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Blood, 15 January 2006, Vol. 107, No. 2, pp. 777-780. Prepublished online as a Blood First Edition Paper on September 29, 2005; DOI 10.1182/blood-2005-06-2437. This Article Full Text Full Text (PDF) Supplemental Methods, Tables, and Figures All Versions of this Article: 2005-06-2437v1 107/2/777    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Weinstock, D. M. Articles by Jasin, M. Search for Related Content PubMed PubMed Citation Articles by Weinstock, D. M. Articles by Jasin, M. Related Collections Neoplasia Oncogenes and Tumor Suppressors Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief report A model of oncogenic rearrangements: differences between chromosomal translocation mechanisms and simple double-strand break repair David M. Weinstock, Beth Elliott, and Maria Jasin From the Department of Medicine and Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY. Recurrent reciprocal translocations are present in many hematologic and mesenchymal malignancies. Because significant sequence homology is absent from translocation breakpoint junctions, non-homologous end-joining (NHEJ) pathways of DNA repair are presumed to catalyze their formation. We developed translocation reporters for use in mammalian cells from which NHEJ events can be selected after precise chromosomal breakage. Translocations were efficiently recovered with these reporters using mouse cells, and their breakpoint junctions recapitulated findings from oncogenic translocations. Small deletions and microhomology were present in most junctions; insertions and more complex events also were observed. Thus, our reporters model features of oncogenic rearrangements in human cancer cells. A homologous sequence at a distance from the break site affected the translocation junction without substantially altering translocation frequency. Interestingly, in a direct comparison, the spectrum of translocation breakpoint junctions differed from junctions derived from repair at a single chromosomal break, providing mechanistic insight into translocation formation. (Blood. 2006;107:777-780) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. Brunet, D. Simsek, M. Tomishima, R. DeKelver, V. M. Choi, P. Gregory, F. Urnov, D. M. Weinstock, and M. Jasin Chromosomal translocations induced at specified loci in human stem cells PNAS, June 30, 2009; 106(26): 10620 - 10625. [Abstract] [Full Text] [PDF] A. Ashworth Drug Resistance Caused by Reversion Mutation Cancer Res., December 15, 2008; 68(24): 10021 - 10023. [Abstract] [Full Text] [PDF] W. Y. Mansour, S. Schumacher, R. Rosskopf, T. Rhein, F. Schmidt-Petersen, F. Gatzemeier, F. Haag, K. Borgmann, H. Willers, and J. Dahm-Daphi Hierarchy of nonhomologous end-joining, single-strand annealing and gene conversion at site-directed DNA double-strand breaks Nucleic Acids Res., July 1, 2008; 36(12): 4088 - 4098. [Abstract] [Full Text] [PDF] J. Guirouilh-Barbat, E. Rass, I. Plo, P. Bertrand, and B. S. Lopez Defects in XRCC4 and KU80 differentially affect the joining of distal nonhomologous ends PNAS, December 26, 2007; 104(52): 20902 - 20907. [Abstract] [Full Text] [PDF] H. Sekine, R. C. Ferreira, Q. Pan-Hammarstrom, R. R. Graham, B. Ziemba, S. S. de Vries, J. Liu, K. Hippen, T. Koeuth, W. Ortmann, et al. Role for Msh5 in the regulation of Ig class switch recombination PNAS, April 24, 2007; 104(17): 7193 - 7198. [Abstract] [Full Text] [PDF]

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