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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3546-3552.
Prepublished online as a Blood First Edition Paper on July 28, 2005; DOI 10.1182/blood-2005-02-0493.
Previous Article | Next Article 
Submitted February 7, 2005
Accepted July 8, 2005
A tumor suppressor function for NFATc3 in T cell lymphomagenesis by murine leukemia virus
Sys Zoffmann Glud, Annette B Sorensen, Mindaugas Andrulis, Bruce Wang, Eisaku Kondo, Randi Jessen, Laszlo Krenacz, Eva Stelkovics, Matthias Wabl, Edgar Serfling, Alois Palmetshofer, and Finn S Pedersen*
Department of Molecular Biology, University of Aarhus, Aarhus, Denmark
Department of Pathology, Institute of Pathology, University of Wuerzburg, Wuerzburg, Germany
Picobella LP, Burlingame, CA, USA
Department of Pathology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan
Laboratory of Tumor Pathology and Molecular Diagnostics, Institute of Biotechnology, Bay Zoltan Foundation for Applied Research, Szeged, Hungary
Department of Microbiology and Immunology, University of California, San Francisco, CA, USA
Department of Molecular Biology, University of Aarhus, Aarhus, Denmark; Department of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark
* Corresponding author; email: fsp{at}mb.au.dk.
NFAT (Nuclear Factor of Activated T cell) transcription factors play a central role in differentiation, activation and elimination of lymphocytes. We here report on the finding of provirus integration into the nfatc3 locus in T cell lymphomas induced by the murine lymphomagenic retrovirus SL3-3 and show that NFATc3 expression is repressed in these lymphomas. The provirus insertions are positioned close to the nfatc3 promoter or a putative polyA region. Furthermore, we demonstrate that NFATc3-deficient mice infected with SL3-3 develop T cell lymphomas faster and with higher frequencies than wild type mice or NFATc2-deficient mice. These results identify NFATc3 as a tumor suppressor for the development of murine T cell lymphomas induced by the retrovirus SL3-3.

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