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Prostate cancer from test. ALL MUST READ!

I find this topic very helpful not that I really know what you guys are writing about. I have two Uncles who had prostate trouble and one did for sure have cancer and surgery to remove it etc. He onced used Steroids although I dont know which ones but he was on steroids for Asthma of all things. Im sure it was Test or maybe some orals but never really asked. He lived through it but its scarey because the Doctors put him on steroids only to have problems later. Everybody like to blame the drug but I agree there has to be some Genetic dispostition here. I hope I can incorporate some preventative measures for myself since it was in the family.
 
this is scaring the shit outta me.... guess i have add finastride to my cycle now..... even though i have no baldness or any kind of cancer in my family... is this what it has to come down to?
 
Realgains said:
Huckleberry Finnaplex.....I may be mistaken but does finasteride only reduce DHT from test, and not the other DHT converting roids?

I may be mistaken,as I have not researched it thoroughly,but I believe Finasteride only inhibits 5 alpha-reductase from enzymatically converting substances into DHT.I'm not sure it would be effective against compounds who are ALREADY DHT,without having to go through this enzymatic conversion.
 
From the mouth of Guru Bill Roberts from Meso-rx.com

"A 5AR inhibitor(Finasteride) is recommended in cases where test is being used and the individual is particularily concerned about the prostate"

I think those concerned about our prostate includes all of us!
 
BILL ROBERTS... :p

Progesterone receptor expression in human prostate cancer: correlation with tumor progression.

Bonkhoff H, Fixemer T, Hunsicker I, Remberger K.

Institute of Pathology, University of the Saarland, Homburg/Saar, Germany. [email protected]

BACKGROUND: The recent discovery of the classical estrogen receptor alpha (ERalpha) in metastatic and recurrent prostatic adenocarcinoma suggests that estrogens are implicated in prostate cancer progression. METHODS: To get more insight into estrogen signaling in prostate cancer tissue, the current study has examined the immunoprofile of the estrogen-inducible progesterone receptor (PR), and evaluated its relation to ERalpha gene expression. RESULTS: In primary tumors, the PR was detectable in 36% of primary Gleason grade 3 (5 of 14 cases), 33% of primary Gleason grade 4 (5 of 15 cases), and in 58% of primary Gleason grade 5 tumors (7 of 12 cases). None of the 41 primary tumors investigated revealed significant PR expression in more than 50% of tumor cells. Conversely, moderate to strong receptor expression was observed in 60% of metastatic lesions (9 of 15 cases), and in 54% of androgen-insensitive tumors (38 of 71 cases). Irrespective of grades and stages, the presence of the PR was invariably associated with high steady state levels of ERalpha mRNA, whereas the ERalpha protein was undetectable by immunohistochemistry (IHC) in a significant number of cases (58 of 97 cases). CONCLUSIONS: The progressive emergence of the PR during tumor progression obviously reflects the ability of metastatic and androgen-insensitive tumors to use estrogens through a ERalpha-mediated pathway. The present data provide a theoretical background for studying the efficiency of antiestrogens and antigestagens in the medical treatment of advanced prostate cancer. Copyright 2001 Wiley-Liss, Inc.

:p
 
LESS CERTAIN INFO HERE.. BUT STILL HELPFUL

Allelic variants of aromatase and the androgen and estrogen receptors: toward a multigenic model of prostate cancer risk.

Modugno F, Weissfeld JL, Trump DL, Zmuda JM, Shea P, Cauley JA, Ferrell RE.

Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA. [email protected]

PURPOSE: The purpose of this study was to determine whether polymorphisms in the CAG repeat in exon 1 of the androgen receptor (AR), two intronic restriction sites in the estrogen receptor (ESR1 XbaI and ESR1 PvuII), and an Arg264Cy5 substitution in the aromatase gene (CYP19) contribute to prostate cancer risk. EXPERIMENTAL DESIGN: A case-control study was performed with 88 Caucasian prostate cancer patients and 241 Caucasian male controls. Logistic regression models were used to assess individual and joint contributions of genotypes to prostate cancer risk. RESULTS: For single polymorphisms, only the AR repeat number was significantly related to increased prostate cancer risk [age- and body mass index (BMI)-adjusted odds ratio (OR), 1.14; 95% confidence interval (CI), 1.04-1.25], suggesting a 14% increase in risk for each missing CAG repeat. When subjects were classified as either long (> or =23 AR CAG repeats) or short (<23 repeats) carriers, a significant increase in risk was also observed (age- and BMI-adjusted OR, 1.75; 95% CI, 1.05-2.95; P = 0.04). The aromatase C/T was associated with an increase in risk of borderline significance (age- and BMI-adjusted OR, 2.50; 95% CI, 0.99-6.28). When examining the effects of two polymorphisms on prostate cancer risk, homozygosity for the ESR1 XbaI restriction site together with a longer AR was more frequent among controls (32%) than cases (18%; age- and BMI-adjusted OR, 0.39; 95% CI, 0.19-0.78). The aromatase C/C genotype together with a longer AR was also more frequent among controls (55%) than cases (41%; age- and BMI-adjusted OR, 0.51; 95% CI, 0.30-0.89). CONCLUSIONS: Estrogen and aromatase may play a role in prostate cancer. A multigenic model of prostate cancer susceptibility is also supported.
 
Macrophage69alpha....really? I would like to hear more about estradiol and prostate cancer. I have never heard such a thing but I have lots to learn bro.

We should all take an estrogen inhibitor like Cytadren or Arimidex too then
 
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