Summary

The p53 null mammary epithelium transplant model has been extensively characterized at the genetic, hormonal, and biological levels. Tumors progress from ductal hyperplasias and ductal carcinoma in-situ (DCIS) and are aneuploid, metastatic and approximately 80% are estrogen receptor (ERa) negative. The normal and premalignant mammary stages of development are positive and hormone responsive. Continuous estrogen (E) or progesterone (P) treatment markedly enhances tumorigenesis in p53-null mammary epithelium. Blocking E signaling by tamoxifen or blocking P signaling by deleting the PR or blocking E and P signaling by ovariectomy markedly decreases hormone-induced mammary tumorigenesis in p53-null epithelium. The tumors that do arise are negative. These results suggest that this model is appropriate to examine issues regarding the timing and duration of tamoxifen treatment on premalignant progression and the use of combined prevention strategies to delay the occurrence of invasive breast cancer (BC).

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