Evidence map›Paper›PMID 39066986›Full record

ArticleBrain tumor pathology2024

Comprehensive genomic analysis reveals clonal origin and subtype-specific evolution in a case of sporadic multiple meningiomas.

Maki Sakaguchi, Masafumi Horie, Yukinobu Ito, Shingo Tanaka, Keishi Mizuguchi, Hiroko Ikeda, Etsuko Kiyokawa, Mitsutoshi Nakada, Daichi Maeda

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PubMed Full text at PMC Publisher
In one paragraph

Article in Brain tumor pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Maki SakaguchiDepartment of Molecular and Cellular Pathology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.
Masafumi HorieDepartment of Molecular and Cellular Pathology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan. mhorie@med.kanazawa-u.ac.jp.
Yukinobu ItoDepartment of Molecular and Cellular Pathology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.
Shingo TanakaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.
Keishi MizuguchiDepartment of Diagnostic Pathology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Hiroko IkedaDepartment of Diagnostic Pathology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Etsuko KiyokawaDepartment of Oncologic Pathology, Kanazawa Medical University, Kanazawa, Ishikawa, Japan.
Mitsutoshi NakadaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.
Daichi MaedaDepartment of Molecular and Cellular Pathology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.

Funding

Japan Society for the Promotion of Science London JP23H05340
6 · The paper itself

Abstract

Meningioma is the most common primary intracranial tumor in adults, with up to 10% manifesting as multiple tumors. Data on the genomic and molecular changes in sporadic multiple meningiomas are scarce, leading to ongoing debates regarding their evolutionary processes. A comprehensive genetic analysis of a large number of lesions, including precursor lesions, is necessary to explore these two possible origins: clonal and independent. In the present study, we performed whole-exome sequencing and analyzed somatic single-nucleotide variants (SNVs), insertions/deletions (INDELs), and copy number alterations (CNAs) in a patient with sporadic multiple meningiomas. These meningiomas included two mass-forming lesions of different histological subtypes (transitional and chordoid) and two small meningothelial nests. Genetic analysis revealed CNAs on chromosomes 22q and Y as common abnormalities in the two largest tumors. Furthermore, we identified SNV/INDELs unique to each focus, with NF2 mutation prevalent in the transitional meningioma and CREBBP mutation in the chordoid meningioma. Loss of chromosome 22 was detected in two small meningothelial nests. Overall, we elucidated the clonal origin and subtype-specific evolution of multiple meningiomas in this case. CNAs may serve as the initial driving event in meningioma development.

Indexed as

Chromosomes, Human, Pair 22DNA Copy Number VariationsMeningeal NeoplasmsMeningiomaClonal EvolutionCREB-Binding ProteinExome SequencingGenomicsHumansINDEL MutationMutationNeurofibromin 2Polymorphism, Single NucleotideCREB-Binding ProteinCREBBP protein, humanNeurofibromin 2NF2 protein, humanCopy number alterationMultiple meningiomasOccult meningiomaWhole-exome sequencing

Identifiers

PMID39066986
PMCPMC11499534

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