Abstract
Abstract
The neonatal mouse has proven to be an excellent model to ascertain the deleterious effects of estrogenic compounds on the developing reproductive tract. This system has been used to determine the morphological consequences after neonatal exposure to coumestrol (a plant estrogen).
The role of estrogens in carcinogenesis (as a cocarcinogen or a tumor promotor) is unresolved at this time. Many studies suggest that estrogens are capable of functioning in this manner and recent evidence in cellular and molecular oncology revealed that estrogens act by genetic and epigenetic mechanisms in cancer cells. This review discusses the long-term morphological alterations in the reproductive tract of mice exposed neonatally to coumestrol.
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