It has recently been recognized that unbalanced translocations resulti
ng in the gain of material from 17q are the most common chromosomal ch
anges in neuroblastoma. These rearrangements are associated with estab
lished indicators of bad prognosis and poor patient survival. We have
used 13 fluorescence in situ hybridization (FISH) probes to map 12 tra
nslocation breakpoints on 17q in 10 neuroblastoma cell lines, identify
ing at least seven different breakpoints, all localized within the pro
ximal half of 17q (268-369 cR, 53-68 cM). These results suggest that t
he dosage of a gene, or genes, in 17q22-qter is responsible for the cl
inical effects of 17q gain, rather than the disruption of a specific g
ene. This region contains two genes, nm23-HI and NGFR, already implica
ted in neuroblastoma biology. (C) 1998 Wiley-Liss, Inc.