Download 105.1 Lastowska

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Regions syntenic to human 17q are gained in mouse and rat neuroblastoma cell
lines
Maria Lastowska1, Yeun-Jun Chung2, Ngan C Cheng3, Michelle Haber3, Murray D Norris3, Ursula R
Kees4, Andrew DJ Pearson1, Michael S Jackson1
The University of Newcastle upon Tyne1 and The Wellcome Trust Sanger Institute2, Hinxton, Cambridge, UK; Children's Cancer
Institute Australia3, Sydney, NSW 2031, and The University of Western Australia4, Perth, Australia.
Gain of chromosome arm 17q is the most frequent chromosomal change in human neuroblastoma
suggesting that this region includes a gene, or genes, critical for tumour pathogenesis. Because the
shortest region of 17q gain (SRG) encompasses >300 genes, it precludes the identification of candidate
genes from human breakpoint data alone. However, mouse chromosome 11, which is syntenic to human
chromosome 17, is gained in up to 30% of neuroblastoma tumours developed in a murine MYCN
transgenic model of this disease. To confirm that this key genetic change indicates the involvement of a
conserved molecular pathway we have used FISH to analyse sporadic cases of both mouse and rat
neuroblastoma. Our results confirm the presence of chromosome 11 gain in all 3 mouse cell lines we
analysed, with the SRG extending from Stat5b to tel. In addition, the rat neuroblastoma cell line harbours
an extra copy of distal chromosome 10 which is also syntenic to human 17q. Comparison of the regions
gained in all three species excludes ~4 Mb from the previously defined region of 17q gain in human as a
likely location of candidate gene/genes, and strongly suggests that the molecular aetiology of
neuroblastoma is similar in all three species. Comparative gene expression analyses from all three
species are currently being performed in an effort to identify candidate genes.
Presentation mode(s): POSTER-PRESENTATION