Estrogen or antiprogestin treatment induces complete regression of pulmonary and axillary metastases in an experimental model of breast cancer progression.

Abstract	In this paper we demonstrate, using the C7-2-HI metastatic transplantable ductal mammary tumor, that endocrine therapy can induce complete regression of spontaneous lymph node and lung metastases in a mouse model of breast cancer progression. This tumor expresses high levels of estrogen and progesterone receptors and shows a high incidence of early axillary lymph nodes and lung metastases; using this model we had previously shown complete tumor regression of subcutaneous implants. Interestingly, although the metastases showed a more differentiated histology as compared with the primary growth, they underwent complete regression when treated with estrogens or antiprogestins. This phenomenon was associated with sustained cytostasis and apoptosis accompanied by increases in p21 and p27 expression and early tissue remodeling. These results highlight the essential role of PR in regulating cell proliferation in this model as well as its possible use as therapeutic target.
Authors	Silvia I Vanzulli, Rocío Soldati, Roberto Meiss, Lucas Colombo, Alfredo A Molinolo, Claudia Lanari
Journal	Carcinogenesis (Carcinogenesis) Vol. 26 Issue 6 Pg. 1055-63 (Jun 2005) ISSN: 0143-3334 [Print] England
PMID	15774491 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Cdkn1a protein, mouse Cdkn1b protein, mouse Cell Cycle Proteins Cyclin-Dependent Kinase Inhibitor p21 Estrogens Progestins Receptors, Estrogen Receptors, Progesterone Tumor Suppressor Proteins Cyclin-Dependent Kinase Inhibitor p27 Mifepristone Estradiol
Topics	Animals Apoptosis (drug effects) Cell Cycle Proteins (biosynthesis) Cyclin-Dependent Kinase Inhibitor p21 Cyclin-Dependent Kinase Inhibitor p27 Estradiol (therapeutic use) Estrogens (therapeutic use) Female Lung Neoplasms (drug therapy, metabolism, secondary) Lymphatic Metastasis Mammary Neoplasms, Experimental (drug therapy, metabolism, pathology) Mice Mice, Inbred BALB C Mifepristone (therapeutic use) Mitosis (drug effects) Progestins (antagonists & inhibitors) Receptors, Estrogen (biosynthesis) Receptors, Progesterone (biosynthesis) Transplantation, Heterologous Tumor Suppressor Proteins (biosynthesis)

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