gms | German Medical Science

63rd Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Japanese Neurosurgical Society (JNS)

German Society of Neurosurgery (DGNC)

13 - 16 June 2012, Leipzig

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ALDH1A1 as a molecular marker with better prognosis for glioblastoma patients

Meeting Abstract

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  • O. Schnell - Neurochirurgische Klinik und Poliklinik, Klinikum der LMU München, Campus Großhadern
  • S.A. Adam - Zentrum für Neuropathologie und Prionenforschung, Ludwig-Maximilians-Universität München
  • S. Eigenbrod - Neurochirurgische Klinik und Poliklinik, Klinikum der LMU München, Campus Großhadern
  • H.A. Kretzschmar - Zentrum für Neuropathologie und Prionenforschung, Ludwig-Maximilians-Universität München
  • J.C. Tonn - Neurochirurgische Klinik und Poliklinik, Klinikum der LMU München, Campus Großhadern
  • U. Schüller - Zentrum für Neuropathologie und Prionenforschung, Ludwig-Maximilians-Universität München

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.01.11

doi: 10.3205/12dgnc175, urn:nbn:de:0183-12dgnc1758

Published: June 4, 2012

© 2012 Schnell et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

Text

Objective: Aldehyde dehydrogenase 1A1 (ALDH1A1) has been identified in a variety of human cancers to be expressed by tumor cells and to serve as a reliable marker to predict patients clinical outcome. However, little is known so far about the function of ALDH1A1 in malignant brain tumors.

Methods: We analyzed the expression of ALDH1A1 protein in developing and mature cerebral and cerebellar tissue as well as in a series of 93 cases of primary glioblastoma. Tissue samples for histopathological diagnosis and molecular genetic analysis were acquired either via microsurgical tumor resection (n = 56) or stereotactical serial biopsy (n = 37). Tumor diagnoses were established based on the criteria of the latest WHO brain tumor classification. Patients were treated mainly with radiochemotherapy followed by adjuvant temozolomide chemotherapie according to the EORTC/NCIC protocol. In case of tumor recurrence, salvage treatment was rendered by our institutional guidelines and on a personalized cancer therapy basis.

Results: While ALDH1A1 was absent in the stem cell niches at varying stages of CNS development, strong ALDH1A1 expression was observed in mature astrocytes, coexpressing GFAP and S100. 92/93 (99%) of the examined glioblastoma cases showed ALDH1A1 expression in up to 49% of tumor cells. The majority of these cells co-expressed GFAP, but not stem cell markers, such as Nestin, OLIG2 or SOX2. Finally, strong expression of ALDH1A1 detected by immunhistochemistry correlated with a significantly better overall survival of the patients and proved to be a prognostic marker (p < 0.01), independent of the MGMT promoter methylation status (p = 0.024) and the age of the patient (p = 0.024).

Conclusions: We suggest ALDH1A1 as a marker of astrocytic differentiation and of better prognosis in patients suffering from glioblastomas.