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estrogen receptors are not created equally.  ER-alpha is the predominant pro-stimulatory signal receptor, whereas the ER-beta is the inhibitory receptor signaling pathway.  SERMS are not created equally as well dependent on how they bind the respective ER receptors.

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Estrogen receptors alpha and beta show dominance in the proliferative phases, with alpha isoform predominating.  In the secretory phase, less expression of ER was present. ER alpha was predominantly expressed in the epithelial and stromal cells in the proliferative phase.  ER beta was predominantly expressed in glandular cells in the same proliferative phase.   in the luteal phase, ER alpha expression declined in the funtionalis layers.  ER alpha in the basalis remained unchanged.  ER beta in the functionalis layers also declined in the luteal phase.   No relative change was found in the weak expression of ER alpha/beta in the myometrium.

estrogen related receptors play a role in estrogen signaling, though they don't bind estradiol. They bind estrogen related elements. Exact role is unknown. They are called "orphan" members of the nuclear family of receptors.

The risks of estrogen metabolism are not clear cut.  Likely never will be due to the complexity of individual metabolism.  This study found no correlation between 2OH-Estrone and 2OH:16alpha-Estrone and breast cancer risk in ER+/PR+ breast cancer.  Translated: no benefit in breast cancer risk in 2OH-Estrone metabolism or increased 2OH:16alpha estrone metabolism.  There was a positive association between 2OH-Estrone and 2:16alpha-Estrone in women with ER-/PR- tumors and low BMI.

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Estrogen receptors are one mechanism of the transmission of the estrogen signal.  The signal can be from estrogens themselves, estrogenic like compounds (xenoestrogens) and via non-estrogens like 3-beta androstane idol that interacts with ER beta to decrease prostate cancer cell proliferation.

estrogen-related receptors.  There are 3 types: alpha, beta, and gamma.  These don't respond to estrogens, but to estrogen related elements

Great article!!  Nice discussion of the complexity of hormones.  Women on aromatase inhibitors can make estrogen from Testosterone.  This is important with estrogen sensitive cancer as in breast cancer.  This will occur via alternative pathways: Testosterone to DHT via 5 alpha reductase and then DHT to 3 beta androstanediol via 3 beta HSD.  3 beta androstanediol is a male hormone metabolite that binds to estrogen receptors.  The affinity is less than Estradiol, but appears to have a higher affinity for ER beta over ER alpha. 

Great read on the effects of bisphenol A as an xenoestrogen.  Bisphenol A is a weak estrogen, but it does increase androgen receptor and estrogen receptor alpha transcription.  This is from fetal exposure.

ER-beta expression appears to regulate estrogenic activity through ER-alpha expression.  Co-expression of ER-alpha and ER-beta is associated with reduced estrogenic signaling, indicating a significant counter regulatory role for ER-beta.

Very nice study.  The authors looked at normal prostate, early disease and late stage prostate cancer.  The authors found that ER beta expression, as a general rule, was lost as progression occurred to the high-grade dysplasias and grad 4/5 carcinomas of the prostate.  Early low/moderate dysplasia was associated with an increase in ER beta--the authors propose that this was due to an attempt of the basal epithelium to counter the paracrine effect of ER alpha.   In contrast, androgen receptors appeared to be equally expressed across all.

5 alpha androstanediol promotes prostate cancer growth and survival independent of androgen receptors.   This study didn't clarify the mechanism.  We no know that this occurs via estrogen receptor alpha.  Thus a Testosterone metabolite signals through an estrogen receptor.

ER-beta found throughout both the proliferative and secretory phases of the menstrual cycle.  ER-beta expression was higher in the proliferative versus the secretory phases, though not statistically significant.  This makes since as estrogen stimulation dominates the proliferative phase.  Additionally, ER-beta expression was found throughout all levels of the endometrium and the myometrium.

this study looked at estrogen in rheumatoid arthritis in mice. They found an anti-inflammatory effect of estrogen in men through ER-alpha. This is in contrast to other studies. Maybe the immunomodulatory effects of estrogen is, in part, through which receptors are activated.

Several interesting points about this article.  Cadmium is a non-carcinogen.  Cadmium acts through estrogen receptors.  Cd acts as an estrogen.  Second, melatonin inhibits ER alpha, which promotes inflammation and growth signaling.

estrogen receptor Beta and alpha discussed in the endometrium through menstrual cycle.  This study focus' on human endometrium

Estrogen receptors and disease

ER-beta inhibits ER-alpha activation of cell proliferation via cyclin D1 gene expression.  This points to ER-beta as a counter regulatory receptor to ER-alpha.  This explains how a loss of ER-beta expression is found to be associated with increased cancers.  

environmental toxin, bisphenol A, shown to increase estrogen receptor and androgen receptor expression in the prostate.  Also, a shift from ER beta to ER alpha occurs, increase the inflammatory and proliferative signal.

Progesterone metabolites and breast cancer

xenoestrogen exposure has been shown to increase ER alpha and ER beta in the pituitary.