gms | German Medical Science

63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

13. - 16. Juni 2012, Leipzig

Enhanced Cathepsin D expression in recurrent glioblastoma

Meeting Abstract

  • N. Pötzsch - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig
  • C. Renner - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig
  • A. Asperger - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig
  • J. Meixensberger - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig
  • F. Gaunitz - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocFR.07.09

DOI: 10.3205/12dgnc222, URN: urn:nbn:de:0183-12dgnc2223

Veröffentlicht: 4. Juni 2012

© 2012 Pötzsch 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: Despite operation, chemotherapy and radiation it seems inevitable that patients with glioblastoma display a recurrent tumor within 7 months. This recurrent tumor is the main cause of death during the therapy of glioblastoma. In our present study we asked whether the recurrent tumor expresses different proteins than the original tumor in hope to identify new therapeutic targets for chemotherapy.

Methods: A comparative proteomic approach was performed using 2-D gel electrophoresis followed by MALDI-TOF peptide mass fingerprinting. Using a surgically removed brain tissue we compared the protein expression pattern of a primary glioblastoma with the recurrent tumor from the same patient. In addition, Western blots were performed with the recurrent tumors and the primary tumors from three other patients.

Results: In a 2D reference experiment with a primary and a recurrent tumor from one patient 43 proteins were detected as differentially expressed. Among other proteins identified by MALDI-TOF analysis and peptide mass fingerprinting we identified Cathepsin D to be roughly 3-times more strongly expressed in the recurrent tumor. In order to substantiate the hypothesis that Cathepsin D expression may be enhanced in recurrent tumors we performed Western blot analysis from the tumor proteins of this patient and with proteins from the primary tumor and the recurrent tumor from three other patients. In all four cases, Western blot analysis demonstrated a stronger expression of Cathepsin D in the recurrent tumors.

Conclusions: Our results indicate that recurrent tumors may be characterized by enhanced expression of the aspartic protease Cathepsin D compared to the original tumor that was removed by surgery. However, further experiments are mandatory to confirm the result for a larger group of recurrent gliomas. In addition, experiments need to be performed to analyze whether Cathepsin D may play a comparable role in brain tumors as it does in other tumors.