gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

Expression of uPA and PAI-1 in meningiomas correlates with malignant progression and brain invasion

uPA- und PAI-1-Expression in Meningeomen korreliert mit maligner Progression und Hirninvasion

Meeting Abstract

  • corresponding author M. Simon - Neurochirurgische Klinik, Universitätskliniken Bonn
  • T. W. Park-Simon - Frauenklinik, Universitätskliniken Bonn
  • P. Koch - Institut für Neuropathologie, Universitätskliniken Bonn
  • R. Mahlberg - Neurochirurgische Klinik, Universitätskliniken Bonn
  • B. Dürkop - Frauenklinik, Universitätskliniken Bonn

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc11.05.-11.02

The electronic version of this article is the complete one and can be found online at:

Published: May 4, 2005

© 2005 Simon et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Brain invasion often causes meningioma recurrence. Brain invasion has been regarded as a decisive (histopathological) parameter for the diagnosis of malignancy in meningiomas. Multiple meningiomas are often of monoclonal origin possibly reflecting subarachnoid spread. Invasion and metastatic spread require the proteolytic degradation of the extracellular matrix, which is mediated, in part, by activation of uPA (urokinase-type plasminogen activator) and its inhibitor PAI-1 (plasminogen activator inhibitor-1). In this study we investigate the role of uPA and PAI-1 in meningiomas.


uPA and PAI-1 protein concentrations were determined in shock-frozen tissue of 26 benign WHO grade I, 17 atypical WHO grade II and 6 anaplastic/malignant WHO grade III meningiomas using an ELISA assay.


Expression of uPA increased significantly with the WHO grade (WHO grade I: 0.247±0.035, WHO grade II: 0.420±0.066, WHO grade III: 1.108±0.736 ng/mg; p<0.05, H test). High levels of PAI-1 were observed primarily in malignant/anaplastic meningiomas (WHO grade I/II: 7.5±1.0, WHO grade III: 237.0±112.3; p<0.025, U test). Expression of PAI-1 correlated significantly with brain invasion (120.3±73.0 vs. 21.5±14.8; p<0.005, U test). High levels of uPA and PAI-1 protein were often seen independently. Tumor multiplicity (>3 tumors) corrrelated neither with uPA nor with PAI-1 expression.


The molecular biology of invasion and (metastatic) subarachnoid spread of meningiomas has not been very well researched. Activation of the plasmin/uPA/PAI-1 system might play a significant role during the malignant progression of meningiomas and meningioma brain invasion. Differential expression of high levels of uPA and PAI-1 protein argues for at least partially independent functions of these proteins in meningiomas. Finally, PAI-1 and uPA could prove useful for meningioma grading. High levels of uPA and PAI expression are already in clinical use as negative prognostic factors in several (mainly gynecological) malignancies.