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Induction of mammary tumors by expression of polyomavirus middle T oncogene: a transgenic mouse model for metastatic disease.

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Guy, C T, Cardiff, R D, Muller, W J·1992·Molecular and Cellular Biology

Abstract

The effect of mammary gland-specific expression of the polyomavirus middle T antigen was examined by establishing lines of transgenic mice that carry the middle T oncogene under the transcriptional control of the mouse mammary tumor virus promoter/enhancer. By contrast to most transgenic strains carrying activated oncogenes, expression of polyomavirus middle T antigen resulted in the widespread transformation of the mammary epithelium and the rapid production of multifocal mammary adenocarcinomas. Interestingly, the majority of the tumor-bearing transgenic mice developed secondary metastatic tumors in the lung. Taken together, these results suggest that middle T antigen acts as a potent oncogene in the mammary epithelium and that cells that express it possess an enhanced metastatic potential.

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Metadata

Authors
Guy, C. T., Cardiff, R. D., & Muller, W. J.
Venue
Molecular and Cellular Biology
Published
1992-03
Volume
12
Issue
3
Pages
954-961
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W2111449140
Cited by
1,631
References
0
FWCI
3.59
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Induction of mammary tumors by expression of polyomavirus middle T oncogene: a transgenic mouse model for metastatic disease. https://app.cochat.ai/papers/10.1128/mcb.12.3.954
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Guy, C. T., Cardiff, R. D., & Muller, W. J. (1992). Induction of mammary tumors by expression of polyomavirus middle T oncogene: a transgenic mouse model for metastatic disease. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.12.3.954

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.