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so its less harmful if you dont use finasteride with deca?...and so notthing can help when on primo right its my best roid..600+mgs a week and i blow up
Prostate cancer from test. ALL MUST READ!
- Thread starter Realgains
- Start date
While I have to agree with Macro, that Estrogen can play its part in promoting prostate cancer, it's still modulated, in most cases through AR, and role of DHT can't be underestimated.
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A mechanism for androgen receptor-mediated prostate cancer recurrence after androgen deprivation therapy.
Cancer Res 2001 Jun 1;61(11):4315-9 (ISSN: 0008-5472)
Gregory CW; He B; Johnson RT; Ford OH; Mohler JL; French FS; Wilson EM [Find other articles with these Authors]
Laboratory for Reproductive Biology, Department of Pediatrics, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.
The development and growth of prostate cancer depends on the androgen receptor and its high-affinity binding of dihydrotestosterone, which derives from testosterone. Most prostate tumors regress after therapy to prevent testosterone production by the testes, but the tumors eventually recur and cause death. A critical question is whether the androgen receptor mediates recurrent tumor growth after androgen deprivation therapy. Here we report that a majority of recurrent prostate cancers express high levels of the androgen receptor and two nuclear receptor coactivators, transcriptional intermediary factor 2 and @#%$ receptor coactivator 1. Overexpression of these coactivators increases androgen receptor transactivation at physiological concentrations of adrenal androgen. Furthermore, we provide a molecular basis for this activation and suggest a general mechanism for recurrent prostate cancer growth.
Androgen receptor expression in prostate cancer lymph node metastases is predictive of outcome after surgery.
J Urol 1999 Apr;161(4):1233-7 (ISSN: 0022-5347)
Sweat SD; Pacelli A; Bergstralh EJ; Slezak JM; Cheng L; Bostwick DG [Find other articles with these Authors]
Department of Laboratory Medicine and Pathology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
PURPOSE: Androgens mediate the growth of prostate cancer cells. The predictive value of androgen receptor immunostaining in patient outcome is controversial. We studied the expression of androgen receptors in a large series of patients with node positive cancer, and correlated the results with clinical progression and survival. MATERIALS AND METHODS: We evaluated 197 patients with a mean age of 65.5 years who had node positive adenocarcinoma, and who underwent bilateral pelvic lymphadenectomy and/or radical prostatectomy at our clinic between 1987 and 1992. Mean followup was 6.3 years. Immunohistochemical studies were performed using an antihuman androgen receptor monoclonal antibody. In each case 100 nuclei were counted from 3 separate areas (total 300 nuclei per diagnostic category) of benign epithelium, cancer and lymph node metastases. Mean androgen receptor expression was determined from the mean of the individual cases. The intensity of immunoreactivity was evaluated on a scale of 0-no staining to 3-strong staining. We assessed the correlation of androgen receptor immunoreactivity, deoxyribonucleic acid ploidy, Gleason score and preoperative serum prostate specific antigen (PSA) with clinical progression, all cause survival and cancer specific survival using the Cox proportional hazards model. Clinical progression was defined as a positive bone scan. RESULTS: There was heterogeneous staining in the majority of cells in benign and malignant prostatic epithelium. The mean number of immunoreactive nuclei was similar in all groups (56, 53 and 56% of benign epithelium, cancer and lymph node metastases, respectively). Pairwise comparisons revealed that the only significant difference was between benign epithelium and cancer (p = 0.001) with greater immunoreactivity in benign epithelium. Intensity was lower in benign epithelium than in cancer and lymph nodes (p <0.05). Androgen receptor expression in lymph node metastases was associated with all cause and cancer specific survival on univariate analysis (p = 0.03 and 0.04, respectively). The 7-year cause specific survival was 98, 94 and 86% in patients with 51 to 69, less than 50 and greater than 70% androgen receptor expression in lymph node metastases, respectively (p <0.05). The association of androgen receptor expression in lymph node metastases was significant on multivariate analysis for cancer specific survival (p = 0.021) but not all cause survival (p = 0.16) after controlling for Gleason score, deoxyribonucleic acid ploidy and preoperative PSA. Androgen receptor immunoreactivity in lymph nodes was not a significant univariate or multivariate predictor of clinical progression, while androgen receptor expression in the primary cancer was not predictive of clinical progression or survival (p >0.05). CONCLUSIONS: Androgen receptor expression was similar in benign epithelium, primary cancer and lymph node metastases with approximately half of the epithelial cell nuclei staining. Androgen receptor immunoreactivity in lymph node metastases was predictive of cancer specific but not all cause survival in univariate and multivariate models. Gleason score was the strongest predictor of all cause survival in this cohort of patients. Our results indicate that it may be clinically useful to determine lymph node androgen receptor expression in men with advanced prostate cancer when combined with Gleason score and PSA.
