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Topic starter
23/09/2019 2:23 pm
Prostate. 2007 Jun 11.
Androgens and prostate cancer risk: A prospective study.
Wirén S, Stocks T, Rinaldi S, Hallmans G, Bergh A, Stenman UH, Kaaks R, Stattin P.
Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
BACKGROUND: Androgens have been implicated in prostate tumorigenesis, but prospective studies have overall reported no association between circulating levels of androgens and risk of prostate cancer. However, some recent studies have shown that a high level of Testosterone increase the risk of non-aggressive tumors but is associated with a decreased risk of aggressive tumors. METHODS: We prospectively measured plasma levels of total testosterone, androstanediol glucuronide (A-diol-g) and sex hormone binding globuline (SHBG) and calculated estimated levels of free testosterone, in a nested case-control study of 392 cases and 392 matched controls. RESULTS: None of the studied hormones were significantly associated with prostate cancer risk in the full study group or in subgroups according to tumor aggressiveness. Odds ratios in the full study group, for top versus bottom quartile, was for total testosterone 1.25 (95% CI = 0.79-2.00; P(trend) = 0.51); free testosterone, 1.31 (95% CI = 0.82-2.07; P(trend) = 0.35); A-diol-g, 0.88 (95% CI = 0.59-1.33; P(trend) = 0.77); and for SHBG, 1.01 (95% CI = 0.64-1.58; P(trend) = 0.94). CONCLUSIONS: We found no significant associations between androgen levels and risk of prostate cancer in this population-based, non-screened cohort.
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dr frankenstein
23/09/2019 2:44 pm
comforting to know.
jb
Topic starter
23/09/2019 3:12 pm
sure.
dr frankenstein
23/09/2019 3:40 pm
Great.
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
23/09/2019 4:01 pm
Cool.
23/09/2019 4:28 pm
It would be nice to see 5AR and DHT in this study.
Topic starter
23/09/2019 4:51 pm
Mol Cell Endocrinol. 2007 Jan 15;263(1-2):46-54.
Estrogen receptor beta (ERbeta) and inhibition of prostate cancer cell proliferation: studies on the possible mechanism of action in DU145 cells.
Pravettoni A, Mornati O, Martini PG, Marino M, Colciago A, Celotti F, Motta M, Negri-Cesi P.
Department of Endocrinology, Center for Endocrinological Oncology, University of Milano, via Balzaretti 9, 20133 Milano, Italy.
Estrogen receptor beta (ERbeta) plays a protective role against uncontrolled cell proliferation. ERbeta is lost during prostate cancer (CaP) progression suggesting its direct involvement in contrasting tumor proliferation in this disease; however, the molecular mechanism at the basis of this effect has not been clearly defined yet. Possible molecular targets of ERbeta were assessed in DU145 cells, a CaP cell line expressing only ERbeta. Cells treated from 1 to 9 days with different doses of estradiol or diarylpropionitrile (DPN, an ERbeta-selective agonist) show a time-dependent decrease in cell proliferation. The reduced proliferation rate is accompanied by the stimulation of ERbeta expression and the increase of cyclin-dependent kinase inhibitor p21. We demonstrate that the endogenous ERbeta is one of the mediator of the antiproliferative action of estrogens enhancing the synthesis of molecules such as p21 that control cell cycle, an effect amplified by the autoregulation of ERbeta expression. Our observations suggest that CaP, when expressing a functional ERbeta, might be sensitive to the antiproliferative action of estrogens; therefore, ERbeta specific agonists might be valid candidates for new pharmacological approaches to this disease.
Endocrinology. 2007 Feb;148(2):566-74.
Essential role for estrogen receptor beta in stromal-epithelial regulation of prostatic hyperplasia.
McPherson SJ, Ellem SJ, Simpson ER, Patchev V, Fritzemeier KH, Risbridger GP.
Centre for Urological Research, Monash Institute of Medical Research, Monash University, Clayton 3168, Australia.
Estrogens, acting via estrogen receptors (ER) alpha and beta, exert direct and indirect actions on prostate growth and differentiation. Previous studies using animal models to determine the role of ERbeta in the prostate have been problematic because the centrally mediated response to estrogen results in reduced androgen levels and prostatic epithelial regression, potentially masking any direct effects via ERbeta. This study overcomes this problem by using the estrogen-deficient aromatase knockout mouse and tissue recombination to provide new insight into estrogen action on prostate growth and pathology. Homo- and heterotypic aromatase knockout tissue recombinants revealed stromal aromatase deficiency induced hyperplasia in normal prostatic epithelium due to disruption of paracrine interaction between stroma and epithelia. Treatment of tissue recombinants with an ERbeta-specific agonist demonstrated that stimulation of ERbeta elicits antiproliferative responses in epithelium that are not influenced by alterations to systemic androgen levels or the activation of ERalpha. Additionally, work performed with intact aromatase knockout mice demonstrated that the administration of an ERbeta-specific agonist ablated preexisting prostatic epithelial hyperplasia, whereas an ERalpha-specific agonist did not. Therefore, failed activation of ERbeta, resulting from local stromal aromatase deficiency, in conjunction with increased androgen levels, results in increased epithelial cell proliferation and prostatic hyperplasia. These data demonstrate essential and beneficial effects of estrogens that are necessary for normal growth of the prostate and distinguishes them from those that adversely alter prostate growth and differentiation. This highlights the potential of selective estrogen-receptor modulators, rather than aromatase inhibitors, for the management of dysregulated prostate growth.
dr frankenstein