Skip Navigation

JNCI Monographs 2008 2008(39):8-11; doi:10.1093/jncimonographs/lgn012
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Lieber, M. R.
Right arrow Articles by Yu, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lieber, M. R.
Right arrow Articles by Yu, K.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published by Oxford University Press 2008.

Mechanistic Aspects of Lymphoid Chromosomal Translocations

Michael R. Lieber, Sathees C. Raghavan, Kefei Yu

Affiliations of authors: USC Norris Comprehensive Cancer Center, Departments of Pathology, Biochemistry & Molecular Biology, Molecular Microbiology & Immunology, and Biological Sciences, University of Southern California Keck School of Medicine, Los Angeles, CA (MRL); Department of Biochemistry, Indian Institute of Science, Bangalore, India (SCR); Department of Microbiology and Molecular Genetics, Michigan State University, 5175 Biomedical Physical Scienses, East Lansing, MI (KY)

Correspondence to: Michael R. Lieber, USC Norris Comprehensive Cancer Center, Rm 5428, Departments of Pathology, Biochemistry & Molecular Biology, Molecular Microbiology & Immunology, and Biological Sciences, University of Southern California Keck School of Medicine, 1441 Eastlake Ave, MC9176, Los Angeles, CA 90089-9176 (e-mail: lieber{at}usc.edu).

Chromosomal translocations require double-strand breakage at two sites, followed by joining of the ends. The joining is usually done by nonhomologous DNA end-joining, though homologous recombination and single-strand annealing play roles in cases where there is homology. The mechanism of breakage can be more difficult to understand at sites other than the antigen receptor loci. Some breakage events in pre–B or pre–T cells are due to the RAG proteins recognizing heptamer/nonamer-like sequences, but most breaks are not. Rather, some of these breaks are due to RAG nicking at non–B DNA conformations. Translocation events in mature B cells, when RAGs are not expressed, may be due to the activation-induced deaminase (AID). But AID only acts on single-stranded DNA, and it is not yet clear how this single-stranded DNA arises at some transcribed sites and not others. During the physiologic process of class switch recombination, R-loops form at transcribed class switch regions, thereby accounting for how single strandedness is facilitated at these sites of AID action.



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J Natl Cancer Inst MonogrHome page
C. S. Rabkin and S. Janz
Overview of Mechanisms and Consequences of Chromosomal Translocation
J Natl Cancer Inst Monographs, July 1, 2008; 2008(39): 1 - 1.
[Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.