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Journal of Virology, February 2008, p. 1808-1818, Vol. 82, No. 4
0022-538X/08/$08.00+0     doi:10.1128/JVI.02115-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Variable Transcriptional Activity of Endogenous Retroviruses in Human Breast Cancer ^,

Medical Clinic III, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany,¹ Department of Pathology, St. James's University Hospital, Leeds, United Kingdom,² Department of Human Genetics, Medical Faculty, University of Saarland, Homburg, Germany,³ Helmholtz Center Munich, German Research Center for Environmental Health, Institute of Molecular Virology, Neuherberg, Germany⁴

Received 25 September 2007/ Accepted 13 November 2007

Human endogenous retroviruses (HERVs) account for up to 9% of the human genome and include more than 800 elements related to betaretroviruses. While mouse mammary tumor virus (MMTV) is the accepted etiological agent of mammary tumors in mice, the role of retroviral elements in human breast cancer remains elusive. Here, we performed a comprehensive microarray-based analysis of overall retroviral transcriptional activities in 46 mammary gland tissue specimens representing pairs of nonmalignant and tumor samples from 23 patients. An analysis of nonmalignant tissue samples revealed a distinct, mammary gland-specific HERV expression profile that consists of 18 constitutively active HERV taxa. For corresponding tumor samples, a general trend toward lower levels of HERV transcription was observed, suggesting common regulatory mechanisms. In various subsets of patients, however, increased transcript levels of single class I HERV families (HERV-T, HERV-E, and HERV-F) and several class II families, including HML-6, were detected. An analysis of transcribed HML-6 sequences revealed either the activation of some or the increased activity of several proviral loci. No evidence for MMTV or human MMTV-like virus transcripts was found, indicating that transcriptionally active, MMTV analogous, exogenous viruses were not present in the breast cancer samples analyzed.

Published ahead of print on 12 December 2007.

Supplemental material for this article may be found at http://jvi.asm.org/.

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