ArticleBrain pathology (Zurich, Switzerland)1999
Clonal origin of recurrent meningiomas.
Article in Brain pathology (Zurich, Switzerland), 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 27 citations in OpenAlex.
- Growth pattern and molecular biological analysis of primary meningioma cell cultures under different conditions.Molecular medicine reports · 2026Article
- Topographic Patterns of Intracranial Meningioma Recurrences-Systematic Review with Clinical Implication.Cancers · 2024Review
- Multiple meningiomas: clinical, radiological, surgical, and pathological findings with outcome in four cats.Journal of feline medicine and surgery · 2007Article
- Absence of histological signs of tumor progression in recurrences of completely resected meningiomas.Journal of neuro-oncology · 2005Article
- Diagnostic impact of ornithine decarboxylase in meningiomas.Journal of neuro-oncology · 2004Article
- Apoptosis detected with monoclonal antibody to single-stranded DNA is a predictor of recurrence in intracranial meningiomas.Journal of neuro-oncology · 2001Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Meningiomas are common intracranial and intraspinal tumors. They are treated primarily by surgical resection. Meningioma recurrence following surgery is frequent despite advances in microneurosurgery. However, it is not clear whether recurrent meningiomas, close or distant to the primary resection site, arise from incomplete resection, dissemination of tumor fragments or from independent tumor growth. In order to address the question of clonality in recurring meningiomas, we examined a series of five patients with a total of 14 tumors for X-chromosome inactivation in the tumor tissues. Four patients with a total of 11 meningiomas were informative for polymorphisms either in the PGK or the AR genes. All recurrent meningiomas were found to be clonal with respect to the primary lesions. This finding suggests a common molecular pathogenesis of primary meningioma and subsequent recurrences (p<0.01). In a sixth patient, we analyzed the NF2 gene for mutations in the primary and 5 recurrent meningiomas. All six lesions carried the identical NF2 mutation, strongly indicating a common origin for these tumors. We conclude that recurrent meningiomas usually arise from dissemination of tumor fragments, most likely at the time of the first surgical resection. Our data should alert to the potential of meningioma cells for seeding during surgical procedures.
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