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Human endogenous retrovirus rec interferes with germ cell development in mice and may cause carcinoma in situ, the predecessor lesion of germ cell tumors

Oncogene volume 24, pages 3223–3228 (2005)Cite this article

Abstract

Germ cell tumors (GCTs) are among the most common malignancies in young men. We have previously documented that patients with GCT frequently produce serum antibodies directed against proteins encoded by human endogenous retrovirus (HERV) type K sequences. Transcripts originating from the env gene of HERV-K, including the rec-relative of human immunodeficiency virus rev, are highly expressed in GCTs. We report here that mice that inducibly express HERV-K rec show a disturbed germ cell development and may exhibit, by 19 months of age, changes reminiscent of carcinoma in situ, the predecessor lesion of classic seminoma in humans. This provides the first direct evidence that the expression of a human endogenous retroviral gene previously established as a marker in human germ cell tumors may contribute to organ-specific tumorigenesis in a transgenic mouse model.

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Acknowledgements

We thank J Mayer, Institute for Human Genetics, University of Saarland Medical School, for discussion. This work was supported by grant Mu 452/5 from the German Research Foundation (DFG) to NM-L.

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Authors and Affiliations

  1. Department of Virology, Bldg. 47, University of Saarland Medical School, 66421, Homburg/Saar, Germany

    Uwe M Galli, Marlies Sauter, Klaus Roemer & Nikolaus Mueller-Lantzsch

  2. M-F-D Diagnostics Laboratory GdbR, Resources Bldg. of the Johannes-Gutenberg University, Obere Zahlbacher Str. 63, 55131, Mainz, Germany

    Bernd Lecher & Simone Maurer

  3. Institute of Pathology, University Hospital, 48149, Muenster, Germany

    Hermann Herbst

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  1. Uwe M Galli
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  2. Marlies Sauter
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Correspondence to Nikolaus Mueller-Lantzsch.

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Galli, U., Sauter, M., Lecher, B. et al. Human endogenous retrovirus rec interferes with germ cell development in mice and may cause carcinoma in situ, the predecessor lesion of germ cell tumors. Oncogene 24, 3223–3228 (2005). https://doi.org/10.1038/sj.onc.1208543

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