Evidence map›Paper›PMID 34148105›Full record

ArticleActa neuropathologica2021

TERT promoter mutation status is necessary and sufficient to diagnose IDH-wildtype diffuse astrocytic glioma with molecular features of glioblastoma.

Kenji Fujimoto, Hideyuki Arita, Kaishi Satomi, Kai Yamasaki, Yuko Matsushita, Taishi Nakamura, Yasuji Miyakita, Toru Umehara, Keiichi Kobayashi, Kaoru Tamura and 17 more

Abstract read
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In one paragraph

Article in Acta neuropathologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
11.7field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

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  5. Independent associations of MGMT promoter methylation and TERT promoter mutation with overall survival in glioblastoma: a single-center retrospective cohort study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

27 authors at 19 institutions in 2 countries.

Kenji FujimotoDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Hideyuki AritaDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Kaishi SatomiDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Kai YamasakiDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Yuko MatsushitaDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Taishi NakamuraDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Yasuji MiyakitaDepartment of Neurosurgery and Neuro-Oncology, National Cancer Center Hospital, Tokyo, Japan.
Toru UmeharaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Keiichi KobayashiDepartment of Neurosurgery, Faculty of Medicine, Kyorin University, Tokyo, Japan.
Kaoru TamuraDepartment of Neurosurgery, Tokyo Medical and Dental University, Tokyo, Japan.
Shota TanakaDepartment of Neurosurgery, The University of Tokyo, Tokyo, Japan.
Fumi HiguchiDepartment of Neurosurgery, Dokkyo Medical University, Tochigi, Japan.
Yoshiko OkitaDepartment of Neurosurgery, Osaka International Cancer Institute, Osaka, Japan.
Yonehiro KanemuraDepartment of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Junya FukaiDepartment of Neurological Surgery, Wakayama Medical University, Wakayama, Japan.
Daisuke SakamotoDepartment of Neurosurgery, Hyogo College of Medicine, Hyogo, Japan.
Takehiro UdaDepartment of Neurosurgery, Osaka City University Graduate School of Medicine, Osaka, Japan.
Ryunosuke MachidaBiostatistics Division, Center for Research Administration and Support, National Cancer Center, Tokyo, Japan.
Aya KuchibaDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Saitama, Japan.
Taketoshi MaeharaDepartment of Neurosurgery, Tokyo Medical and Dental University, Tokyo, Japan.
Motoo NaganeDepartment of Neurosurgery, Faculty of Medicine, Kyorin University, Tokyo, Japan.
Ryo NishikawaDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Saitama, Japan.
Hiroyoshi SuzukiDepartment of Pathology and Laboratory Medicine, National Hospital Organization, Sendai Medical Center, Sendai, Japan.
Makoto ShibuyaCentral Clinical Laboratory, Hachioji Medical Center, Tokyo Medical University, Tokyo, Japan.
Takashi KomoriDepartment of Laboratory Medicine and Pathology (Neuropathology), Tokyo Metropolitan Neurological Hospital, Tokyo, Japan.
Yoshitaka NaritaDepartment of Neurosurgery and Neuro-Oncology, National Cancer Center Hospital, Tokyo, Japan.
Koichi IchimuraDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan. k.ichimura.uk@juntendo.ac.jp.ORCID 0000-0002-3851-2349
Kyorin University · JPSaitama Medical University · JPThe University of Osaka · JPTokyo Medical and Dental University · JPDokkyo Medical University · JPHyogo Medical University · JPJuntendo University · JPKumamoto University · JPOsaka City General Hospital · JPOsaka City University · JPOsaka International Cancer Institute · JPOsaka National Hospital · JPSendai Medical Center · JPThe University of Tokyo · JPTokyo Medical University Hachioji Medical Center · JPTokyo Metropolitan Neurological Hospital · JPTokyo National Hospital · JPWakayama Medical University · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Consortium to Inform Molecular and Practical Approaches to CNS Tumor Taxonomy (cIMPACT-NOW) update 3 recommends that histologic grade II and III IDH-wildtype diffuse astrocytic gliomas that harbor EGFR amplification, the combination of whole chromosome 7 gain and whole chromosome 10 loss (7 + /10 -), or TERT promoter (pTERT) mutations should be considered as glioblastomas (GBM), World Health Organization grade IV. In this retrospective study, we examined the utility of molecular classification based on pTERT status and copy-number alterations (CNAs) in IDH-wildtype lower grade gliomas (LGGs, grade II, and III). The impact on survival was evaluated for the pTERT mutation and CNAs, including EGFR gain/amplification, PTEN loss, CDKN2A homozygous deletion, and PDGFRA gain/amplification. We analyzed 46 patients with IDH-wildtype/pTERT-mutant (mut) LGGs and 85 with IDH-wildtype/pTERT-wildtype LGGs. EGFR amplification and a combination of EGFR gain and PTEN loss (EGFR + /PTEN -) were significantly more frequent in pTERT-mut patients (p < 0.0001). Cox regression analysis showed that the pTERT mutation was a significant predictor of poor prognosis (hazard ratio [HR] 2.79, 95% confidence interval [CI] 1.55-4.89, p = 0.0008), but neither EGFR amplification nor EGFR + /PTEN - was an independent prognostic factor in IDH-wildtype LGGs. PDGFRA gain/amplification was a significant poor prognostic factor in IDH-wildtype/pTERT-wildtype LGGs (HR 2.44, 95% CI 1.09-5.27, p = 0.03, Cox regression analysis). The IDH-wildtype LGGs with either pTERT-mut or PDGFRA amplification were mostly clustered with GBM by DNA methylation analysis. Thus, our study suggests that analysis of pTERT mutation status is necessary and sufficient to diagnose IDH-wildtype diffuse astrocytic gliomas with molecular features of glioblastoma. The PDGFRA status may help further delineate IDH-wildtype/pTERT-wildtype LGGs. Methylation profiling showed that IDH-wildtype LGGs without molecular features of GBM were a heterogeneous group of tumors. Some of them did not fall into existing categories and had significantly better prognoses than those clustered with GBM.

Indexed as

AdultBrain NeoplasmsDNA Copy Number VariationsFemaleGliomaHomozygoteHumansIsocitrate DehydrogenaseMaleMiddle AgedMutationPTEN PhosphohydrolaseSequence DeletionTelomeraseIsocitrate DehydrogenasePTEN PhosphohydrolasePTEN protein, humanTelomeraseTERT protein, humanCopy-number alterationIDH-wildtypeLower grade gliomaTERT promoter mutation

Identifiers

PMID34148105
OpenAlexW3174191211

What OpenQuestion holds

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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.