gms | German Medical Science

57th Annual Meeting of the German Society of Neurosurgery
Joint Meeting with the Japanese Neurosurgical Society

German Society of Neurosurgery (DGNC)

11 - 14 May, Essen

Increased expression of the oncogenic tyrosine kinase recepor Axl in human malignant glioma

Erhöhte Expression der onkogenen Tyrosin-Kinase Axl in malignen Gliomen

Meeting Abstract

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  • corresponding author R. Erber - Neurochirurgische Klinik, Universitätsklinikum Mannheim
  • S. Behrndt - Neurochirurgische Klinik, Universitätsklinikum Mannheim
  • P. Vajkoczy - Neurochirurgische Klinik, Universitätsklinikum Mannheim

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocFR.03.05

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

Published: May 8, 2006

© 2006 Erber 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.



Objective: The genetic and molecular events underlying glioma progression and growth have remained obscure. Recently, we have identified the receptor tyrosine kinase Axl as a novel mediator of glioma cell migration and invasion. Inhibition of Axl signaling resulted in a suppressed tumor growth and reduced tumor invasion in mice. To further study the relevance of Axl for glioma progression we have analyzed its expression in human tumor specimens.

Methods: Axl expression was analysed in n=20 high-grade glioma (all glioblastoma multiforme), 5 low-grade glioma (all astrocytoma WHO grade II), and 2 non-neoplastic brain specimens by means of RT-PCR, quantitative PCR (q-PCR), immunohistochemistry and western blotting.

Results: RT-PCR revealed a low-level baseline expression of Axl already in normal brain samples. q-PCR demonstrated stepwise upregulation of Axl expression in low grade glioma (2-fold increase when compared to normal brain) and high-grade glioma (up to 4-fold increase when compared to normal brain). Immunohistochemistry and western blotting confirmed elevated Axl expression in neoplastic tissue on the protein level.

Conclusions: Axl expression correlates with an increased malignancy of astroglial tumors, supporting a novel role for Axl in mediating glioma progression and growth. Specific targeting of Axl may represent a novel strategy to intervene with glioma growth and progression.