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60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Expression of cyclooxygenase-2 in vestibular schwannomas

Meeting Abstract

  • B. Hong - Neurochirurgische Klinik, Medizinische Hochschule Hannover
  • C. Krusche - Institut für Pathologie, Medizinische Hochschule Hannover
  • R. Klein - Institut für Pathologie, Medizinische Hochschule Hannover
  • S. Winter - Neurochirurgische Klinik, Medizinische Hochschule Hannover
  • J. Krauss - Neurochirurgische Klinik, Medizinische Hochschule Hannover
  • M. Nakamura - Neurochirurgische Klinik, Medizinische Hochschule Hannover

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocP08-04

DOI: 10.3205/09dgnc332, URN: urn:nbn:de:0183-09dgnc3321

Veröffentlicht: 20. Mai 2009

© 2009 Hong et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Recent studies have shown that cyclooxygenase-2 (COX-2) plays an important role in tumor growth and tumor neovascularization. A growing body of literature supports the use of COX-2 inhibitors in treatment of various cancers. Up until now no data concerning potential COX-2 expression are available for intracranial schwannomas. The aim of this study is to analyze the pattern of COX-2 expression in sporadic vestibular schwannomas (sporadic VS) and neurofibromatosis type 2 associated vestibular schwannomas (NF2 associated VS).

Methods: Using immunohistochemistry, we investigated the expression of COX-2 in NF2 associated VS and in sporadic VS. Fifteen paraffin-embedded specimens of each NF2 associated VS and sporadic VS were evaluated. An immunohistochemical score was used to interpret the extent and intensity of COX-2 staining. Tumor proliferation was analyzed using Ki-67 immunohistochemistry. More than 1000 cells per tumor were evaluated by light microscopy on high-field power by a blinded observer. In addition, microvascular density was analyzed using von-Willebrand-factor.

Results: Expression of COX-2 was detected in 29 specimens (96.7%). The intensity and extension of the staining was heterogeneous: 11 tumors (36.7%) were graded as weakly, 9 (30%) as moderately, and 9 (30%) as strongly COX-2 positive, without difference between sporadic and NF2 associated VS. One specimen (3.3%) was COX-2 negative. Proliferation of sporadic VS was significantly higher than of NF2 associated VS (p<0,001). No statistically significant difference was found between the microvascular densities of both groups.

Conclusions: Our data demonstrate that COX-2 is expressed in the majority of VS with heterogeneous intensity. This suggests that the COX-2 pathway is involved in the pathophysiology of VS, and that COX-2 might become a therapeutic target in the treatment of VS.