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E Enmark and J Å Gustafsson

The recent discovery of a second estrogen receptor, ER&B;, shows that the mechanisms behind the effects of estrogen are far more complicated than previously assumed, and gives unique opportunities to gain a better understanding of these phenomena. ER&B; is expressed in many important target tissues for estrogen, and a better insight into the respective mechanisms of action of ERalpha and ER&B; might give clues concerning the etiology and pathogenesis of for example prostate or ovarian cancer. Development of ERalpha and ER&B; specific ligands may furthermore open up interesting new possibilities for treatment of e.g. postmenopausal symptoms and breast cancer. In this review, we will try to summarize what is known sofar about estrogen receptor &B;, with some emphasis on the human receptor and its expression. We will furthermore try so summarize what is known about different isoforms of the receptor, in view of what is known about isoforms and variants of other receptors, in particular estrogen receptor alpha (ERalpha) and the progesterone receptor (PR).

Acknowledgements

This study was supported by a grant from the Swedish Cancer Society.

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C Palmieri, G J Cheng, S Saji, M Zelada-Hedman, A Wärri, Z Weihua, S Van Noorden, T Wahlstrom, R C Coombes, M Warner, and J-A Gustafsson

Estrogen is essential for normal growth and differentiation in the mammary gland. It also supports growth of approximately 50% of primary breast cancers. For this reason, removal of estrogen or blocking of its action with the anti-estrogen, tamoxifen, is the main treatment for estrogen receptor alpha (ERalpha)-positive tumors. In 1996, when oncologists became aware of a second ER, ERbeta, there was some doubt as to whether this receptor would be of importance in breast cancer because the clinical consensus was that responsiveness to tamoxifen is related to the presence of ERalpha in breast cancer. Today we know that ERalpha and ERbeta have distinct cellular distributions, regulate separate sets of genes and can oppose each other's actions on some genes. We also know that ERbeta is widely expressed in both the normal and malignant breast and that there are proliferating cells in the breast which express ERbeta. In this review we summarize what is known about ERbeta in breast cancer and examine the possibility that ERbeta-selective ligands may well represent a useful class of pharmacological tools with a novel target, namely proliferating cells expressing ERbeta.