| First Author | Robbiani DF | Year | 2009 |
| Journal | Mol Cell | Volume | 36 |
| Issue | 4 | Pages | 631-41 |
| PubMed ID | 19941823 | Mgi Jnum | J:154731 |
| Mgi Id | MGI:4398751 | Doi | 10.1016/j.molcel.2009.11.007 |
| Citation | Robbiani DF, et al. (2009) AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations. Mol Cell 36(4):631-41 |
| abstractText | Cancer-initiating translocations such as those associated with lymphomas require the formation of paired DNA double-strand breaks (DSBs). Activation-induced cytidine deaminase (AID) produces widespread somatic mutation in mature B cells; however, the extent of 'off-target' DSB formation and its role in translocation-associated malignancy is unknown. Here, we show that deregulated expression of AID causes widespread genome instability, which alone is insufficient to induce B cell lymphoma; transformation requires concomitant loss of the tumor suppressor p53. Mature B cell lymphomas arising as a result of deregulated AID expression are phenotypically diverse and harbor clonal reciprocal translocations involving a group of Immunoglobulin (Ig) and non-Ig genes that are direct targets of AID. This group includes miR-142, a previously unknown micro-RNA target that is translocated in human B cell malignancy. We conclude that AID produces DSBs throughout the genome, which can lead to lymphoma-associated chromosome translocations in mature B cells. |
