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low dose xenoestrogen exposure increases prostate growth and future disease through fetal exposure and increased ER alpha expression.

xenoestrogens are estrogen receptor agonists.  This is a good discussion of there interaction with xenoestrogens and particularly ER alpha.

Estrogen receptors are primarily located inside the nucleus and in the cytoplasm; not on the cell membrane surface. This article specifically focus' on the non-genomic action of ER-beta.  ER-alpha and ER-beta are classic transcription factors.

Increased survival in those with ER beta + and ER alpha -.  Early relapse was associated with lack of ER beta expression.  ER beta is transcribed from a different genomic location than ER alpha.  

DES exposure feminizes male mice through ER alpha receptor.

Good discussion of the different effects of ER-alpha and ER-beta in breast cancer.  ER-beta inhibits growth in contrast to ER-alpha.

This article discusses the failure of androgen deprivation therapy and prostate cancer.  This failure is quite common.  The authors point to alpha-DHT as the primary mechanism through AR stimulation.  However, we know that DHT metabolites also stimulate estrogen receptors.

review of melatonins activity in cancer battle.

ER-alpha plays role in TMJ.  This study looked to see if inflammation and E2 would modulate ER-alpha expression.  They found this to be tissue dependent and whether inflammation was present or not.  In the presence of inflammation, ER-alpa expression was reduced, but in inflamed joint, ER-alph expression stayed unchanged.

Fantastic read on the effects of progesterone metabolism on tumor and cancer growth.  Tumorigenesis is not just about the hormone, hormone balance, but about the metabolism of hormones.  This is why premarin is so carcinogenic: it is primarily metabolized by the 4-OH estrone pathway.

5-beta androstanediol doesn't have affinity for androgen receptors, but for estrogen receptors. Affinity for ER beta exceeds that for ER alpha.

Study finds ER and PR increase along the timeline of tumor initiation.  The authors point to likely association that ER and PR expression is associated with and key to initiating colorectal transformation.  A lot to be determined from this study.  IF this were entirely true, then what to explain the 35% lower colorectal cancer risk in women vs men?  Likely ER and PR pertubance plays a significant role is likely, but the mere expression--yet to be determined.

Androgens antagonize ER-alpha receptors in breast cancer.

Estrogen receptors play a role in prostate cancer.  TMPRSS2-ERG expression is associated with increased aggressive cancer phenotype--ER beta decreases TMPRSS2-ERG expression, whereas ER alpha increases it.

In vitro study finds that progesterone metabolites effect expression of estrogen receptors.  The progesterone metabolite 5alphaP increased ER alpha expression.  This is important as ER alpha promotes growth and inflammation.

DHT metabolite 3-beta androstanediol inhibits prostate cancer via its interaction with ER beta not AR.  This study finds increased E-cadherin transcription to reduce metastasis.  Estrogen was not active, according to this study.  This implies that estrogen in early disease may have a different signal than late.

Melanoma is a known estrogen sensitive cancer.  This study finds ER Beta loss correlates with thickness of lesion.  The authors propose ERalpha/ERbeta ratio be assessed.  ERbeta has been shown to decrease proliferation, promotes differentiation, and decrease inflammation in breast studies.  In contrast, ERalpha promotes proliferation, decreases differentiation, and promotes inflammation.  Here, the same effects seem to apply to melanoma. Of interesting note, men have lower skin ERbeta than women and ERbeta declines with age and menopause in women.  Essentially, the loss of the ability to differentiate, decrease proliferation and inflammation  occurs with increase estrogen stimulus--set up for estrogen promoting cancers.

ER beta expression and the ratio of ER alpha/ER beta is important in prognosis and effectiveness of SERM therapy like tamoxifen.  This study looked at the aromatase inhibitor anastrazole as well.

Just the abstract, but Testosterone to estrogen production through aromatase activity plays role in prostate cancer.  This is due to the lack of correlation in androgens and prostate cancer in the androgen hypothesis.  Estrogen receptors alpha/beta balance equally play a role.  

Estradiol increases prolactin receptor transcription through their ER-alpha receptor.