For the last 25 years my laboratory has explored the mechanisms of action of sex hormones (estrogens and androgens) on the control of proliferation of their target cells. To this purpose, we have used human breast and prostate cancer cell lines and correlated the data collected in culture conditions with what these sex steroids do to their target cells in rodents and humans. Sex steroids affect the proliferation of their target cells through a two-step mechanism (Step 1 = proliferation: Step 2 = inhibition). Currently, somatic cell genetics and recombinant DNA technology (subtracted libraries) allow us to search for unique genes having a regulatory role on the inhibition of cell proliferation.

In addition to the line of investigation described above, research is designed and conducted to identify possible links between the reproductive impairment observed in wildlife and humans and environmental estrogens. I am interested and dedicated to uncovering the relationship between estrogenic environmental mimics and breast and prostate cancers. To achieve these ends, I am using 2 parallel approaches: (1) the identification of estrogenic xenobiotics by assessing their ability to induce cell proliferation on breast cancer cells, as estrogens do. The E-SCREEN test, developed in this lab, is used as a simple, reliable laboratory standard test for estrogenicity; and (2) the development of technology to measure the total environmental estrogen burden in tissues and body fluids from wildlife and humans.

Research Associates:

Fantahun Diba

Post Docs:

Maricel Maffini

Research Technicians:

Cheryl Michaelson
John Raynor

Selected Publications:

Soto, A.M., Lin, T-M., Sakabe, K., Olea, N., Damassa, D.A., and Sonnenschein, C. 1995. Variants of the human prostate LNCaP cell line as tools of study discrete components of the androgen-mediated proliferative response. Oncology Research 7:5454-558.

Sonnenschein, C., Soto, A.M., Fernandez, M.F., Olea, N., Olea-Serrano, M.F., and Ruiz-Lopez, M.D. 1995. Development of marker of estrogenic exposure in human serum. Clinical Chemistry 41:1888-1895.

Olea, N., Pulgar, R., Perez, P., Olea-Serrano, F., Rivas, A., Novillo-Fertrell, A., Pedraza, V., Soto, A.M. and Sonnenschein, C. 1996. Estrogenicity of resin-based composites and sealants used in dentistry. Env. Health Prospect. 104-298-305.

Sonnenschein, C., Soto, A.M., and Michaelson, C.L. 1996. Human serum albumin shares the properties of estrocolyone-I, the inhibitor of the proliferation of estrogen-target cells. J. steroid Biochem. & Molec. Biol. 59:147-154.

Szelei, J., Jimenez, J., Soto, A.M., Luizzi, M.F., and Sonnenschein, C. 1997. Androgen-induced proliferative shutoff in androgen receptor-transfected human estrogen-target breast cancer MCF7 cells. Endocrinology 138:1406-1412.

Geck, P., Szelei, J., Jimenez, J., Lin, T.M., Sonnenschein, C., and Soto, A.M. Expression of novel genes linked to the androgen-induced, proliferative shutoff in prostate cancer cells. Journal of Steroid Biochemistry and Molecular Biology 93: (in press), 1997.