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Nathan Goodyear

The role of 5-alpha reductase inhibitors in prostate pathophysiology: Is there an addit... - 1 views

www.ncbi.nlm.nih.gov/...PMC2698784

prostate 5 alpha reductase 5 alpha reductase inhibitors hormones male men male hormones

shared by Nathan Goodyear on 01 Jul 16 - No Cached
  • Nathan Goodyear on 01 Jul 16
     
    good review of 5-alpha reductase inhibitor and prostate pathophysiology.  Type I is increased in prostate cancer.  
Nathan Goodyear

Prostate Biopsy in Response to a Change in Nadir Prostate Specific Antigen of... - 0 views

www.jurology.com/...abstract

5 alpha reductase 5 alpha reductase inhibitors PSA prostate cancer men male hormone hormones

shared by Nathan Goodyear on 09 Feb 15 - No Cached
  • Nathan Goodyear on 09 Feb 15
     
    5 alpha reductase inhibitor therapy reduces PSA and prostate volume.  The level of change may be used to aid in prostate cancer diagnosis.  Those with eventual diagnosis had Gleason 7 or higher.
Nathan Goodyear

Progesterone-induced stimulation of mammary tumorigenesis is due to the proge... - 0 views

www.sciencedirect.com/...S0960076015000060

5 alpha reductase inhibitors 5 alpha reductase progesterone 5alpha-pregnane breast cancer

shared by Nathan Goodyear on 07 Jul 20 - No Cached
  • Nathan Goodyear on 07 Jul 20
     
    5 alpha reductase inhibitor, finasteride inhibits pro-tumor progesterone metabolite pathway.
Nathan Goodyear

Use of 5α-reductase inhibitors for lower urinary tract symptoms and risk of p... - 0 views

www.bmj.com/bmj.f3406

5 alpha reductase 5 alpha reductase inhibitors prostate cancer LUTS men male hormone hormones

shared by Nathan Goodyear on 09 Feb 15 - No Cached
  • Nathan Goodyear on 09 Feb 15
     
    5alpha reductase inhibitors associated with decreased risk of Gleason 2-7 prostate cancer in men with LUTS and enlarged prostate.
Nathan Goodyear

Pharmacological approaches to reducing the risk of... [Eur Urol. 2009] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...19200641

finasteride 5 alpha-reductase inhibitors prostate cancer

shared by Nathan Goodyear on 02 Mar 11 - No Cached
  • 5alpha-reductase inhibitors (5-ARIs).
  • there is no evidence that 5-ARIs or any other approach to prostate cancer risk reduction will reduce the risk of lethal prostate cancers
  • Nathan Goodyear on 02 Mar 11
     
    5 alpha-reductase inhibitors, such as finasteride, have not been shown to reduce lethal prostate cancer
Nathan Goodyear

The Dark Side of 5α-Reductase Inhibitors' Ther... [Korean J Urol. 2014] - Pub... - 0 views

www.ncbi.nlm.nih.gov/...24955220

5 alpha reductase 5 alpha reductase inhibitors men male hormone hormones

shared by Nathan Goodyear on 24 Jun 14 - No Cached
  • Nathan Goodyear on 24 Jun 14
     
    Nice review of the inherent risks associated with 5alpha-reductase inhibition therapy.
Nathan Goodyear

The androgen metabolite 5alpha-androstane-3beta,17beta-diol (3betaAdiol) induces breast... - 0 views

www.researchgate.net/...aromatase_inhibitor_resistance

breast cancer aromatase aromatase inhibitors estradiol estrogen 3-beta androstanediol Testosterone DHT 3 beta HSD receptor receptors ER alpha ER-alpha ER beta ER-beta hormone hormones women

shared by Nathan Goodyear on 21 Jan 14 - No Cached
  • Nathan Goodyear on 21 Jan 14
     
    Great article!!  Nice discussion of the complexity of hormones.  Women on aromatase inhibitors can make estrogen from Testosterone.  This is important with estrogen sensitive cancer as in breast cancer.  This will occur via alternative pathways: Testosterone to DHT via 5 alpha reductase and then DHT to 3 beta androstanediol via 3 beta HSD.  3 beta androstanediol is a male hormone metabolite that binds to estrogen receptors.  The affinity is less than Estradiol, but appears to have a higher affinity for ER beta over ER alpha. 
Nathan Goodyear

High-grade prostate cancer and finasteride. - 0 views

www.ncbi.nlm.nih.gov/...19930174

finasteride 5 alpha reductase 5 alpha reductase inhibitors prostate disease cancer men male hormones PSA

shared by Nathan Goodyear on 14 Oct 15 - No Cached
  • Nathan Goodyear on 14 Oct 15
     
    finasteride lacks the 5 alpha reductase specificity (type 1 > 2) for high grade prostate cancer.
Nathan Goodyear

