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ISRN Neurosci. 2013 Dec 19;2013:626290. doi: 10.1155/2013/626290. eCollection 2013.

Caspase-3 and survivin expression in primary atypical and malignant meningiomas.

ISRN neuroscience

Andrej Vranic

Affiliations

  1. Department of Neurosurgery, University Medical Center Ljubljana, Zaloska 7, 1525 Ljubljana, Slovenia ; Génomique Fonctionnelle des Tumeurs Solides, Unité INSERM U674, 75010 Paris, France.

PMID: 25006573 PMCID: PMC4061719 DOI: 10.1155/2013/626290

Abstract

Objective. Information about possible prognostic factors of the survival of patients with atypical and malignant meningiomas (AMM) is sparse. The aim of our study was to evaluate prognostic significance of apoptotic marker caspase-3 and apoptotic inhibitor survivin in a series of primary AMM. Methods. 86 AMM (76 atypical and 10 malignant) were analyzed. Caspase-3 and survivin expression was evaluated immunohistochemically. The correlation between caspase-3, survivin, and other possible factors of meningioma recurrence was evaluated. Uni- and multivariate recurrence-free survival (RFS) and overall survival (OS) analyses were performed. Results. The intensity of caspase-3 expression correlated with the tumor grade (P = 0.004), the proliferation index (P = 0.019), and the mitotic count (P = 0.013). Survivin tended to be more expressed in female patients (P = 0.072). Survivin expression was stronger in malignant compared to atypical meningiomas, however, the difference was not statistically important (P = 0.491). Neither survivin nor caspase-3 expression significantly predicted OS or RFS in patients with AMM. Conclusions. Strong caspase-3 expression on AMM cells could reflect a cellular attempt at the homeostatic autoregulation of the tumor size. Survivin expression on AMM cells is similar to the survivin expression reported on benign meningiomas. Caspase-3 and survivin expression has no prognostic significance on the survival of patients with AMM.

References

  1. Brain Pathol. 2005 Apr;15(2):109-15 - PubMed
  2. J Neurooncol. 2003 Aug-Sep;64(1-2):71-6 - PubMed
  3. J Neurooncol. 2009 Dec;95(3):367-375 - PubMed
  4. J Neurosci Res. 2002 Jul 15;69(2):197-206 - PubMed
  5. Acta Neurochir (Wien). 2004 Jan;146(1):37-44; discussion 44 - PubMed
  6. Brain Res. 2008 Jan 10;1188:25-34 - PubMed
  7. Neurosurgery. 2009 Jan;64(1):56-60; discussion 60 - PubMed
  8. Cancer Res. 2005 Feb 15;65(4):1547-53 - PubMed
  9. Neuropathology. 2007 Apr;27(2):114-20 - PubMed
  10. Histopathology. 2003 Sep;43(3):280-90 - PubMed
  11. Oncol Rep. 2009 May;21(5):1181-8 - PubMed
  12. Neurosci Lett. 2005 Jun 10-17;381(1-2):69-73 - PubMed
  13. Acta Neurochir (Wien). 1999;141(9):921-32 - PubMed
  14. Cancer Lett. 2003 Apr 25;193(2):217-23 - PubMed
  15. Acta Neuropathol. 2002 Jul;104(1):105-9 - PubMed
  16. Neurosurg Focus. 2007;23(4):E9 - PubMed
  17. Oncogene. 2004 Sep 30;23(45):7494-506 - PubMed
  18. J Neurooncol. 2005 May;72(3):203-8 - PubMed
  19. J Neurosurg. 2007 Mar;106(3):455-62 - PubMed
  20. Int J Oncol. 2007 Jan;30(1):123-8 - PubMed
  21. Neurosurgery. 2010 Oct;67(4):1124-32 - PubMed
  22. Apoptosis. 2007 Apr;12(4):695-705 - PubMed
  23. J Neurooncol. 2004 Mar-Apr;67(1-2):209-14 - PubMed
  24. J Neurooncol. 2001 Oct;55(1):1-9 - PubMed

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