Evidence map›Paper›PMID 34525976›Full record

ArticleBMC cancer2021

Infrequent RAS mutation is not associated with specific histological phenotype in gliomas.

Yasuhide Makino, Yoshiki Arakawa, Ema Yoshioka, Tomoko Shofuda, Sachiko Minamiguchi, Takeshi Kawauchi, Masahiro Tanji, Daisuke Kanematsu, Masahiro Nonaka, Yoshiko Okita and 6 more

Open access · goldAbstract readCase Reports
In one paragraph

Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Molecular features in gangliogliomas: a systematic review.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2026
    Pooled it
  2. Article
  3. Radiosensitization of Glioblastoma by the K-ras Inhibitor RMC-6236.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The Role of RAS in CNS Tumors: A Key Player or an Overlooked Oncogene?International journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
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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

16 authors at 5 institutions in 1 country.

Yasuhide MakinoDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yoshiki ArakawaDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan. yarakawa@kuhp.kyoto-u.ac.jp.
Ema YoshiokaDepartment of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Tomoko ShofudaDepartment of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Sachiko MinamiguchiDepartment of Diagnostic Pathology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takeshi KawauchiDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masahiro TanjiDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Daisuke KanematsuDepartment of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Masahiro NonakaDepartment of Neurosurgery, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Yoshiko OkitaDepartment of Neurosurgery, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Yoshinori KodamaDepartment of Central Laboratory and Surgical Pathology, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Masayuki ManoDepartment of Central Laboratory and Surgical Pathology, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Takanori HiroseDepartment of Diagnostic Pathology, Hyogo Cancer Center, Hyogo, Japan.
Yohei MineharuDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Susumu MiyamotoDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yonehiro KanemuraDepartment of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, Osaka, Japan. yonehirok@gmail.com.
Osaka National Hospital · JPKyoto University · JPHyogo Prefectural Cancer Center · JPKansai Medical University · JPOsaka Medical Center for Cancer and Cardiovascular Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMutations in driver genes such as IDH and BRAF have been identified in gliomas. Meanwhile, dysregulations in the p53, RB1, and MAPK and/or PI3K pathways are involved in the molecular pathogenesis of glioblastoma. RAS family genes activate MAPK through activation of RAF and PI3K to promote cell proliferation. RAS mutations are a well-known driver of mutation in many types of cancers, but knowledge of their significance for glioma is insufficient. The purpose of this study was to reveal the frequency and the clinical phenotype of RAS mutant in gliomas.

methodsThis study analysed RAS mutations and their clinical significance in 242 gliomas that were stored as unfixed or cryopreserved specimens removed at Kyoto University and Osaka National Hospital between May 2006 and October 2017. The hot spots mutation of IDH1/2, H3F3A, HIST1H3B, and TERT promoter and exon 2 and exon 3 of KRAS, HRAS, and NRAS were analysed with Sanger sequencing method, and 1p/19q codeletion was analysed with multiplex ligation-dependent probe amplification. DNA methylation array was performed in some RAS mutant tumours to improve accuracy of diagnosis.

resultsRAS mutations were identified in four gliomas with three KRAS mutations and one NRAS mutation in one anaplastic oligodendroglioma, two anaplastic astrocytomas (IDH wild-type in each), and one ganglioglioma. RAS-mutant gliomas were identified with various types of glioma histology.

conclusionRAS mutation appears infrequent, and it is not associated with any specific histological phenotype of glioma.

Indexed as

MutationAdolescentAdultAgedAged, 80 and overAstrocytomaBrain NeoplasmsChildChild, PreschoolDNA MethylationDNA Modification MethylasesDNA Mutational AnalysisDNA Repair EnzymesExonsFemaleGenes, rasDNA Modification MethylasesDNA Repair EnzymesH3-3A protein, humanH3C2 protein, humanHistonesIDH1 protein, humanIDH2 protein, humanIsocitrate DehydrogenaseMGMT protein, humanTelomeraseTERT protein, humanTumor Suppressor ProteinsAstrocytomaGangliogliomaGliomaHistological phenotypeOligodendrogliomaRAS mutation

Identifiers

PMID34525976
PMCPMC8442437
OpenAlexW3199759982

What OpenQuestion holds

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LicenceCC BY
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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.