Group items tagged

ER beta appears to be expressed through the menstruation cycle with predominance follicular and early secretory phases. Contrast with ER alpha predominance in late follicular and early secretory phases.

ER alpha increases aromatase expression in the prostate.  PGE2 increased the ER alpha receptor.  Vicious cycle in men.  Increased aromatase activity increases estrogen production which increases ER alpha (pro growth) and further aromatase activity.

good discussion of estrogen receptors and their role of estrogen signaling transmission.This article goes deep into coregulators, corepressors, cofactors, agonists, antagonists...

estrogen receptors are transported to the cell membrane after production in the rat hippocampus.  The membrane receptors have the same origin as the intracellular receptors.

another awesome article dealing with hormone metabolites. Physicians that don't understand metabolites and receptors may be doing more harm than good.   One of the mainstays of the treatment of metastatic prostate disease is androgen deprivation therapy.  This article requires a reassessment of this due to the DHT metabolite 3-beta androstanediol.  This metabolite is produced from DHT production via the enzyme 3beta HSD.  This metabolite binds to ER beta, an estrogen receptor, and inhibits proliferation, migration, promotes adhesion (limits spreading), and stimulates apoptosis.  This is contrast to 3-alpha androstanediol.  Androgen deprivation therapy will decrease 3-beta androstanediol.  This is the likely reason for the increased aggressive prostate cancer found in those men using 5 alpha reductase inhibitors.

very nice article that looks at the balance of ER-alpha/ER-beta and their role in metabolic syndrome.  This article discusses the balance of  these receptors are tissue dependent in their effect.  I like their conclusion: "...but these mechanisms will never be completely understood if they are not considered in the context of a whole system.

Study shows that decreased androgens up regulates estrogen receptor alpha.  ER alpha promotes growth preferentially over ER beta, and is inflammatory.  Thus in the picture of low T, increased aromatase activity and thus increase Estradiol/Estrone production, we should not be surprised to find increased stimulus for prostate growth.

Nice review of the literature of Estrogens, estrogen receptors and their effect on cytokine production and Lupus.

Article discusses the the conversion of 3-alpha-diol back to DHT and this role in prostate cancer in androgen deprivation therapy.  What we now know is that this metabolite interacts with ER alpha receptor to promote proliferation.  Carcinogenesis appears to be primarily an estrogen driven process and her in prostate cancer, the androgen metabolites are promoting proliferation through estrogen receptors.

Studies in breast cancer and prostate cancer have revealed different effects by ER alpha vs ER beta.  It is no surprise that the same effects are found in ovarian cancer.  This study found ER alpha antagonists and ER beta agonists "significantly" suppressed growth in the ovarian cancer cell lines SKOV3 and OV2008.  Also, ER alpha agonist and ER beta antagonist "significantly" increased growth in the same cell lines.  These findings point to in increased proliferation with ER alpha and decreased with ER beta.  This is consistent with breast and prostate cancer also.

Estrogen associated with improved MetS.  This study finds that it is not through the ER alpha receptor.

bisphenol A increases estrogen signaling.

This study looked at estrogen receptors and inflammatory breast cancer.  ER-alpha36 varian and ER-beta were found to be present in non-genomic signaling in this disease.  ER-alpha is regular absent in this disease.  There is both genomic and non-genomic pathways with regards to signaling with ER

How do environmental chemicals interfere?  This study shows how Bisphenol A actually interferes at the site of the estrogen receptor alpha.  Bisphenol A decreased the efficacy of chemotherapy in ER +/- breast cancer.  Again, the focus is on the interaction with ER alpha.

Estrogen Receptor alpha expression is decreased in the nucleus of hippocampus in Alzheimer's disease.

Bisphenol A causes shift in ER-beta to ER-alpha through increase ER alpha transcription in the testis.  This only looked at ER expression in the testis.

ER alpha and ER beta found to be expressed in meningiomas.  ER alpha was expressed more by the meningiomas.

Great review article on the endocrine disrupting role of Cadmium.  Cadmium binds to the ER-alpha inducing an estrogen signal.  Cadmium also binds to the androgen receptor as well.  This study proposes a similar activation of ER-alpha and AR by Cadmium.

This is a dissertation, but they found ER alpha expression in all meningioma samplings. This is in contrast to previous studies. As further research has come with meningiomas, more ER presence is found, likely due to improved testing techniques. What is interesting here is that Low/no PR status was associated with Increased ER alpha status. This has been shown to be a more pro-inflammatory/pro-growth picture in disease states, such as breast and prostate CA.

ER and PR are suggested to play role in colon cancer.  The question is do they play a role in carcinogenesis or does the expression of the receptors indicate something else i.e. attempt at differentiation through progesterone.  Also, what receptors are involver here: ER alpha or beta.  Likewise for the progesterone receptors