gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Uniform MDM2 overexpression despite divergent EGFR and p53 expression status in a panel of glioblastoma multiforme cell lines suggests an independent role of MDM2 in glioblastoma pathogenesis

Die uniforme MDM2-Überexpression in Glioblastoma multiforme-Zellinien mit unterschiedlichem EGFR- und p53-Status als Ausdruck autonomer Funktion von MDM2 in der Pathogenese des Glioblastoms

Meeting Abstract

  • corresponding author M.-E. Halatsch - Ruprecht-Karls-Universität, Klinik und Poliklinik für Neurochirurgie, Heidelberg
  • K. Mursch - Neurochirurgie, Zentralklinik, Bad Berka
  • S. Löw - Ruprecht-Karls-Universität, Klinik und Poliklinik für Neurochirurgie, Heidelberg
  • A. Unterberg - Ruprecht-Karls-Universität, Klinik und Poliklinik für Neurochirurgie, Heidelberg
  • V. I. Vougioukas - Albert-Ludwigs-Universität, Abteilung Allgemeine Neurochirurgie, Freiburg

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocDO.02.04

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

Published: April 11, 2007

© 2007 Halatsch 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: Overexpression and deletion mutation of the epidermal growth factor receptor (EGFR) gene as well as murine double minute 2 (MDM2) overexpression have been linked to the absence of p53 gene mutations in human glioblastoma multiforme (GBM). In this study, we examined whether overexpression of MDM2 may also occur independently of EGFR and p53 status, which would be consistent with an autonomous function of MDM2 in the pathogenesis of GBM.

Methods: We examined EGFR and MDM2 messenger RNA expression profiles and p53 status by reverse transcription-polymerase chain reaction and gene sequencing, respectively, in a set of human wild-type (wt) p53 GBM cell lines (U-87MG, U-87MG.wtEGFR and U-87MG.ΔEGFR) that exclusively differ in EGFR expression (endogenous wt EGFR expression, exogenous wt EGFR overexpression and exogenous 801-bp deletion-mutant (Δ) EGFR overexpression, respectively) as well as in two human mutant p53 GBM cell lines that differ approximately two-fold in endogenous wt EGFR mRNA expression.

Results: Regardless of the underlying heterogeneity in EGFR mRNA expression and p53 status, MDM2 was similarly overexpressed among the cell lines.

Conclusions: In this report, a panel of human GBM cell lines with diverse constellations of EGFR and p53 status exhibited uniform levels of MDM2 overexpression, suggesting that MDM2 may assume an autonomous role in GBM regardless of the status of genes that according to current concepts are functionally interrelated or mutually exclusive. Thus, targeting of intrinsically oncogenic MDM2 may constitute an attractive therapeutic approach for a subset of GBM.