

Abstract read
In one paragraph

Article in Translational stroke research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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. Article
  2. Epidural cavernous hemangioma misdiagnosed as a schwannoma: A case report.The Journal of international medical research · 2025
    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

23 authors.

Hiroki HongoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Satoru MiyawakiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan. smiya-nsu@m.u-tokyo.ac.jp.
Keisuke TakaiDepartment of Neurosurgery, Tokyo Metropolitan Neurological Hospital, Fuchu, Japan.
Hideaki OnoDepartment of Neurosurgery, Fuji Brain Institute and Hospital, Fujinomiya, Japan.
Masahiro ShimizuDepartment of Neurosurgery, Kanto Neurosurgical Hospital, Kumagaya, Japan.
Takashi MatsukawaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Shotaro OgawaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Yu TeranishiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Satoshi KiyofujiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Kenta OharaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Daiichiro IshigamiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Yu SakaiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Seiei TorazawaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Yudai HiranoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Daisuke ShimadaDepartment of Neurosurgery, Kyorin University Faculty of Medicine, Mitaka, Japan.
Naoto KuniiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Seijiro ShimadaDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Jun MitsuiDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hiroto KatohDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Daisuke KomuraDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hirofumi NakatomiDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Shumpei IshikawaDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Nobuhito SaitoDepartment of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Funding

Japan Society for the Promotion of Science 21H03041Japan Society for the Promotion of Science 23K27709Japan Society for the Promotion of Science 24K02555
6 · The paper itself

Abstract

Somatic PIK3CA and MAP3K3 mutations in cerebral and spinal cavernous malformations (CMs) have been identified in recent studies. However, their significance in the clinical presentation and risk of hemorrhage in CMs remains poorly understood. We aimed to analyze the association between these mutations and the clinical characteristics of CMs. Among patients with CMs who underwent surgical resection of lesions between July 2002 and March 2022, those with complete clinical and radiological data at the time of initial surgery were included. Somatic PIK3CA and MAP3K3 mutations were detected using droplet digital polymerase chain reaction. Subsequently, the clinical and radiological characteristics correlated with these mutations were assessed. Furthermore, the effect of these mutations on the first symptomatic intraparenchymal hemorrhage during follow-up was evaluated. In total, 72 patients were included; among them, 50 had sufficient mutation data. PIK3CA E542K, E545K, and H1047R mutations were identified in 7 (14%), 7 (14%), and 15 (30%) patients, respectively. MAP3K3 I441M was identified in 10 (20%) patients (8 [16%] had both PIK3CA and MAP3K3 mutations). MAP3K3 I441M was more common in patients with Zabramski classification type II lesions than in those with CMs of other types (p = 0.024). Multivariate Cox regression analyses identified the presence of a PIK3CA mutation as a risk factor for early (re)hemorrhage. The results suggest that PIK3CA and MAP3K3 mutations are associated with clinical and radiological characteristics in patients with CMs and that the presence of a somatic PIK3CA mutation increases susceptibility to hemorrhage. These findings may help guide future therapeutic strategies.

Indexed as

Class I Phosphatidylinositol 3-KinasesHemangioma, Cavernous, Central Nervous SystemMAP Kinase Kinase Kinase 3MutationAdolescentAdultChildClinical RelevanceFemaleHumansMaleMiddle AgedYoung AdultClass I Phosphatidylinositol 3-KinasesMAP3K3 protein, humanMAP Kinase Kinase Kinase 3PIK3CA protein, humanCavernous malformationsHemorrhageMAP3K3PIK3CASomatic mutations

Identifiers

PMID40478424
PMCPMC12596314

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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.