@article{MurphyKittrellGayetal.1999, author = {Kristen L. Murphy and Frances S. Kittrell and Jason P. Gay and Richard J{\"a}ger and Daniel Medina and Jeffrey M. Rosen}, title = {Bcl-2 expression delays mammary tumor development in dimethylbenz(a)anthracene-treated transgenic mice}, series = {Oncogene}, volume = {18}, number = {47}, publisher = {Nature Publishing Group}, issn = {0950-9232}, doi = {10.1038/sj.onc.1203099}, pages = {6597 -- 6604}, year = {1999}, 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.}, language = {en} }