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Molecular cytogenetic delineation of 17q translocation breakpoints in neuroblastoma cell lines
Author(s) -
|fLastowska Maria,
Van Roy Nadine,
Bown Nick,
Speleman Frank,
Lunec John,
Strachan Tom,
Pearson Andrew D. J.,
Jackson Michael S.
Publication year - 1998
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199810)23:2<116::aid-gcc4>3.0.co;2-5
Subject(s) - chromosomal translocation , breakpoint , neuroblastoma , fluorescence in situ hybridization , biology , gene , cytogenetics , genetics , microbiology and biotechnology , gene duplication , karyotype , fish <actinopterygii> , chromosome , cancer research , cell culture , fishery
It has recently been recognized that unbalanced translocations resulting in the gain of material from 17q are the most common chromosomal changes in neuroblastoma. These rearrangements are associated with established indicators of bad prognosis and poor patient survival. We have used 13 fluorescence in situ hybridization (FISH) probes to map 12 translocation breakpoints on 17q in 10 neuroblastoma cell lines, identifying at least seven different breakpoints, all localized within the proximal half of 17q (268–369 cR, 53–68 cM). 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. This region contains two genes, nm23‐H1 and NGFR , already implicated in neuroblastoma biology. Genes Chromosomes Cancer 23:116–122, 1998. © 1998 Wiley‐Liss, Inc.