Carcinogenesis Advance Access originally published online on April 16, 2004
Carcinogenesis 2004 25(9):1599-1609; doi:10.1093/carcin/bgh173
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Carcinogenesis vol.25 no.9 © Oxford University Press 2004; all rights reserved.
ARTICLE |
Oligonucleotide microarray analysis of gene expression in neuroblastoma displaying loss of chromosome 11q
1 National Centre for Medical Genetics, Our Lady's Hospital for Sick Children, Crumlin, Dublin 12, 2 Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, 3 Department of Histopathology, Our Lady's Hospital for Sick Children, Crumlin, Dublin 12, 4 Department of Oncology, Our Lady's Hospital for Sick Children, Crumlin, Dublin 12, Ireland and 5 Tumor Bank, The Children's Hospital at Westmead, Sydney, Australia
6 To whom correspondence should be addressed Email: ray.stallings{at}olhsc.ie
A number of distinct subtypes of neuroblastoma exist with different genetic abnormalities that are predicative of outcome. Whole chromosome gains are usually associated with low stage disease and favourable outcome, whereas loss of 1p, 3p and 11q, unbalanced gain of 17q and MYCN amplification (MNA) are indicative of high stage disease and unfavourable prognosis. Although MNA and loss of 11q appear to represent two distinct genetic subtypes of advanced stage neuroblastoma, a detailed understanding of how these subtypes differ in terms of global gene expression is still lacking. We have used metaphase comparative genomic hybridization (CGH) analysis in combination with oligonucleotide technology to identify patterns of gene expression that correlate with specific genomic imbalances found in primary neuroblastic tumours and cell lines. The tumours analysed in this manner included a ganglioneuroma, along with various ganglioneuroblastoma and neuroblastoma of different stages and histopathological classifications. Oligonucleotide microarray-based gene expression profile analysis was performed with Affymetrix HU133A arrays representing 
14 500 unique genes. The oligonucleotide microarray results were subsequently validated by quantitative real-time PCR, immunohistochemical staining, and by comparison of specific gene expression patterns with published results. Hierarchical clustering of gene expression data distinguished tumours on the basis of stage, differentiation and genetic abnormalities. A number of genes were identified whose patterns of expression were highly correlated with 11q loss; supporting the concept that loss of 11q represents a distinct genetic subtype of neuroblastoma. The implications of these results in the process of neuroblastoma development and progression are discussed.
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