Evidence map›Paper›PMID 41742683›Full record

ArticleCancer science2026

Clinical and Genetic Landscape of Glioblastoma, IDH-Wildtype With FGFR Gene Family Alterations.

Yasuhito Kegoya, Yoshihiro Otani, Ryo Mizuta, Ryosuke Ikemachi, Mako Kamiura, Joji Ishida, Shinichi Toyooka, Daisuke Ennishi, Shuta Tomida, Shota Tanaka

Abstract read
In one paragraph

Article in Cancer science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Yasuhito KegoyaDepartment of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Yoshihiro OtaniDepartment of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.ORCID https://orcid.org/0000-0002-1615-5125
Ryo MizutaDepartment of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Ryosuke IkemachiDepartment of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Mako KamiuraDepartment of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Joji IshidaDepartment of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Shinichi ToyookaCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.ORCID https://orcid.org/0000-0002-7588-6745
Daisuke EnnishiCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Shuta TomidaCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.ORCID https://orcid.org/0000-0003-3786-936X
Shota TanakaDepartment of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.ORCID https://orcid.org/0009-0002-9484-2980

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma, isocitrate dehydrogenase wildtype (GBM, IDH-wt), is a highly aggressive brain tumor with a poor prognosis. Alterations in the fibroblast growth factor receptor (FGFR) gene family-such as FGFR::TACC fusions and FGFR1 mutations-have emerged as potential therapeutic targets; however, their clinical and genetic features in GBM, IDH-wt remain unclear. We analyzed 1076 GBM, IDH-wt cases using comprehensive genomic profiling data from the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database in Japan. FGFR alterations were detected in 8.0% of patients, including FGFR::TACC fusions (3.3%) and FGFR1 mutations (2.9%). The FGFR::TACC fusion-positive group was older at diagnosis and showed higher frequencies of TERT promoter mutation and MDM2 amplification, and lower frequencies of EGFR amplification and TP53 mutation, compared with the fusion-negative group. The FGFR1 mutation-positive group was enriched for ATRX, NF1, and PIK3CA mutations and had significantly fewer TERT promoter and PTEN mutations, compared with the mutation-negative group. No significant differences in overall survival were observed, although both groups tended to have longer median overall survival compared with their respective negative groups. This study represents the largest genomic cohort to date of FGFR alterations in GBM, IDH-wt. FGFR::TACC fusion-positive and FGFR1 mutation-positive GBMs exhibited distinct genetic profiles, highlighting the clinical relevance of molecular subclassification and providing insight for future therapeutic strategies.

Indexed as

Brain NeoplasmsGlioblastomaIsocitrate DehydrogenaseReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorAdultAgedFemaleHumansMaleMiddle AgedMutationOncogene Proteins, FusionPromoter Regions, GeneticTelomeraseFGFR1 protein, humanIsocitrate DehydrogenaseOncogene Proteins, FusionReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorTelomeraseTERT protein, humancomprehensive genomic profilingcopy number alterationFGFRglioblastomasingle‐nucleotide variant

Identifiers

PMID41742683
PMCPMC13134525

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.