Evidence map›Paper›PMID 28531337›Full record

ArticleNeuro-oncology2017

Correlation of immune phenotype with IDH mutation in diffuse glioma.

Anna Sophie Berghoff, Barbara Kiesel, Georg Widhalm, Dorothee Wilhelm, Orsolya Rajky, Sebastian Kurscheid, Philip Kresl, Adelheid Wöhrer, Christine Marosi, Monika E Hegi and 1 more

Abstract read
In one paragraph

Article in Neuro-oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 4 pooled it
–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

178 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  7. Immune Subtypes and Survival in Patients with Primary Glioma.medRxiv : the preprint server for health sciences · 2026
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  18. Getting the right combination to break the epigenetic code.Nature reviews. Clinical oncology · 2025
    Review
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118 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Anna Sophie BerghoffInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Barbara KieselInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Georg WidhalmInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Dorothee WilhelmInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Orsolya RajkyInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Sebastian KurscheidInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Philip KreslInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Adelheid WöhrerInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Christine MarosiInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Monika E HegiInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Matthias PreusserInstitute of Neurology, Medical University of Vienna, Vienna, Austria; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Neurosurgery, Medical University of Vienna, Vienna, Austria; Department of Genome Science, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia; Laboratory of Brain Tumor Biology and Genetics, Service of Neurosurgery & Neuroscience Research Center, Lausanne University Hospital (CHUV), Lausanne, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor infiltrating lymphocytes (TILs) and programmed death ligand 1 (PD-L1) are targets of immune checkpoint inhibitors.

methodsForty-three World Health Organization (WHO) grade II/III gliomas (39 IDH-mutant [mut], 4 IDH-wildtype [wt]) and 14 IDH-mut glioblastomas (GBM) were analyzed for TIL (CD3+; PD1+) infiltration and PD-L1 expression. Results were compared with the data of a previously published series of 117 IDH-wt glioblastomas. PD-L1 gene expression levels were evaluated in 677 diffuse gliomas grades II-IV from The Cancer Genome Atlas (TCGA) database.

resultsTIL and PD-L1 expression were observed in approximately half of WHO grade II/III gliomas. IDH-wt status was associated with significantly higher TIL infiltration and PD-L1 expression among all (grades II-IV) cases (n = 174, P < 0.001) and within the cohort of glioblastomas (n = 131, P < 0.001). In low-grade glioma (LGG) and glioblastoma cohorts of TCGA, significantly higher PD-L1 gene expression levels were evident in IDH-wt compared with IDH-mut samples (LGG: N = 516; P = 1.933e-11, GBM: N = 161; P < 0.009). Lower PD-L1 gene expression was associated with increased promoter methylation (Spearman correlation coefficient -0.36; P < 0.01) in the LGG cohort of TCGA. IDH-mut gliomas had higher PD-L1 gene promoter methylation levels than IDH-wt gliomas (P < 0.01).

conclusionsThe immunological tumor microenvironment of diffuse gliomas differs in association with IDH mutation status. IDH-wt gliomas display a more prominent TIL infiltration and higher PD-L1 expression than IDH-mut cases. Mechanistically this may be at least in part due to differential PD-L1 gene promoter methylation levels. Our findings may be relevant for immune modulatory treatment strategies in glioma patients.

Indexed as

MutationAdultAgedB7-H1 AntigenBiomarkers, TumorBrain NeoplasmsCohort StudiesFemaleFollow-Up StudiesGliomaHumansIsocitrate DehydrogenaseLymphocytes, Tumor-InfiltratingMaleMiddle AgedPhenotypeB7-H1 AntigenBiomarkers, TumorCD274 protein, humanIDH1 protein, humanIDH2 protein, humanIsocitrate DehydrogenaseglioblastomaIDH mutationimmune microenvironmentlow grade gliomaPD-L1promoter methylation

Identifiers

PMID28531337
PMCPMC5737620

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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.