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[Cancer Research 66, 7837-7839, August 15, 2006]
© 2006 American Association for Cancer Research

Reviews

Switching on Chromosomal Translocations

Almudena R. Ramiro1, Michel C. Nussenzweig2,3 and André Nussenzweig4

1 DNA Hypermutation Group, Spanish National Cancer Center, Madrid, Spain; 2 Laboratory of Molecular Immunology, The Rockefeller University; 3 Howard Hughes Medical Institute, New York, New York; and 4 Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, Maryland

Requests for reprints: Almudena R. Ramiro, DNA Hypermutation Group, Spanish National Cancer Center, Madrid 28029, Spain. Phone: 34-91-732-8055; Fax: 34-917-8033; E-mail: arodriguezr{at}cnio.es.

Activation-induced deaminase initiates three different antibody diversification reactions: class switch recombination, somatic hypermutation (SHM), and gene conversion. We have shown that, in addition to antibody diversification, activation-induced deaminase can also initiate Burkitt's lymphoma–like c-myc/IgH translocations. However, distinct DNA damage- and oncogene-induced checkpoints operate in B cells to produce a normal intrachromosomal class switch recombination event or an aberrant interchromosomal fusion. These findings open the way to study the molecular pathways taking place at the early stages of malignant transformation. (Cancer Res 2006; 66(16): 7837-9)




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Copyright © 2006 by the American Association for Cancer Research.