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[Cancer Research 62, 2798-2805, May 15, 2002]
© 2002 American Association for Cancer Research

Carcinogenesis

Lack of Ductal Development in the Absence of Functional Estrogen Receptor {alpha} Delays Mammary Tumor Formation Induced by Transgenic Expression of ErbB2/neu

Sylvia Curtis Hewitt, Wayne P. Bocchinfuso1, Jun Zhai, Chuck Harrell, Linwood Koonce, James Clark, Page Myers and Kenneth S. Korach2

Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology [S. C. H., W. P. B., C. H., L. K., K. S. K. [and Comparative Medicine Branch [J. C., P. M.], National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, and Analytical Sciences, Inc., Durham, North Carolina 27713 [J. Z.]

Expression of the mouse mammary tumor virus (MMTV) neu/erbB2 transgene in mice induces mammary tumors. To examine the effect of removing estrogen receptor {alpha} (ER{alpha}) signaling on the ability of an MMTV-neu/erbB2 transgene to induce mammary tumors, the neu transgene was expressed in the ER{alpha} knockout ({alpha}ERKO) mouse, which lacks functional ER{alpha}. MMTV-neu females that lacked ER{alpha} still developed mammary tumors; however, tumor onset was significantly delayed. This study indicates that ER{alpha} is not required for mammary tumor induction by overexpression of neu/erbB2, but plays a role in the rate of tumor onset. The removal of ovarian steroid by ovariectomy in adults did not alter the onset rate. In contrast, prepubertal ovariectomy, which arrested mammary epithelial development, significantly delayed onset. In addition, manipulations that increase progesterone also accelerate the tumor onset, indicating the slower onset in the {alpha}ERKO is primarily attributable to the anovulatory phenotype resulting in lack of progesterone stimulation and a decreased abundance of target cells in the {alpha}ERKO mammary gland.




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