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 Blood, 2 July 2009, Vol. 114, No. 1, pp. 119-127.
Prepublished online as a Blood First Edition Paper on March 30, 2009; DOI 10.1182/blood-2009-01-198937.

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LYMPHOID NEOPLASIA

A mouse model for chronic lymphocytic leukemia based on expression of the SV40 large T antigen

Petra J. ter Brugge1, Van B. T. Ta1,2, Marjolein J. W. de Bruijn2, Guido Keijzers3, Alex Maas3, Dik C. van Gent3, and Rudi W. Hendriks2

Departments of 1 Immunology, 2 Pulmonary Medicine, and 3 Cell Biology and Genetics, Erasmus MC Rotterdam, Rotterdam, The Netherlands

The simian virus 40 (SV40) T antigen is a potent oncogene able to transform many cell types and has been implicated in leukemia and lymphoma. In this report, we have achieved sporadic SV40 T-antigen expression in mature B cells in mice, by insertion of a SV40 T antigen gene in opposite transcriptional orientation in the immunoglobulin (Ig) heavy (H) chain locus between the D and JH segments. SV40 T-antigen expression appeared to result from retention of the targeted germline allele and concomitant antisense transcription of SV40 large T in mature B cells, leading to chronic lymphocytic leukemia (CLL). Although B-cell development was unperturbed in young mice, aging mice showed accumulation of a monoclonal B-cell population in which the targeted IgH allele was in germline configuration and the wild-type IgH allele had a productive V(D)J recombination. These leukemic B cells were IgDlowCD5+ and manifested nonrandom usage of V, D, and J segments. VH regions were either unmutated, with preferential usage of the VH11 family, or manifested extensive somatic hypermutation. Our findings provide an animal model for B-CLL and show that pathways activated by SV40 T antigen play important roles in the pathogenesis of B-CLL.


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