Format

Send to

Choose Destination
See comment in PubMed Commons below
Int J Cancer. 2005 Mar 20;114(2):249-56.

Microarray-based gene expression profiling of benign, atypical and anaplastic meningiomas identifies novel genes associated with meningioma progression.

Author information

1
Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.

Abstract

To identify gene expression profiles associated with human meningiomas of different World Health Organization (WHO) malignancy grades, we analyzed 30 tumors (13 benign meningiomas, WHO grade I; 12 atypical meningiomas, WHO grade II; 5 anaplastic meningiomas, WHO grade III) for the expression of 2,600 genes using cDNA-microarray technology. Receiver operator curve (ROC) analysis with a cutoff value of 45% selection probability identified 37 genes with decreased and 27 genes with increased expression in atypical and anaplastic meningiomas, compared to benign meningiomas. Supervised classification of the tumors did not reveal specific expression patterns representative of each WHO grade. However, anaplastic meningiomas could be distinguished from benign meningiomas by differential expression of a distinct set of genes, including several ones associated with cell cycle regulation and proliferation. Investigation of potential correlations between microarray expression data and genomic aberrations, detected by comparative genomic hybridization (CGH), demonstrated that losses on chromosomes 10 and 14 were associated with distinct expression profiles, including increased expression of several genes related to the insulin-like growth factor (IGF) (IGF2, IGFBP3 and AKT3) or wingless (WNT) (CTNNB1, CDK5R1, ENC1 and CCND1) pathways. Taken together, our microarray-based expression profiling revealed interesting novel candidate genes and pathways that may contribute to meningioma progression.

PMID:
15540215
DOI:
10.1002/ijc.20733
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center