Molecular cytogenetic delineation of 17q translocation breakpoints in neuroblastoma cell lines

被引:0
|
作者
Lastowska, M
Van Roy, N
Brown, N
Speleman, F
Lunec, J
Strachan, T
Pearson, ADJ
Jackson, MS
机构
[1] Newcastle Univ, Dept Human Genet, Newcastle Upon Tyne NE2 4AA, Tyne & Wear, England
[2] Inst Paediat, Clin Paediat Haematol & Oncol, Poznan, Poland
[3] Univ Hosp, Dept Med Genet, Ghent, Belgium
[4] Newcastle Univ, Canc Res Unit, Newcastle Upon Tyne NE2 4AA, Tyne & Wear, England
[5] Newcastle Univ, Inst Child Hlth, Newcastle Upon Tyne NE2 4AA, Tyne & Wear, England
来源
GENES CHROMOSOMES & CANCER | 1998年 / 23卷 / 02期
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中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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-HI and NGFR, already implicated in neuroblastoma biology. (C) 1998 Wiley-Liss, Inc.
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页码:116 / 122
页数:7
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