Functional analysis of androgen receptor N-terminal and ligand binding domain interacting coregulators in prostate cancer.
J Formos Med Assoc (China 2000 Dec;99(12):885-94 (ISSN: 0929-6646)
Yeh S; Sampson ER; Lee DK; Kim E; Hsu CL; Chen YL; Chang HC; Altuwaijri S; Huang KE; Chang C [Find other articles with these Authors]
George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, Radiation Oncology, and Cancer Center, University of Rochester, Rochester, NY 14642, USA.
Several new androgen receptor (AR) coregulators, including ARA70, ARA55, ARA54, ARA160 and ARA24, associated with the N-terminal or the ligand-binding domain (LBD) of AR, have been identified by our group. We first identified the AR-LBD coregulators ARA70, ARA55, and ARA54. Our previous reports suggest that ARA70 can enhance the androgenic activity of 17 beta-estradiol (E2) and antiandrogens toward AR. It is of interest to compare and determine if the specificity of sex hormones and antiandrogens can be modulated by different coregulators. Our results indicate that, ARA70 is the best coregulator for increasing the androgenic activity of E2. Only ARA70 and ARA55 were able to significantly increase the androgenic activity of hydroxyflutamide, the active metabolite of a widely-used antiandrogen for the treatment of prostate cancer. Furthermore, our results suggest that among the LBD coregulators, ARA70 has a relatively high specificity for AR in the human prostate cancer cell line DU145. Together, our data suggest that the androgenic activity of some sex hormones and antiandrogens can be modulated by selective AR coactivators. In addition to the AR-LBD associated proteins, ARA24 and ARA160 have been identified as AR coregulators, interacting with the AR N-terminal instead of the LBD. Functional analysis revealed that the AR N-terminal coregulator ARA160 could cooperate with the AR LBD-associated coregulator ARA70. Our data indicate that ARA24 could also interact with AR, and that this binding is decreased by an expanding poly-glutamine (Q) length within AR. The length of the poly-Q stretch in the AR N-terminal domain is inversely correlated with the transcriptional activity of AR. Our data suggest that optimal AR transactivation may require interaction of AR with AR coregulators. The identification of factors or peptides that can interrupt androgen-mediated AR-ARA interactions may be useful in the development of better antiandrogens for treating androgen-related diseases, such as prostate cancer.
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A mechanism for androgen receptor-mediated prostate cancer recurrence after androgen deprivation therapy.
Cancer Res 2001 Jun 1;61(11):4315-9 (ISSN: 0008-5472)
Gregory CW; He B; Johnson RT; Ford OH; Mohler JL; French FS; Wilson EM [Find other articles with these Authors]
Laboratory for Reproductive Biology, Department of Pediatrics, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.
The development and growth of prostate cancer depends on the androgen receptor and its high-affinity binding of dihydrotestosterone, which derives from testosterone. Most prostate tumors regress after therapy to prevent testosterone production by the testes, but the tumors eventually recur and cause death. A critical question is whether the androgen receptor mediates recurrent tumor growth after androgen deprivation therapy. Here we report that a majority of recurrent prostate cancers express high levels of the androgen receptor and two nuclear receptor coactivators, transcriptional intermediary factor 2 and @#%$ receptor coactivator 1. Overexpression of these coactivators increases androgen receptor transactivation at physiological concentrations of adrenal androgen. Furthermore, we provide a molecular basis for this activation and suggest a general mechanism for recurrent prostate cancer growth.
