Translocation-excision-deletion-amplification mechanism leading to nonsyntenic coamplification of MYC and ATBF1
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/421340
- author
- Van Roy, N ; Vandesompele, J ; Menten, B ; Nilsson, Helén LU ; De Smet, E ; Rocchi, M ; De Paepe, A ; Påhlman, Sven LU and Speleman, F
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Genes, Chromosomes and Cancer
- volume
- 45
- issue
- 2
- pages
- 107 - 117
- publisher
- John Wiley & Sons Inc.
- 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
- 2022-03-05 04:13:57
@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 & Sons Inc.}}, 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}}, }