Proteomics separates adult-type diffuse high-grade gliomas in metabolic subgroups independent of 1p/19q codeletion and across IDH mutational status.


Journal

Cell reports. Medicine
ISSN: 2666-3791
Titre abrégé: Cell Rep Med
Pays: United States
ID NLM: 101766894

Informations de publication

Date de publication:
17 01 2023
Historique:
received: 25 08 2021
revised: 15 07 2022
accepted: 07 12 2022
pubmed: 31 12 2022
medline: 21 1 2023
entrez: 30 12 2022
Statut: ppublish

Résumé

High-grade adult-type diffuse gliomas are malignant neuroepithelial tumors with poor survival rates in combined chemoradiotherapy. The current WHO classification is based on IDH1/2 mutational and 1p/19q codeletion status. Glioma proteome alterations remain undercharacterized despite their promise for a better molecular patient stratification and therapeutic target identification. Here, we use mass spectrometry to characterize 42 formalin-fixed, paraffin-embedded (FFPE) samples from IDH-wild-type (IDHwt) gliomas, IDH-mutant (IDHmut) gliomas with and without 1p/19q codeletion, and non-neoplastic controls. Based on more than 5,500 quantified proteins and 5,000 phosphosites, gliomas separate by IDH1/2 mutational status but not by 1p/19q status. Instead, IDHmut gliomas split into two proteomic subtypes with widespread perturbations, including aerobic/anaerobic energy metabolism. Validations with three independent glioma proteome datasets confirm these subgroups and link the IDHmut subtypes to the established proneural and classic/mesenchymal subtypes in IDHwt glioma. This demonstrates common phenotypic subtypes across the IDH status with potential therapeutic implications for patients with IDHmut gliomas.

Identifiants

pubmed: 36584682
pii: S2666-3791(22)00441-4
doi: 10.1016/j.xcrm.2022.100877
pmc: PMC9873829
pii:
doi:

Substances chimiques

Proteome 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

100877

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

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Auteurs

Jakob Maximilian Bader (JM)

Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.

Nikolaus Deigendesch (N)

Pathology, Institute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.

Martin Misch (M)

Department of Neurosurgery, Charité, Universitätsmedizin Berlin Corporate Member of Freie Universität Berlin, and Humboldt-Universität zu Berlin, Berlin Institute of Health, 13353 Berlin, Germany.

Matthias Mann (M)

Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany; Novo Nordisk Foundation Center for Protein Research, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.

Arend Koch (A)

Department of Neuropathology, Charité, Universitätsmedizin Berlin Corporate Member of Freie Universität Berlin, and Humboldt-Universität zu Berlin, Berlin Institute of Health, 13353 Berlin, Germany. Electronic address: arend.koch@charite.de.

Felix Meissner (F)

Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany; Department of Systems Immunology and Proteomics, Institute of Innate Immunity, University Hospital Bonn, 53127 Bonn, Germany. Electronic address: felix.meissner@uni-bonn.de.

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