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Carcinogenesis Advance Access originally published online on March 17, 2005
Carcinogenesis 2005 26(6):1055-1063; doi:10.1093/carcin/bgi060
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Carcinogenesis vol.26 no.6 © Oxford University Press 2005; all rights reserved.

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

Silvia I. Vanzulli 2, {dagger}, Rocío Soldati 1, {dagger}, Roberto Meiss 2, Lucas Colombo 3, Alfredo A. Molinolo 1, 4 and Claudia Lanari 1, *

1 Laboratory of Hormonal Carcinogenesis, Instituto de Biología y Medicina Experimental, CONICET (Consejo Nacional de Investigaciones Científicas y Técnicas), Buenos Aires, Argentina, 2 Instituto de Estudios Oncológicas, Academia Nacional de Medicina and 3 Instituto Angel Roffo, Buenos Aires, Argentina
4 Present address: Molecular Carcinogenesis Unit, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, Building 30, Room 213, National Institutes of Health, Bethesda, MD 20892-4340, USA

* To whom correspondence should be addressed at: Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, C1428ADN Buenos Aires, Argentina. Tel: +54 11 4783 2869; Fax: +54 11 4786 2564; Email: clanari{at}dna.uba.ar

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.


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