Androgen receptor expression in prostate cancer lymph node metastases is predictive of outcome after surgery.
J Urol 1999 Apr;161(4):1233-7 (ISSN: 0022-5347)
Sweat SD; Pacelli A; Bergstralh EJ; Slezak JM; Cheng L; Bostwick DG [Find other articles with these Authors]
Department of Laboratory Medicine and Pathology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
PURPOSE: Androgens mediate the growth of prostate cancer cells. The predictive value of androgen receptor immunostaining in patient outcome is controversial. We studied the expression of androgen receptors in a large series of patients with node positive cancer, and correlated the results with clinical progression and survival. MATERIALS AND METHODS: We evaluated 197 patients with a mean age of 65.5 years who had node positive adenocarcinoma, and who underwent bilateral pelvic lymphadenectomy and/or radical prostatectomy at our clinic between 1987 and 1992. Mean followup was 6.3 years. Immunohistochemical studies were performed using an antihuman androgen receptor monoclonal antibody. In each case 100 nuclei were counted from 3 separate areas (total 300 nuclei per diagnostic category) of benign epithelium, cancer and lymph node metastases. Mean androgen receptor expression was determined from the mean of the individual cases. The intensity of immunoreactivity was evaluated on a scale of 0-no staining to 3-strong staining. We assessed the correlation of androgen receptor immunoreactivity, deoxyribonucleic acid ploidy, Gleason score and preoperative serum prostate specific antigen (PSA) with clinical progression, all cause survival and cancer specific survival using the Cox proportional hazards model. Clinical progression was defined as a positive bone scan. RESULTS: There was heterogeneous staining in the majority of cells in benign and malignant prostatic epithelium. The mean number of immunoreactive nuclei was similar in all groups (56, 53 and 56% of benign epithelium, cancer and lymph node metastases, respectively). Pairwise comparisons revealed that the only significant difference was between benign epithelium and cancer (p = 0.001) with greater immunoreactivity in benign epithelium. Intensity was lower in benign epithelium than in cancer and lymph nodes (p <0.05). Androgen receptor expression in lymph node metastases was associated with all cause and cancer specific survival on univariate analysis (p = 0.03 and 0.04, respectively). The 7-year cause specific survival was 98, 94 and 86% in patients with 51 to 69, less than 50 and greater than 70% androgen receptor expression in lymph node metastases, respectively (p <0.05). The association of androgen receptor expression in lymph node metastases was significant on multivariate analysis for cancer specific survival (p = 0.021) but not all cause survival (p = 0.16) after controlling for Gleason score, deoxyribonucleic acid ploidy and preoperative PSA. Androgen receptor immunoreactivity in lymph nodes was not a significant univariate or multivariate predictor of clinical progression, while androgen receptor expression in the primary cancer was not predictive of clinical progression or survival (p >0.05). CONCLUSIONS: Androgen receptor expression was similar in benign epithelium, primary cancer and lymph node metastases with approximately half of the epithelial cell nuclei staining. Androgen receptor immunoreactivity in lymph node metastases was predictive of cancer specific but not all cause survival in univariate and multivariate models. Gleason score was the strongest predictor of all cause survival in this cohort of patients. Our results indicate that it may be clinically useful to determine lymph node androgen receptor expression in men with advanced prostate cancer when combined with Gleason score and PSA.
Functional analysis of androgen receptor N-terminal and ligand binding domain interacting coregulators in prostate cancer.
J Formos Med Assoc (China 2000 Dec;99(12):885-94 (ISSN: 0929-6646)
Yeh S; Sampson ER; Lee DK; Kim E; Hsu CL; Chen YL; Chang HC; Altuwaijri S; Huang KE; Chang C [Find other articles with these Authors]
George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, Radiation Oncology, and Cancer Center, University of Rochester, Rochester, NY 14642, USA.
