@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}
}