Background. Unbalanced translocations resulting in the gain of material fro
m 17q are the most common chromosomal changes in neuroblastoma and are asso
ciated with poor patient survival, and are established indicators of bad pr
ognosis. Procedure. We have used 13 fluorescent in situ hybridisation probe
s 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 ge
nes, in 17q22-qter is responsible for the clinical effects of 17q gain, rat
her than the disruption of a specific gene. Med. Pediatr. Oncol. 36: 20-23,
2001. (C) 2001 Wiley-Liss, Inc.