6533b7dafe1ef96bd126e15c

RESEARCH PRODUCT

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

Klaus RoemerUwe M GalliBernd Dr. LecherNikolaus Mueller-lantzschSimone MaurerMarlies SauterHermann Herbst

subject

MaleCancer ResearchTime FactorsvirusesTransgeneBlotting WesternEndogenous retrovirusApoptosisMice TransgenicEndogenyBiologymedicine.disease_causeMiceViral Envelope ProteinsCell Line TumorGeneticsmedicineAnimalsHumansHuman endogenous retrovirus KRNA MessengerMolecular BiologyModels GeneticReverse Transcriptase Polymerase Chain ReactionEndogenous RetrovirusesSeminomaNeoplasms Germ Cell and EmbryonalSeminiferous Tubulesmedicine.diseaseVirologyProtein Structure TertiaryAlternative SplicingGerm Cellsmedicine.anatomical_structureMicroscopy FluorescenceCancer researchGerminomaGerm cell tumorsCarcinogenesisCarcinoma in SituGerm cell

description

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.

yearjournalcountryeditionlanguage
2005-02-28Oncogene
https://doi.org/10.1038/sj.onc.1208543