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 Blood, 1 March 2005, Vol. 105, No. 5, pp. 2135-2137.
Prepublished online as a Blood First Edition Paper on November 2, 2004; DOI 10.1182/blood-2004-07-2573.

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NEOPLASIA
Brief report

Deregulated expression of the Myc cellular oncogene drives development of mouse "Burkitt-like" lymphomas from naive B cells

Delin Zhu, Chen Feng Qi, Herbert C. Morse, III, Siegfried Janz, and Freda K. Stevenson

From the Molecular Immunology Group, Tenovus Laboratory, Southampton University Hospitals Trust, United Kingdom; Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD; and Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD.

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 Eµ, 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 VH 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.


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