Estrogens, antiestrogens and cell proliferation

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Abstract
The classical estrogen receptor model does not sufficiently account for the tumor‐promoting activity of extrogens or for the antiproliferative effect of antiestrogens in estrogen‐dependent tumors. Particular difficulties not readily accommodated within the model are that hormonal autonomy can supervene without loss of the estrogen receptor and that antiestrogen effects are highly context‐dependent, without apparent differences in the estrogen receptor itself or in metabolic transformation of antiestrogens. Recent studies suggest that estrogens may promote cell proliferation, in part, through the mediation of growth factors and that antiestrogens may exert some of their effects by mechanisms unrelated to the estrogen receptor.