Artikel
Parasagittal tumour location strongly predicts hTERT promoter mutations in high-grade meningiomas
Parasagittale Tumorlokalisation als starker Prädiktor für hTERT Promoter-Mutationen in höhergradigen Meningeomen
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Autoren
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Susanne Peetz-Dienhart
- Universitätsklinikum Münster, Institut für Neuropathologie, Münster, Deutschland
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Dorothee Cäcilia Spille
- Universitätsklinikum Münster, Klinik und Poliklinik für Neurochirurgie, Münster, Deutschland
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Peter B. Sporns
- Universitätsklinikum Münster, Institut für Klinische Radiologie, Münster, Deutschland
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Alborz Adeli
- Universitätsklinikum Münster, Institut für Klinische Radiologie, Münster, Deutschland
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Eva Christine Bunk
- Universitätsklinikum Münster, Klinik und Poliklinik für Neurochirurgie, Münster, Deutschland
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Andrea Wagner
- Universitätsklinikum Münster, Institut für Neuropathologie, Münster, Deutschland
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Werner Paulus
- Universitätsklinikum Münster, Institut für Neuropathologie, Münster, Deutschland
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Walter Stummer
- Universitätsklinikum Münster, Klinik und Poliklinik für Neurochirurgie, Münster, Deutschland
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Katharina Heß
- Universitätsklinikum Münster, Institut für Neuropathologie, Münster, Deutschland
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Benjamin Brokinkel
- Universitätsklinikum Münster, Klinik und Poliklinik für Neurochirurgie, Münster, Deutschland
| Veröffentlicht: | 26. Juni 2020 |
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Gliederung
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Objective: Mutations of the human Telomerase Reverse Transcriptase (hTERT) promoter and loss of histone H3K27M trimethylation (Me3) have been shown to predict recurrence in meningiomas. While unselected screening is critical regarding their low frequency and the considerable financial expense, risk factors for these alterations are sparsely known.
Methods: Correlations of hTERT promoter mutations and loss of H3K27Me3 with radiological variables (including tumour and edema volumes, contrast heterogeneity and intensity of the tumour on T2-weighted imaging, contrast-enhancement of the capsule, intratumoural calcifications, integrity of the arachnoid layer, tumour shape and location) were analyzed in samples from 96 surgeries for high-grade meningiomas in 72 patients in uni- and multivariate analyses.
Results: hTERT promoter mutations were found in 16 (17%) and loss of H3K27Me3 in three samples (3%). None of the tumours harbored both alterations. Recurrence occurred in 33 of 72 patients (46%). hTERT promoter mutations (HR: 2.81, 95%CI 1.20-6.59; p=.018) were correlated with progression. One of the three individuals with loss of H3K27Me3 developed recurrence. Promoter mutations were found in 47% of parasagittal meningiomas (N=9 of 19) but only in 11% (N=5 of 46), 7% (N=2 of 27) and 0% of tumours arising from the convexity, the skull base and other locations, respectively (p=.001). While parasagittal tumour location was confirmed as an independent predictor in multivariate analyses (OR: 8.20, 95%CI 2.21-30.39; p=.002), no correlations between hTERT promoter mutations and any of the other variables were found. Loss of H3K27Me3 was observed in two convexity and one parasagittal meningioma. Hence, 53% of the samples from parasagittal/falcine meningiomas carried one of the two analyzed alterations.
Conclusion: Prediction of prognostic molecular alterations in high-grade meningiomas utilizing variables available in the routine preoperative setup is difficult. Determination in parasagittal meningiomas will reveal promoter mutations in almost 50% and can improve estimation of prognosis in these often incompletely resected tumours. However, determination of hTERT promoter mutations in H3K27Me deficient samples might not improve estimation of prognosis.
