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

Author:
  • N Van Roy
  • J Vandesompele
  • B Menten
  • Helén Nilsson
  • E De Smet
  • M Rocchi
  • A De Paepe
  • Sven Påhlman
  • F Speleman
Publishing year: 2006
Language: English
Pages: 107-117
Publication/Series: Genes, Chromosomes and Cancer
Volume: 45
Issue: 2
Document type: Journal article
Publisher: John Wiley & Sons

Abstract english

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.

Keywords

  • Cancer and Oncology

Other

Published
  • ISSN: 1045-2257
Sven Påhlman
E-mail: sven [dot] pahlman [at] med [dot] lu [dot] se

Professor

Division of Translational Cancer Research

+46 46 222 64 21

MV406 312K1

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