Journal
CELL
Volume 135, Issue 6, Pages 1028-1038Publisher
CELL PRESS
DOI: 10.1016/j.cell.2008.09.062
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Funding
- NIH
- National Cancer Institute
- Center for Cancer Research
- Leukemia and Lymphoma Society
- Howard Hughes Medical Institute Investigator
- BBSRC [BB/F012217/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C163, BB/F012217/1] Funding Source: researchfish
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Chromosomal translocation requires formation of paired double-strand DNA breaks (DSBs) on heterologous chromosomes. One of the most well characterized oncogenic translocations juxtaposes c-myc and the immunoglobulin heavy-chain locus (IgH) and is found in Burkitt's lymphomas in humans and plasmacytomas in mice. DNA breaks in IgH leading to c-myc/IgH translocations are created by activation-induced cytidine deaminase ( AID) during antibody class switch recombination or somatic hypermutation. However, the source of DNA breaks at c-myc is not known. Here, we provide evidence for the c-myc promoter region being required in targeting AID-mediated DNA damage to produce DSBs in c-myc that lead to c-myc/IgH translocations in primary B lymphocytes. Thus, in addition to producing somatic mutations and DNA breaks in antibody genes, AID is also responsible for the DNA lesions in oncogenes that are required for their translocation.
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