Concurrent gliomas in patients with multiple sclerosis.


Journal

Communications medicine
ISSN: 2730-664X
Titre abrégé: Commun Med (Lond)
Pays: England
ID NLM: 9918250414506676

Informations de publication

Date de publication:
18 Dec 2023
Historique:
received: 22 12 2022
accepted: 10 10 2023
medline: 19 12 2023
pubmed: 19 12 2023
entrez: 19 12 2023
Statut: epublish

Résumé

Concurrent malignant brain tumors in patients with multiple sclerosis (MS) constitute a rare but paradigmatic phenomenon for studying neuroimmunological mechanisms from both molecular and clinical perspectives. A multicenter cohort of 26 patients diagnosed with both primary brain tumors and multiple sclerosis was studied for disease localization, tumor treatment-related MS activity, and molecular characteristics specific for diffuse glioma in MS patients. MS neither predisposes nor protects from the development of gliomas. Patients with glioblastoma WHO grade 4 without isocitratdehydrogenase (IDH) mutations have a longstanding history of MS, whereas patients diagnosed with IDH-mutant astrocytoma WHO grade 2 receive multiple sclerosis diagnosis mostly at the same time or later. Concurrent MS is associated with a lesser extent of tumor resection and a worse prognosis in IDH-mutant glioma patients (PFS 32 vs. 64 months, p = 0.0206). When assessing tumor-intrinsic differences no distinct subgroup-defining methylation pattern is identified in gliomas of MS patients compared to other glioma samples. However, differential methylation of immune-related genetic loci including human leukocyte antigen locus on 6p21 and interleukin locus on 5q31 is found in MS patients vs. matched non-MS patients. In line, inflammatory disease activity increases in 42% of multiple sclerosis patients after brain tumor radiotherapy suggesting a susceptibility of multiple sclerosis brain tissue to pro-inflammatory stimuli such as ionizing radiation. Concurrent low-grade gliomas should be considered in multiple sclerosis patients with slowly progressive, expansive T2/FLAIR lesions. Our findings of typically reduced extent of resection in MS patients and increased MS activity after radiation may inform future treatment decisions. Brain tumors such as gliomas can evade attacks by the immune system. In contrast, some diseases of the central nervous system such as multiple sclerosis (MS) are caused by an overactive immune system. Our study looks at a cohort of rare patients with both malignant glioma and concurrent MS and examines how each disease and their treatments affect each other. Our data suggest that even in patients with known MS, if medical imaging findings are unusual, a concurrent brain tumor should be excluded at an early stage. Radiotherapy, as is the standard of care for malignant brain tumors, may worsen the inflammatory disease activity in MS patients, which may be associated with certain genetic risk factors. Our findings may help to inform treatment of patients with brain tumors and MS.

Sections du résumé

BACKGROUND BACKGROUND
Concurrent malignant brain tumors in patients with multiple sclerosis (MS) constitute a rare but paradigmatic phenomenon for studying neuroimmunological mechanisms from both molecular and clinical perspectives.
METHODS METHODS
A multicenter cohort of 26 patients diagnosed with both primary brain tumors and multiple sclerosis was studied for disease localization, tumor treatment-related MS activity, and molecular characteristics specific for diffuse glioma in MS patients.
RESULTS RESULTS
MS neither predisposes nor protects from the development of gliomas. Patients with glioblastoma WHO grade 4 without isocitratdehydrogenase (IDH) mutations have a longstanding history of MS, whereas patients diagnosed with IDH-mutant astrocytoma WHO grade 2 receive multiple sclerosis diagnosis mostly at the same time or later. Concurrent MS is associated with a lesser extent of tumor resection and a worse prognosis in IDH-mutant glioma patients (PFS 32 vs. 64 months, p = 0.0206). When assessing tumor-intrinsic differences no distinct subgroup-defining methylation pattern is identified in gliomas of MS patients compared to other glioma samples. However, differential methylation of immune-related genetic loci including human leukocyte antigen locus on 6p21 and interleukin locus on 5q31 is found in MS patients vs. matched non-MS patients. In line, inflammatory disease activity increases in 42% of multiple sclerosis patients after brain tumor radiotherapy suggesting a susceptibility of multiple sclerosis brain tissue to pro-inflammatory stimuli such as ionizing radiation.
CONCLUSIONS CONCLUSIONS
Concurrent low-grade gliomas should be considered in multiple sclerosis patients with slowly progressive, expansive T2/FLAIR lesions. Our findings of typically reduced extent of resection in MS patients and increased MS activity after radiation may inform future treatment decisions.
Brain tumors such as gliomas can evade attacks by the immune system. In contrast, some diseases of the central nervous system such as multiple sclerosis (MS) are caused by an overactive immune system. Our study looks at a cohort of rare patients with both malignant glioma and concurrent MS and examines how each disease and their treatments affect each other. Our data suggest that even in patients with known MS, if medical imaging findings are unusual, a concurrent brain tumor should be excluded at an early stage. Radiotherapy, as is the standard of care for malignant brain tumors, may worsen the inflammatory disease activity in MS patients, which may be associated with certain genetic risk factors. Our findings may help to inform treatment of patients with brain tumors and MS.

