gms | German Medical Science

68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

AXL tyrosine kinase receptor is widely activated in glioblastoma tissue and is associated with a significant shorter overall survival

Meeting Abstract

  • Julia Sophie Onken - Neurosurgery Charité Berlin, Berlin, Deutschland
  • Radke Josefine - Neuropathology Charité Berlin, Berlin, Deutschland
  • Hempt Claudia - Neuropathology Charité Berlin, Berlin , Deutschland
  • Vajkoczy Peter - Neurosurgery Charité Berlin, Berlin, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocMO.14.02

doi: 10.3205/17dgnc079, urn:nbn:de:0183-17dgnc0794

Published: June 9, 2017

© 2017 Onken et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at



Objective: Receptor tyrosine kinase AXL (RTK-AXL) is regarded as suitable target in glioma therapy. Here we evaluate the expression and localization of the biological active RTK-AXL (P-AXL) in human glioblastoma (GBM) tissue in order to define a suitable subgroup for future anti-AXL therapy.

Methods: We analyzed 100 tissue samples from newly diagnosed glioblastoma patients according to their P-AXL expression. The tissue was analyzed in terms of P-AXL expression by immunohistochemistry and immunofluorescence, antibody specificity has been proven with positive and negative controls. Co-staining of P-AXL and mesenchymal markers like vimentin and fibronectin was performed. Results were correlated with survival data.

Results: We stained a total of 100 patients and showed that P-AXL is expressed in each patient. We identified three main distribution patterns within the tumor. In 9% of patients P-AXL was found exclusively in perivascular/ vascular regions, in 91% P-AXL was expressed in hypercellular tumor tissue, pseudopalisades or vessels. P-AXL is found in mesenchymal-like areas and is co-localized with mesenchymal markers like vimentin and fibronectin. Expression of P-AXL in tumor tissue and tumor vasculature is associated with a significant decreased overall survival (Hazard ratio 2.349, 95% confidence interval 1.069 to 5.162, *p=0.03).

Conclusion: The broad expression of P-AXL among our patient collective and impaired survival in these patients strongly suggest that P-AXL serves as a target in the majority of GBM patients. Its role in EMT (epithelial to mesenchymal transition) and (neo-) vascularization of GBMs needs to be further investigated.