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Translocation-excision-deletion-amplification mechanism leading to nonsyntenic coamplification of MYC and ATBF1

Van Roy, N ; Vandesompele, J ; Menten, B ; Nilsson, Helén LU ; De Smet, E ; Rocchi, M ; De Paepe, A ; Påhlman, Sven LU and Speleman, F (2006) In Genes, Chromosomes and Cancer 45(2). p.107-117
Abstract
Despite oncogene amplification being a characteristic of many tumor types, the mechanisms leading to amplicon formation have remained largely unresolved. In this study, we used a combinatorial approach of fluorescence in situ hybridization and single-nucleotide polymorphism chip gene copy number analyses to unravel the mechanism leading to nonsyntenic coamplification of MYC and ATBF1 in SJNB-12 cells. To explain our findings, we propose a complex series of events consisting of multiple double-strand breaks, accompanied (or triggered) by the formation of a reciprocal translocation t(8; 16), as well as excisions and deletions near the translocation breakpoints. This study provides evidence for a translocation-excision-deletion-amplification... (More)
Despite oncogene amplification being a characteristic of many tumor types, the mechanisms leading to amplicon formation have remained largely unresolved. In this study, we used a combinatorial approach of fluorescence in situ hybridization and single-nucleotide polymorphism chip gene copy number analyses to unravel the mechanism leading to nonsyntenic coamplification of MYC and ATBF1 in SJNB-12 cells. To explain our findings, we propose a complex series of events consisting of multiple double-strand breaks, accompanied (or triggered) by the formation of a reciprocal translocation t(8; 16), as well as excisions and deletions near the translocation breakpoints. This study provides evidence for a translocation-excision-deletion-amplification sequence of events rather than a breakage-fusion-bridge model, which has been more frequently proposed to explain proto-oncogene amplification. Furthermore, it illustrates the power of presently available tools for detailed analysis of the complex rearrangements that accompany amplicon formation. (Less)
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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Genes, Chromosomes and Cancer
volume
45
issue
2
pages
107 - 117
publisher
John Wiley and Sons
external identifiers
  • pmid:16235245
  • wos:000234553000001
  • scopus:31944434940
  • pmid:16235245
ISSN
1045-2257
DOI
10.1002/gcc.20272
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Molecular Medicine (013031200)
id
793fd0ec-ed12-4899-8b70-0d8644829197 (old id 421340)
date added to LUP
2016-04-01 11:38:13
date last changed
2021-01-06 07:37:02
@article{793fd0ec-ed12-4899-8b70-0d8644829197,
  abstract     = {Despite oncogene amplification being a characteristic of many tumor types, the mechanisms leading to amplicon formation have remained largely unresolved. In this study, we used a combinatorial approach of fluorescence in situ hybridization and single-nucleotide polymorphism chip gene copy number analyses to unravel the mechanism leading to nonsyntenic coamplification of MYC and ATBF1 in SJNB-12 cells. To explain our findings, we propose a complex series of events consisting of multiple double-strand breaks, accompanied (or triggered) by the formation of a reciprocal translocation t(8; 16), as well as excisions and deletions near the translocation breakpoints. This study provides evidence for a translocation-excision-deletion-amplification sequence of events rather than a breakage-fusion-bridge model, which has been more frequently proposed to explain proto-oncogene amplification. Furthermore, it illustrates the power of presently available tools for detailed analysis of the complex rearrangements that accompany amplicon formation.},
  author       = {Van Roy, N and Vandesompele, J and Menten, B and Nilsson, Helén and De Smet, E and Rocchi, M and De Paepe, A and Påhlman, Sven and Speleman, F},
  issn         = {1045-2257},
  language     = {eng},
  number       = {2},
  pages        = {107--117},
  publisher    = {John Wiley and Sons},
  series       = {Genes, Chromosomes and Cancer},
  title        = {Translocation-excision-deletion-amplification mechanism leading to nonsyntenic coamplification of MYC and ATBF1},
  url          = {http://dx.doi.org/10.1002/gcc.20272},
  doi          = {10.1002/gcc.20272},
  volume       = {45},
  year         = {2006},
}