| First Author | Zhu D | Year | 2005 |
| Journal | Blood | Volume | 105 |
| Issue | 5 | Pages | 2135-7 |
| PubMed ID | 15522957 | Mgi Jnum | J:95904 |
| Mgi Id | MGI:3527987 | Doi | 10.1182/blood-2004-07-2573 |
| Citation | Zhu D, et al. (2005) Deregulated expression of the Myc cellular oncogene drives development of mouse 'Burkitt-like' lymphomas from naive B cells. Blood 105(5):2135-7 |
| abstractText | Chromosomal translocations juxtaposing immunoglobulin (Ig) and MYC genes are the hallmarks of human Burkitt lymphoma (BL), with deregulated MYC expression being a critical factor in pathogenesis. By inserting an intact mouse Myc gene into the mouse genome, proximal to the Ig enhancer Emu, the effect of a precise mimic of the major t(8;14) translocation of human endemic BL (eBL) could be investigated. Knock-in mice developed IgM-positive B-cell tumors, with most being typical of eBL by histology and immunophenotype, including expression of the germinal center (GC)-associated protein, BCL6. Unlike eBL, however, analysis of Ig V(H) sequences revealed no significant level of somatic mutation. Thus, constitutive expression of Myc in the knock-in mice is apparently able to induce 'Burkitt-like' lymphomas before antigen stimulation and formation of a GC. In contrast, human eBL development occurs in a GC or post-GC site with a likely contribution to pathogenesis from Epstein-Barr virus (EBV) and other epigenetic factors. |
