Gyriform infiltration as imaging biomarker for molecular glioblastomas.


Journal

Journal of neuro-oncology
ISSN: 1573-7373
Titre abrégé: J Neurooncol
Pays: United States
ID NLM: 8309335

Informations de publication

Date de publication:
May 2022
Historique:
received: 02 02 2022
accepted: 23 03 2022
pubmed: 3 4 2022
medline: 10 5 2022
entrez: 2 4 2022
Statut: ppublish

Résumé

Molecular glioblastomas (i.e. without the histological but with the molecular characteristics of IDH-wild-type glioblastoma) frequently lack contrast enhancement, which can wrongly lead to suspect a lower-grade glioma. Herein, we aimed to assess the diagnostic value of gyriform infiltration as an imaging marker for molecular glioblastomas. Two independent investigators reviewed the MRI scans from patients with newly diagnosed gliomas for the presence of a gyriform infiltration defined as an elective cortical hypersignal on MRI FLAIR sequence. Diagnostic test performance of this sign for the diagnosis of molecular glioblastoma were calculated. A total of 426 patients were included, corresponding to 31 molecular glioblastoma, 294 IDH-wild-type glioblastoma, 50 IDH-mutant astrocytoma, and 51 IDH-mutant 1p19q-codeleted oligodendroglioma. A gyriform infiltration was observed in 16/31 (52%) molecular glioblastoma, 40/294 (14%) IDH-wild-type glioblastoma, and none of the IDH-mutant glioma. All the 56 gyriform-infiltration-positive tumors were IDH-wild-type and all but two had a TERT promoter mutation. The inter-rater agreement was good (κ = 0.69, p < 0.001). The sensitivity, specificity, positive predictive value and negative predictive value of the presence of a gyriform infiltration for the diagnosis of molecular glioblastoma were 52%, 90%, 29%, 96%, respectively. The median overall survival was better for gyriform-infiltration-negative patients compared to gyriform-infiltration-positive patients in the whole series and in patients with non-enhancing lesions (n = 95) (25.6 vs 16.9 months, p = 0.005 and 20.2 months vs not reached, p < 0.001). Gyriform infiltration is a specific imaging marker of molecular glioblastomas that can help distinguishing these tumors from IDH-mutant lower-grade gliomas.

Sections du résumé

BACKGROUND BACKGROUND
Molecular glioblastomas (i.e. without the histological but with the molecular characteristics of IDH-wild-type glioblastoma) frequently lack contrast enhancement, which can wrongly lead to suspect a lower-grade glioma. Herein, we aimed to assess the diagnostic value of gyriform infiltration as an imaging marker for molecular glioblastomas.
METHODS METHODS
Two independent investigators reviewed the MRI scans from patients with newly diagnosed gliomas for the presence of a gyriform infiltration defined as an elective cortical hypersignal on MRI FLAIR sequence. Diagnostic test performance of this sign for the diagnosis of molecular glioblastoma were calculated.
RESULTS RESULTS
A total of 426 patients were included, corresponding to 31 molecular glioblastoma, 294 IDH-wild-type glioblastoma, 50 IDH-mutant astrocytoma, and 51 IDH-mutant 1p19q-codeleted oligodendroglioma. A gyriform infiltration was observed in 16/31 (52%) molecular glioblastoma, 40/294 (14%) IDH-wild-type glioblastoma, and none of the IDH-mutant glioma. All the 56 gyriform-infiltration-positive tumors were IDH-wild-type and all but two had a TERT promoter mutation. The inter-rater agreement was good (κ = 0.69, p < 0.001). The sensitivity, specificity, positive predictive value and negative predictive value of the presence of a gyriform infiltration for the diagnosis of molecular glioblastoma were 52%, 90%, 29%, 96%, respectively. The median overall survival was better for gyriform-infiltration-negative patients compared to gyriform-infiltration-positive patients in the whole series and in patients with non-enhancing lesions (n = 95) (25.6 vs 16.9 months, p = 0.005 and 20.2 months vs not reached, p < 0.001).
CONCLUSION CONCLUSIONS
Gyriform infiltration is a specific imaging marker of molecular glioblastomas that can help distinguishing these tumors from IDH-mutant lower-grade gliomas.

Identifiants

pubmed: 35364762
doi: 10.1007/s11060-022-03995-9
pii: 10.1007/s11060-022-03995-9
doi:

Substances chimiques

Biomarkers 0
Isocitrate Dehydrogenase EC 1.1.1.41

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

511-521

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Emmanuel Mesny (E)

Department of Neuro-Oncology, Hôpital Neurologique, Hospices Civils de Lyon, Lyon, France. emmanuel.mesny@chu-lyon.fr.
Department of Radiotherapy, Centre Hospitalier Universitaire Lyon Sud, Pierre-Bénite, France. emmanuel.mesny@chu-lyon.fr.
Service d'oncologie Radiothérapie CHU Lyon Sud, Hospices Civil de Lyon, 165 Chem. du Grand Revoyet, 69310, Pierre-Bénite, France. emmanuel.mesny@chu-lyon.fr.

Marc Barritault (M)

Institut de Pathologie de L'Est, Hospices Civils de Lyon, Lyon, France.
Department of Cancer Cell Plasticity, Cancer Research Centre of Lyon, INSERM U1052, CNRS UMR5286, Lyon, France.
Universités de Lyon, Université Claude Bernard, Lyon 1, Lyon, France.

Cristina Izquierdo (C)

Service of Neurology, Department of Neuroscience, Hospital Universitari Germans Trias I Pujol, Barcelona, Spain.

Delphine Poncet (D)

Institut de Pathologie de L'Est, Hospices Civils de Lyon, Lyon, France.
Universités de Lyon, Université Claude Bernard, Lyon 1, Lyon, France.

Anne d'Hombres (A)

Department of Radiotherapy, Centre Hospitalier Universitaire Lyon Sud, Pierre-Bénite, France.

Jacques Guyotat (J)

Department of Neurosurgery, Hospices Civils de Lyon, Lyon, France.

Emmanuel Jouanneau (E)

Universités de Lyon, Université Claude Bernard, Lyon 1, Lyon, France.
Department of Neurosurgery, Hospices Civils de Lyon, Lyon, France.
Signaling, Metabolism and Tumor Progression, Cancer Research Centre of Lyon, INSERM U1052, CNRS UMR 5286, Lyon, France.

Roxana Ameli (R)

Department of Neuro-Radiology, Hôpital Neurologique, Hospices Civils de Lyon, Lyon, France.

Jérôme Honnorat (J)

Department of Neuro-Oncology, Hôpital Neurologique, Hospices Civils de Lyon, Lyon, France.
Universités de Lyon, Université Claude Bernard, Lyon 1, Lyon, France.
Synaptopathies and Autoantibodies, SynatAc) Team, Institut NeuroMyoGène, INSERM U1217/CNRS UMR 5310, Lyon, France.

David Meyronet (D)

Institut de Pathologie de L'Est, Hospices Civils de Lyon, Lyon, France.
Department of Cancer Cell Plasticity, Cancer Research Centre of Lyon, INSERM U1052, CNRS UMR5286, Lyon, France.
Universités de Lyon, Université Claude Bernard, Lyon 1, Lyon, France.

François Ducray (F)

Department of Neuro-Oncology, Hôpital Neurologique, Hospices Civils de Lyon, Lyon, France.
Department of Cancer Cell Plasticity, Cancer Research Centre of Lyon, INSERM U1052, CNRS UMR5286, Lyon, France.
Universités de Lyon, Université Claude Bernard, Lyon 1, Lyon, France.

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