Several new androgen receptor (AR) coregulators, including ARA70, ARA55, ARA54, ARA160 and ARA24, associated with the N-terminal or the ligand-binding domain (LBD) of AR, have been identified by our group. We first identified the AR-LBD coregulators ARA70, ARA55, and ARA54. Our previous reports suggest that ARA70 can enhance the androgenic activity of 17 beta-estradiol (E2) and antiandrogens toward AR. It is of interest to compare and determine if the specificity of sex hormones and antiandrogens can be modulated by different coregulators. Our results indicate that, ARA70 is the best coregulator for increasing the androgenic activity of E2. Only ARA70 and ARA55 were able to significantly increase the androgenic activity of hydroxyflutamide, the active metabolite of a widely-used antiandrogen for the treatment of prostate cancer. Furthermore, our results suggest that among the LBD coregulators, ARA70 has a relatively high specificity for AR in the human prostate cancer cell line DU145. Together, our data suggest that the androgenic activity of some sex hormones and antiandrogens can be modulated by selective AR coactivators. In addition to the AR-LBD associated proteins, ARA24 and ARA160 have been identified as AR coregulators, interacting with the AR N-terminal instead of the LBD. Functional analysis revealed that the AR N-terminal coregulator ARA160 could cooperate with the AR LBD-associated coregulator ARA70. Our data indicate that ARA24 could also interact with AR, and that this binding is decreased by an expanding poly-glutamine (Q) length within AR. The length of the poly-Q stretch in the AR N-terminal domain is inversely correlated with the transcriptional activity of AR. Our data suggest that optimal AR transactivation may require interaction of AR with AR coregulators. The identification of factors or peptides that can interrupt androgen-mediated AR-ARA interactions may be useful in the development of better antiandrogens for treating androgen-related diseases, such as prostate cancer.
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Stan O'Zolol
New member
It is also important to note that there are two isozymes of 5-alpha reductase. Finsasteride only inhibits 5AR type II. Therefore, conversion to DHT will still take place, though at a lesser rate (about a 70% reduction).
Stan O'Zolol
New member
Reading those abstracts that panerai posted are more along the lines of what I understood about prostate cancer and androgens...that they facilitate the growth of existing tumours, not cause them explicitly.
Most likely, it's a synergism between DHT and oestradiol that most effectively promote growth of tumor cell in prostate.
DHT, by itself, will only make your penis grow...
Saw Palmetto suppose to be able to inhibit, to some degree 5AR type I, as well as other ways, but more studies are needed to be done, to state it as a fact.
DHT, by itself, will only make your penis grow...
Saw Palmetto suppose to be able to inhibit, to some degree 5AR type I, as well as other ways, but more studies are needed to be done, to state it as a fact.
I agree with you, most of the men are predisposed genetically to get prostate cancer, and the only reason, not all of us get it, is because a lot died for other reasons before prostate cancer happens. Still, statistics are not very favorable.
We all are going to die anyway, right? So, even if we all are going to get prostate cancer, it doesn't mean, that by preventing it effectively for years we can't postpone the occurence before dying from other causes.
And that would be the same as never getting it, even if we are genetically predisposed to it.
It's all about working around risk factors and AAS are one of those.
We all are going to die anyway, right? So, even if we all are going to get prostate cancer, it doesn't mean, that by preventing it effectively for years we can't postpone the occurence before dying from other causes.
And that would be the same as never getting it, even if we are genetically predisposed to it.
It's all about working around risk factors and AAS are one of those.
Diesel3d
New member
i was taking a look at Super saw palmetto at http://www.lef.org/prod_desc/item00428.html
. Anyone Think a high dosage would produce the same results as finastride? Saw plametto seems to do the exact same thing as it.
____________________
Prevention and Treatment of Benign Prostate Enlargement
Enlargement of the prostate gland occurs in most men with advancing age and is accompanied by reduced urinary flow and increased residual urine volume. Hormonal imbalances have previously been blamed for age related prostate disorders, but other factors have been identified as causes of the benign proliferation of prostate cells (BPH) and accompanying urinary impairment caused by this condition. Men with severe BPH often use a combination of saw palmetto and pygeum to improve urine flow and bladder voiding. These men usually wake up less frequently at night to urinate.
