Abstract

ObjectiveMeningiomas are among the most frequent intracranial tumors. Although the majority of meningiomas can be cured by surgical resection, up to 20% of the patients develop an aggressive clinical course with tumor recurrence or progressive disease.Cytogenetically, meningiomas frequently harbour a normal karyotype or monosomy of chromosome 22 as the sole anomaly. However, progression of meningiomas is associated with a non-random pattern of secondary losses of the chromosomes and chromosomal regions 1p, 6, 10, 14, 18, and 19. There is evidence, that loss of chromosome 17 might be involved in the clonal cytogenetic evolution of recurrent meningiomas. The aim of this study was to determine the role of deletions in the 17q chromosomal region in patients with recurrent meningiomas.ResultsThe authors retrospectively reviewed all patients that underwent repeated surgery for recurrent meningiomas between 1999 and 2015 at the Department of Neurosurgery of the Saarland University Hospital. Patients were included in this study if tumor samples from two or more different meningiomas were available.A total of 7 patients underwent repeated surgery for recurrent meningiomas (4 males, 3 females, mean age: 45.4 years at the date of surgery) between 1999 and 2015. Collectively, 22 biopsies were analyzed with FISH (fluorescence-in-situ-hybridization) for the chromosomal region 17q23.3. In 20/22 (90.1%) specimens, the tumor samples harboured a significant deletion in the chromosomal region 17q (range: 10 to 63% of the cells). In 3/3 (100%) cases, deletion in the 17q chromosomal region was detectable in the primary tumor. In the tumor evolution, there was no steady in- or decrease in the percentage of this deletion.ConclusionDeletion in the 17q chromosomal region was present in the patients’ primary tumors as well as in late recurrences. Overall, a significant deletion in the 17q chromosomal region was detected in 90.1% of the tumors. Thus, the authors assume that deletion in the 17q chromosomal region displays rather an early event in meningioma progression. Accordingly, deletion in the 17q chromosomal region might clinically serve as a potential early marker for malignancy and a higher risk for recurrence in meningiomas.

Highlights

  • Meningiomas are the most frequent intracranial tumors

  • A significant deletion in the 17q chromosomal region was detected in 90.1% of the tumors

  • The authors assume that deletion in the 17q chromosomal region displays rather an early event in meningioma progression

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Summary

Introduction

Meningiomas are the most frequent intracranial tumors They account for about 30% of all brain tumors with an annual incidence rate of 10.5 cases per 100,000 females and 4.8 cases per 100,000 males [1]. They are among the cytogenetically best studied tumors and typically reveal a normal karyotype or losses – mostly monosomy and only rarely deletions - of chromosome 22. Increasing hypodiploidy and complex aberrations are known to induce higher tumor malignancy in meningiomas. As described in the literature, meningiomas with a complex karyotype show higher rates of malignancy [4,5,6]. Loss of the chromosomal region 1p and mutations in SMO, AKT1 and the TERT promoter are independent (cyto-)genetic predictors for meningioma recurrence [3, 7, 10,11,12]

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