ArticleOncogene2001
The SV40 small t-antigen prevents mammary gland differentiation and induces breast cancer formation in transgenic mice; truncated large T-antigen molecules harboring the intact p53 and pRb binding region do not have this effect.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Functional Domains of the Early Proteins and Experimental and Epidemiological Studies Suggest a Role for the Novel Human Polyomaviruses in Cancer.Frontiers in microbiology · 2022Review
- Aging Mouse Models Reveal Complex Tumor-Microenvironment Interactions in Cancer Progression.Frontiers in cell and developmental biology · 2018Review
- Comparisons between murine polyomavirus and Simian virus 40 show significant differences in small T antigen function.Journal of virology · 2011Article
- Cellular transformation by Simian Virus 40 and Murine Polyoma Virus T antigens.Seminars in cancer biology · 2009Review
- PP2A-dependent disruption of centrosome replication and cytoskeleton organization in Drosophila by SV40 small tumor antigen.Oncogene · 2008Article
- GATA-3 links tumor differentiation and dissemination in a luminal breast cancer model.Cancer cell · 2008Article
- Gene expression profiling: cell cycle deregulation and aneuploidy do not cause breast cancer formation in WAP-SVT/t transgenic animals.Journal of molecular medicine (Berlin, Germany) · 2005Article
- pRb inactivation in mammary cells reveals common mechanisms for tumor initiation and progression in divergent epithelia.PLoS biology · 2004Review
- HBX causes cyclin D1 overexpression and development of breast cancer in transgenic animals that are heterozygous for p53.Oncogene · 2003Article
- Simian virus 40 small tumor antigen induces deregulation of the actin cytoskeleton and tight junctions in kidney epithelial cells.Journal of virology · 2003Article
- Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?Breast cancer research : BCR · 2002Review
- Suppression of p53 function in normal human mammary epithelial cells increases sensitivity to extracellular matrix-induced apoptosis.The Journal of cell biology · 2001Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We report here for the first time, that the SV40 small t-antigen inhibits mammary gland differentiation during mid-pregnancy and that about 10% of multiparous WAP-SVt transgenic animals develop breast tumors with latencies ranging from 10-17 months. Cyclin D1 is deregulated and over expressed in the small t-antigen positive mammary gland epithelial cells (ME-cells) and in the breast tumor cells. SV40 small t-antigen immortalized ME-cells (t-ME-cells) exhibit a strong intranuclear cyclin D1 staining, also in the absence of external growth factors and the cells continue to divide for several days without serum. In addition, the expression rate of cyclin E and p21(Waf1) but not of p53 is increased. Coimmunoprecipitation experiments revealed that p21(Waf1) is mainly associated with the cyclin D/CDK4 but not with the cyclin E/CDK2 complex. WAP-SVT transgenic animals exhibit an almost regular mammary gland development until late pregnancy but the majority of the ME-cells are eliminated by apoptosis during the early lactation period. Tumor formation is delayed and less efficient than in T/t-antigen positive animals. Sequestration of p53 and pRb by the N-terminal truncated T-antigen molecules (T1-antigen and T2-antigen) does not affect mammary gland differentiation and the transgenic animals (WAP-SVBst-Bam) do not develop breast tumors.
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