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Relationship between Gene Expression and Enhancement in Glioblastoma Multiforme: Exploratory DNA Microarray Analysis¹

¹ From the Departments of Radiological Sciences (W.B.P., J.H.C.), Human Genetics (J.D., M.R.J.C., A.P., S.F.N.), Neurology (T.F.C., P.N., A.L.), Neurological Surgery (L.M.L.), and Pathology and Laboratory Medicine (P.S.M.), David Geffen School of Medicine at University of California–Los Angeles (UCLA) Medical Center, 10833 Le Conte Ave, BL-428/CHS, Los Angeles, CA 90095-1721. Received November 15, 2007; revision requested February 25, 2008; revision received March 14; accepted April 18; final version accepted April 28. Supported in part by the Harry Allgauer Foundation through the Doris R. Ullmann Fund for Brain Tumor Research Technologies, the Henry E. Singleton Brain Cancer Program at UCLA, the Ziering Family Foundation in memory of Sigi Ziering, the Art of the Brain, the Roven Family Fund in memory of Dawn Steel, and the Joseph Drown Foundation in memory of Mark Schackman for the funding for tumor collection, gene expression analysis, database maintenance, and image archiving). Address correspondence to W.B.P. (e-mail: wpope{at}mednet.ucla.edu).

Purpose: To determine the difference in gene expression between completely versus incompletely enhancing glioblastoma multiforme (GBM).

Materials and Methods: Gene expression was determined for 52 newly diagnosed GBMs by using DNA microarrays, and the relationship to enhancement pattern and survival was analyzed. This study was approved by the institutional review board and was HIPAA compliant; informed consent was obtained.

Results: Thirty-eight percent (20 of 52) of GBMs were incompletely enhancing (IE). The expression of eight genes was increased more than twofold in IE GBM when compared with completely enhancing (CE) GBM. Among these were tight junction protein-2 (2.2-fold increase, P = .019), and the oligodendroglioma markers oligodendrocyte lineage transcription factor 2 (2.4-fold increase, P = .029) and Achaete-scute complex-like 1 (ASCL1; 2.7-fold increase, P = .023). The expression of 71 genes showed relative overexpression in CE when compared with IE GBM. These included several proangiogenic and edema-related genes, including vascular endothelial growth factor (2.1-fold, P = .005) and neuronal pentraxin-2 (3.0-fold, P = .029). Several genes associated with primary GBM were overexpressed in CE tumors, whereas ASCL1, which is associated with secondary GBM, was overexpressed in IE tumors. Many genes overexpressed in IE GBM were associated with longer survival, whereas several genes overexpressed in CE GBM correlated with shortened survival.

Conclusion: The enhancement pattern divides GBM in two groups with differing prognoses. By comparing gene expression between IE and CE GBMs, it was possible to identify genes that may affect magnetic resonance imaging features of edema and enhancement, and genes whose expression levels are predictive of both improved and shortened survival.

© RSNA, 2008