| Molecular cytogenetic delineation of 17q translocation breakpoints in neuroblastoma cell lines. | |
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MedLine Citation:
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PMID: 9739014 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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M Lastowska; N Van Roy; N Bown; F Speleman; J Lunec; T Strachan; A D Pearson; M S Jackson |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Genes, chromosomes & cancer Volume: 23 ISSN: 1045-2257 ISO Abbreviation: Genes Chromosomes Cancer Publication Date: 1998 Oct |
Date Detail:
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Created Date: 1999-04-13 Completed Date: 1999-04-13 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9007329 Medline TA: Genes Chromosomes Cancer Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 116-22 Citation Subset: IM |
Affiliation:
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Department of Human Genetics, University of Newcastle upon Tyne, United Kingdom. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Chromosome Breakage
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genetics* Chromosomes, Human, Pair 17 / genetics* Genetic Markers Humans In Situ Hybridization, Fluorescence Metaphase Neuroblastoma / genetics*, pathology Translocation, Genetic / genetics* Tumor Cells, Cultured |
| Chemical | |
Reg. No./Substance:
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0/Genetic Markers |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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