Lastowska M, Van Roy N, Bown N, Speleman F, Lunec J, Strachan T, Pearson A D, Jackson M S
Department of Human Genetics, University of Newcastle upon Tyne, United Kingdom.
Genes Chromosomes Cancer. 1998 Oct;23(2):116-22. doi: 10.1002/(sici)1098-2264(199810)23:2<116::aid-gcc4>3.0.co;2-5.
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.
最近人们认识到，导致17q物质增加的不平衡易位是神经母细胞瘤中最常见的染色体变化。这些重排与既定的不良预后指标和患者生存率低相关。我们使用了13种荧光原位杂交（FISH）探针来定位10个神经母细胞瘤细胞系中17q上的12个易位断点，确定了至少7个不同的断点，所有断点都位于17q的近端一半（268-369 cR，53-68 cM）内。这些结果表明，17q22-qter区域中一个或多个基因的剂量是导致17q增加的临床效应的原因，而不是特定基因的破坏。该区域包含两个已经与神经母细胞瘤生物学相关的基因，nm23-H1和NGFR。
