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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.

Loss of ER-beta expression in the prostate associated with increased progression from a normal prostate to prostate cancer.

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.

It is important to understand that hormones in serum do not reflect the hormonal environment in the prostate.  Additionally, the diseased prostate does not respond the same as a healthy prostate.  That is high advanced Prostate cancer will respond to estrogen therapy and early prostate disease will increase with increased aromatase Testosterone to Estradiol conversion.

A revisit of the saturation model of Testosterone therapy and prostate cancer.  Review finds Testosterone therapy does not "appear to promote prostate cancer growth".  The saturation model is the thought around the AR.  At low concentrations, there is a greater sensitivity of Testosterone to AR binding at very low T levels; but above those very low T levels, prostate cancer becomes insensitive to the Testosterone.

Artesunate found to have broad range of anti-cancer activity, such as pro-apoptosis attenuation of tumor growth, metastasis, and angiogenesis. This study primarily looked at the effect in a prostate cancer mouse model. It found that the artesunate down regulated androgen receptors. Now, there is debate about how and when AR and androgens play a role in prostate cancer as studies have also pointed to estrogen and ER in carcinogenesis of the prostate.

PSA increased more in men with prostate cancer compared to no disease in men on finasteride therapy. This supports the idea that finasteride has a greater PSA reduction in benign prostate disease compared to prostate cancer.

environmental toxins that have estrogenic activity, i.e. BPA alter the prostate stem cells.  These and other xenoestrogens, as they are collectively called, increase the sensitivity of the prostate to estrogen.  This increases the risk of prostate Ca.  This just sets the pattern of signal interpretation and sensitivity.  Add in the continued estrogenic environment, add in the excess weight, the increased aromatase activity and resultant estrogen production and one has all the ingredients for prostate cancer.

The genesis of cancer is complex.  To simply say that cancer is genetic is both niave and uninformed.  This study displays the complexity of the timing of hormones and cancer genesis.  This rat study found that Estradiol added to Testosterone increased "markedly".  Estrogen plays a role in the genesis of prostate disease.  However, this varies among individuals.  The response of prostate cancer to estradiol appears to change according to the progression of the cancer.

not really much can be gleamed from this other than lower cholesterol i.e. < 200 is associated with high grade, gleason 8-10, prostate cancer.  No association was found with prostate cancer in general.

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.

High aromatase activity and ER alpha expression/signaling associated with prostate disease.

testosterone therapy does not increase prostate cancer.

study finds high incidence of prostate cancer in those with low Testosterone at the time of biopsy for HGPIN. What is also interesting, is that the authors found a higher SHBG.  It is well known that Estradiol increases SHBG.  It is also well known that Testosterone to Estradiol in the prostate plays a role in prostate cancer.

The tide is beginning to shift on testosterone and Prostate Cancer.  A literature review finds no support for Testosterone and Prostate carcinogenesis or low Testosterone providing any protection against prostate cancer.  

a good read!

low T:E2 ratio increases inflammation in prostate.  This has implications in prostatitis and prostate cancer.

Great confusion exists in the medical profession about Testosterone and PSA and the health of the prostate. The conversion of Estrogen, whether E2 or E1, and other variables are responsible for increases in PSA while on Testosterone therapy. This study points out that Estradiol in men stimulates cell line growth of prostate cancer. In contrast, Epitestosterone, an androgen metabolite, has antiandrogen, inhibits this estrogen activity. Epitestosterone exists in an inverse relationship to Estradiol and IGF-1.

Is prostate cancer, in part, a result of viral insult.  Study finds XMRV is highly associated with high-grade prostate cancer.

study shows that over expression of aromatase activity and resultant increased estradiol/estrone production increases prostatitis and plays a role in prostate cancer.  

Review, only abstract available--Testosterone therapy does not affect prostate size, intraprostatic Testosterone levels, or prostate cancer progression.  Carcinogenesis of the prostate is not a androgen driven process.  It is an aromatase process.  DHT metabolites can promote tumor growth via Estrogen receptors later, but initiation, via all accounts, occurs through aromatase expression and production of estrogen in the prostate.