Autres résumés

Type: plain-language-summary (eng)
Brain tumors such as gliomas can evade attacks by the immune system. In contrast, some diseases of the central nervous system such as multiple sclerosis (MS) are caused by an overactive immune system. Our study looks at a cohort of rare patients with both malignant glioma and concurrent MS and examines how each disease and their treatments affect each other. Our data suggest that even in patients with known MS, if medical imaging findings are unusual, a concurrent brain tumor should be excluded at an early stage. Radiotherapy, as is the standard of care for malignant brain tumors, may worsen the inflammatory disease activity in MS patients, which may be associated with certain genetic risk factors. Our findings may help to inform treatment of patients with brain tumors and MS.

Identifiants

pubmed: 38110626
doi: 10.1038/s43856-023-00381-y
pii: 10.1038/s43856-023-00381-y
doi:

Types de publication

Journal Article

Langues

eng

Pagination

186

Subventions

Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 39404578
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 39404578
Organisme : Gemeinnützige Hertie-Stiftung (Hertie Foundation)
ID : P1200013
Organisme : Else Kröner-Fresenius-Stiftung (Else Kroner-Fresenius Foundation)
ID : 2019_EKMS.23

Informations de copyright

© 2023. The Author(s).

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Auteurs

Katharina Sahm (K)

Department of Neurology, Medical Faculty Mannheim, Mannheim Center for Translational Neurosciences (MCTN), University of Heidelberg, Mannheim, Germany. k.sahm@dkfz.de.
Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany. k.sahm@dkfz.de.

Tobias Kessler (T)

Clinical Cooperation Unit Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Department of Neurology and Neurooncology Program, National Center for Tumor Diseases (NCT), Heidelberg University Hospital, Heidelberg, Germany.

Philipp Eisele (P)

Department of Neurology, Medical Faculty Mannheim, Mannheim Center for Translational Neurosciences (MCTN), University of Heidelberg, Mannheim, Germany.

Miriam Ratliff (M)

Department of Neurosurgery, Medical Faculty Mannheim, Mannheim Center for Translational Neurosciences (MCTN), University of Heidelberg, Mannheim, Germany.

Elena Sperk (E)

Department of Radiation Oncology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.

Laila König (L)

Department of Radiation Oncology, Heidelberg University Hospital, Heidelberg, Germany.

Michael O Breckwoldt (MO)

Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.

Corinna Seliger (C)

Department of Neurology and Neurooncology Program, National Center for Tumor Diseases (NCT), Heidelberg University Hospital, Heidelberg, Germany.
Wilhelm Sander-NeuroOncology Unit and Department of Neurology, Regensburg University Hospital, Regensburg, Germany.

Iris Mildenberger (I)

Department of Neurology, Medical Faculty Mannheim, Mannheim Center for Translational Neurosciences (MCTN), University of Heidelberg, Mannheim, Germany.
Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.

Daniel Schrimpf (D)

Department of Neuropathology, Heidelberg University Hospital, Heidelberg, Germany.
Clinical Cooperation Unit Neuropathology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.

Christel Herold-Mende (C)

Division of Experimental Neurosurgery, Department of Neurosurgery, Heidelberg University Hospital, Heidelberg, Germany.

Pia S Zeiner (PS)

Dr Senckenberg Institute of Neurooncology, University of Frankfurt, Frankfurt, Germany.

Ghazaleh Tabatabai (G)

Department of Neurology & Interdisciplinary Neurooncology, University Hospital Tübingen, Hertie Institute for Clinical Brain Research, Eberhard Karls University Tübingen, Tübingen, Germany.

Sven G Meuth (SG)

Department of Neurology, Institute of Translational Neurology, University Hospital Münster, Münster, Germany.

David Capper (D)

Department of Neuropathology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
German Cancer Consortium (DKTK), Partner Site Berlin, German Cancer Research Center, Heidelberg, Germany.

Martin Bendszus (M)

Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.

Andreas von Deimling (A)

Department of Neuropathology, Heidelberg University Hospital, Heidelberg, Germany.
Clinical Cooperation Unit Neuropathology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.

Wolfgang Wick (W)

Clinical Cooperation Unit Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Department of Neurology and Neurooncology Program, National Center for Tumor Diseases (NCT), Heidelberg University Hospital, Heidelberg, Germany.

Felix Sahm (F)

Department of Neuropathology, Heidelberg University Hospital, Heidelberg, Germany.
Clinical Cooperation Unit Neuropathology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.

Michael Platten (M)

Department of Neurology, Medical Faculty Mannheim, Mannheim Center for Translational Neurosciences (MCTN), University of Heidelberg, Mannheim, Germany. m.platten@dkfz.de.
Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany. m.platten@dkfz.de.

Classifications MeSH