Evidence map›Paper›PMID 35474103›Full record

ArticleScientific reports2022

Glioma facilitates the epileptic and tumor-suppressive gene expressions in the surrounding region.

Kazuki Komiyama, Keiya Iijima, Reika Kawabata-Iwakawa, Kazuyuki Fujihara, Toshikazu Kakizaki, Yuchio Yanagawa, Yuhei Yoshimoto, Shigeo Miyata

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% of its field
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

16 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  5. The molecular landscape of glioblastoma-associated epilepsy.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
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  7. Article
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  16. Application of spatial transcriptome technologies to neurological diseases.Frontiers in cell and developmental biology · 2023
    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

8 authors at 2 institutions in 1 country.

Kazuki KomiyamaDepartment of Neurosurgery, Gunma University Graduate School of Medicine, Maebashi, Japan.
Keiya IijimaDepartment of Neurosurgery, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Japan.
Reika Kawabata-IwakawaDivision of Integrated Oncology Research, Gunma University Initiative for Advanced Research, Maebashi, Japan.
Kazuyuki FujiharaDepartments of Psychiatry and Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan.
Toshikazu KakizakiDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan.
Yuchio YanagawaDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan.
Yuhei YoshimotoDepartment of Neurosurgery, Gunma University Graduate School of Medicine, Maebashi, Japan.
Shigeo MiyataDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan. s_miyata@gunma-u.ac.jp.
Gunma University · JPNational Center of Neurology and Psychiatry · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with glioma often demonstrate epilepsy. We previously found burst discharges in the peritumoral area in patients with malignant brain tumors during biopsy. Therefore, we hypothesized that the peritumoral area may possess an epileptic focus and that biological alterations in the peritumoral area may cause epileptic symptoms in patients with glioma. To test our hypothesis, we developed a rat model of glioma and characterized it at the cellular and molecular levels. We first labeled rat C6 glioma cells with tdTomato, a red fluorescent protein (C6-tdTomato), and implanted them into the somatosensory cortex of VGAT-Venus rats, which specifically expressed Venus, a yellow fluorescent protein in GABAergic neurons. We observed that the density of GABAergic neurons was significantly decreased in the peritumoral area of rats with glioma compared with the contralateral healthy side. By using a combination technique of laser capture microdissection and RNA sequencing (LCM-seq) of paraformaldehyde-fixed brain sections, we demonstrated that 19 genes were differentially expressed in the peritumoral area and that five of them were associated with epilepsy and neurodevelopmental disorders. In addition, the canonical pathways actively altered in the peritumoral area were predicted to cause a reduction in GABAergic neurons. These results suggest that biological alterations in the peritumoral area may be a cause of glioma-related epilepsy.

Indexed as

Brain NeoplasmsEpilepsyGliomaAnimalsBrainGene ExpressionHumansRats

Identifiers

PMID35474103
PMCPMC9042955
OpenAlexW4224437464

What OpenQuestion holds

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Registered trials

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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.