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| Article |
| Bcl-2 expression delays mammary tumor development in dimethylbenz(a)anthracene-treated transgenic mice |
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| Kristen L Murphy1,2, Frances S Kittrell2, Jason P Gay2, Richard Jäger3, Daniel Medina2 and Jeffrey M Rosen2 |
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1Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, Texas, TX 77030, USA
2Department of Cell Biology, Baylor College of Medicine, Houston, Texas, TX 77030, USA
3Institut fuer Genetik, Forschungszentrum Karlsruhe, Postfach 3640, D-76021 Karlsruhe, Germany
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Correspondence to: Jeffrey M Rosen, Department of Cell Biology, Baylor College of Medicine, Houston, Texas, TX 77030, USA
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| Abstract |
| Bcl-2 is known to have dual antiproliferative and antiapoptotic roles. Overexpression of Bcl-2 in the mammary gland using a whey acidic protein (WAP) promoter-driven Bcl-2 transgene inhibits apoptosis in the mammary gland during pregnancy, lactation, and involution, and also counteracts apoptosis induced by overexpression of a mutant p53 transgene (WAP-p53 172 R-L). WAP-Bcl-2 mice and nontransgenic controls were treated with the carcinogen dimethylbenz(a)anthracene (DMBA). Surprisingly, the nontransgenic mice developed mammary tumors with decreased latency. Tumors arising in WAP-Bcl-2 mice displayed substantially reduced levels of proliferation relative to those seen in nontransgenic mice (P<0.015), perhaps resulting in the observed increase in tumor latency following carcinogen treatment. This WAP-Bcl-2 mouse tumor model reflects the situation seen in some human breast cancers overexpressing Bcl-2, where expression of Bcl-2 has been shown to correlate with a lower proliferative index in tumors. |
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| Keywords |
| Bcl-2; mammary tumorigenesis; DMBA; transgenic mice |
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| Received 28 April 1999; revised 19 July 1999; accepted 20 July 1999 |
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| 11 November 1999, Volume 18, Number 47, Pages 6597-6604 |
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