Published scientific literature, along with ten years of reports from members of the Life Extension Foundation, show that saw palmetto extract is effective in alleviating symptoms of BPH in most men. Pygeum extract has been shown to specifically inhibit prostate cell proliferation by blocking the binding of dihydrotestosterone (DHT) and other growth factors to prostate cell membranes. Pygeum has anti-edema effects that shrink the prostate gland significantly. Recent studies show it also inhibits the proliferation of prostate cells, by interfering with the activity of the enzyme kinase C that is needed by all rapidly growing benign and malignant cells.
Although more than 80% of men report improvement after using saw palmetto and/or pygeum extracts, some prostate enlargement often remains that continues to interfere with urinary flow and bladder evacuation. Urtica dioica, an herbal extract of nettle root that has been used in Germany for more than a decade to treat BPH, has been shown to reduce symptoms by 86% after 3 months of use. Learning of these studies, researchers at St. Luke’s/Roosevelt Hospital in New York conducted a study to discover the mechanism by which standardized nettle root extract relieves the symptoms of BPH. In their study, published in 1995, these scientists showed Urtica dioica inhibits the binding of a testosterone-related protein to receptor sites on prostate cell membranes. In January 1998, the Foundation made nettle root extract available in one formula combined with saw palmetto and pygeum. Saw palmetto, pygeum and Urtica dioica are approved drugs in Germany for the treatment of BPH.
Saw palmetto has been shown to work by inhibiting the enzyme (5-alpha reductase) in the prostate gland that converts testosterone to DHT. New studies show saw palmetto also reduces smooth muscle contraction, relaxing the bladder and sphincter muscles that cause urinary urgency. Super Saw Palmetto contains the highly effective super-critical extract from saw palmetto.
For complete information about the treatment of early and late stage prostate cancer and BPH, see the Life Extension Foundation’s newest book, Disease Prevention and Treatment, 3rd edition.
. Anyone Think a high dosage would produce the same results as finastride? Saw plametto seems to do the exact same thing as it.
____________________
Prevention and Treatment of Benign Prostate Enlargement
Enlargement of the prostate gland occurs in most men with advancing age and is accompanied by reduced urinary flow and increased residual urine volume. Hormonal imbalances have previously been blamed for age related prostate disorders, but other factors have been identified as causes of the benign proliferation of prostate cells (BPH) and accompanying urinary impairment caused by this condition. Men with severe BPH often use a combination of saw palmetto and pygeum to improve urine flow and bladder voiding. These men usually wake up less frequently at night to urinate.
Published scientific literature, along with ten years of reports from members of the Life Extension Foundation, show that saw palmetto extract is effective in alleviating symptoms of BPH in most men. Pygeum extract has been shown to specifically inhibit prostate cell proliferation by blocking the binding of dihydrotestosterone (DHT) and other growth factors to prostate cell membranes. Pygeum has anti-edema effects that shrink the prostate gland significantly. Recent studies show it also inhibits the proliferation of prostate cells, by interfering with the activity of the enzyme kinase C that is needed by all rapidly growing benign and malignant cells.
Although more than 80% of men report improvement after using saw palmetto and/or pygeum extracts, some prostate enlargement often remains that continues to interfere with urinary flow and bladder evacuation. Urtica dioica, an herbal extract of nettle root that has been used in Germany for more than a decade to treat BPH, has been shown to reduce symptoms by 86% after 3 months of use. Learning of these studies, researchers at St. Luke’s/Roosevelt Hospital in New York conducted a study to discover the mechanism by which standardized nettle root extract relieves the symptoms of BPH. In their study, published in 1995, these scientists showed Urtica dioica inhibits the binding of a testosterone-related protein to receptor sites on prostate cell membranes. In January 1998, the Foundation made nettle root extract available in one formula combined with saw palmetto and pygeum. Saw palmetto, pygeum and Urtica dioica are approved drugs in Germany for the treatment of BPH.
Saw palmetto has been shown to work by inhibiting the enzyme (5-alpha reductase) in the prostate gland that converts testosterone to DHT. New studies show saw palmetto also reduces smooth muscle contraction, relaxing the bladder and sphincter muscles that cause urinary urgency. Super Saw Palmetto contains the highly effective super-critical extract from saw palmetto.
For complete information about the treatment of early and late stage prostate cancer and BPH, see the Life Extension Foundation’s newest book, Disease Prevention and Treatment, 3rd edition.
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