Background: Unbalanced translocations resulting in the gain of material from 17q are the most common chromosomal changes in neuroblastoma and are associated with poor patient survival, and are established indicators of bad prognosis.
Procedure: We have used 13 fluorescent in situ hybridisation probes to map 17q translocation breakpoints in ten neuroblastoma cell lines and 21 primary tumours.
Results: At least seven different breakpoints have been identified, all localised within the proximal half of 17q (53-68 cM, 17cen-17q22).
Conclusion: These results suggest that the dosage of a gene, or genes, in 17q22-qter is responsible for the clinical effects of 17q gain, rather than the disruption of a specific gene.