| First Author | Nepal RM | Year | 2008 |
| Journal | Oncogene | Volume | 27 |
| Issue | 34 | Pages | 4752-6 |
| PubMed ID | 18408759 | Mgi Jnum | J:138509 |
| Mgi Id | MGI:3805259 | Doi | 10.1038/onc.2008.111 |
| Citation | Nepal RM, et al. (2008) AID and RAG1 do not contribute to lymphomagenesis in Emu c-myc transgenic mice. Oncogene 27(34):4752-6 |
| abstractText | DNA breaks caused by recombination-activating gene 1 (RAG1) and activation-induced cytidine deaminase (AID) induce c-myc/immunoglobulin (Ig) heavy chain chromosomal translocations and thereby stimulate lymphomagenesis. However, constitutive expression of c-myc alone is not sufficient to induce lymphomas. Because RAG1 and AID activity occurs outside of Ig genes, we assessed whether these enzymes provide the secondary genetic lesions in Emu c-myc transgenic mice to promote lymphoma development. We found that the tumor incidence and tumor phenotype in Emu c-myc transgenic mice is similar in AID+/+, AID+/- and AID-/- backgrounds in both specific pathogen-free and conventional animal facilities, indicating that AID does not contribute to lymphoma development in Emu c-myc transgenic mice. To examine the role of RAG proteins in Emu c-myc mice, we examined Emu c-myc transgenic mice that harbor the Ig-HEL heavy- and light-chain transgenes, and thus have reduced RAG expression in B cells. We found that tumor incidence was not affected by these Ig transgenes. However, we found that RAG1-/- Emu c-myc mice exhibited accelerated tumor development compared to controls. This data combined with our finding that Emu c-myc mice lived longer in the conventional facility than in the specific pathogen-free facility suggest an immune-mediated activity that suppresses lymphoma development. |