Testosterone replacement in prostate cancer survivors with hypogonadal symptoms - Leibo... - 0 views

onlinelibrary.wiley.com/...full

testosterone replacement prostate cancer PSA 5-alpha reductase inhibitor

shared by Nathan Goodyear on 25 Sep 13 - No Cached
  • Nathan Goodyear on 25 Sep 13
     
    Good article.  This article (case series) found that 40% of the men included had no increase in PSA with Testosterone.  One point on the Testosterone dosage is that they used androgen, which is an overdose of Testosterone.  That gives 60% that the PSA did increase.  These men had higher PSA to begin with which leads to the suggestion that the prostate cells were abnormal.  Those men that had a prostatectomy were more likely to have little if any increase in PSA.  This study did use a the 5 alpha reductase inhibitor dutasteride.
Nathan Goodyear

Clinical dose ranging studies with finasteride, a type 2 5α-reductase inhibit... - 0 views

www.eblue.org/...abstract

finasteride propecia male-pattern baldness

shared by Nathan Goodyear on 31 Mar 11 - No Cached
  • Nathan Goodyear on 31 Mar 11
     
    propecia, 5-alpha reductase inhibitor, improves male pattern baldness
Nathan Goodyear

Dutasteride affects progesterone metabolizing enzyme activity/expression in human breas... - 0 views

www.sciencedirect.com/...S0960076006001397

hormones progesterone cancer breast cancer 5alpha-pregnane 4-pregnenes progesterone metabolites 5 alpha reductase 5 alpha reductase inhibitors

shared by Nathan Goodyear on 07 Oct 16 - No Cached
  • Nathan Goodyear on 07 Oct 16
     
    Cell culture study finds that 5alpha-reductase inhibition decreased 5alpha-pregnanes and thus inhibited cell proliferation and detachment; this is in contrast to the 4 pregnenes that occur through the enzymes 3alpha-hydroxysteroid oxidoreductase and the 20alpha-hydroxysteroid oxidoreductase, which show anti cell proliferation and cell detachment.
Nathan Goodyear

Estrogen receptor β and the progression of prostate cancer: role of 5α-andros... - 0 views

erc.endocrinology-journals.org/...731.long

3-beta androstanediol DHT Testosterone androgens prostate cancer ER beta ER-beta receptors ER men male hormone hormones

shared by Nathan Goodyear on 21 Jan 14 - No Cached
  • In the prostate, ERβ is highly expressed in the epithelial compartment, where it is the prevailing isoform
  • In the gland, DHT may be either reversibly 3α- or irreversibly 3β-hydroxylated by the different 3α- and 3β-hydroxysteroid dehydrogenases respectively (Steckelbroeck et al. 2004); these transformations generate two metabolites respectively 3α-diol and 3β-Adiol, which are both unable to bind the AR. Instead, 3β-Adiol displays a high affinity for ERβ (Kuiper et al. 1998, Nilsson et al. 2001), and it has been proposed that this metabolite may play a key role in prostate development
  • ERβ signaling, in contrast to ERα, seems to act as a suppressor of prostate growth, and may be positively involved in breast cancer
  • ...4 more annotations...
  • 3β-Adiol counteracts PC cell proliferation in vitro
  • 3β-Adiol counteracts the biological actions of its androgenic precursors testosterone and DHT
  • functional antagonism of 3β-Adiol appears to be molecularly independent from the activation of the androgenic pathway
  • the action of 3β-Adiol is mediated, at the molecular levels, by the estrogenic pathway.
  • Nathan Goodyear on 21 Jan 14
     
    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.
Nathan Goodyear

Promoting effects and mechanisms of action of androgen in bladder c... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9129932

bladder cancer bladder cancer Testosterone men male hormone hormones

shared by Nathan Goodyear on 04 Jan 15 - No Cached
  • Nathan Goodyear on 04 Jan 15
     
    Another animal study finds Testosterone plays a role in bladder cancer development.  The study used anti androgen and 5 alpha reductase inhibitor therapy to see if these add on therapies provided anything to ADR whether via castration or pituitary suppression--the answer was no.  The authors concluded that Testosterone played more of a role with AR versus the more active 5alpha-DHT metabolite.
Nathan Goodyear

Long-term effects of finasteride on prostate specific antigen levels: results from the ... - 0 views

www.ncbi.nlm.nih.gov/...16093979

5 alpha reductase finasteride 5 alpha reductase inhibitors PSA BPH prostate disease cancer men male hormones

shared by Nathan Goodyear on 14 Oct 15 - No Cached
  • Nathan Goodyear on 14 Oct 15
     
    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.
Nathan Goodyear

Progesterone metabolites regulate induction, growth, and suppression of estrogen- and p... - 0 views

www.ncbi.nlm.nih.gov/...PMC3706910

progesterone metabolites metabolite 5-alpha pregnene 5-alpha pregnenes 5alpha-dihydroprogesterone 4-pregnene 4-pregnenes 3alpha-dihydroprogesterone breast cancer ER PR hormone hormones receptors estrogen

shared by Nathan Goodyear on 28 Jan 14 - No Cached
  • in vitro studies had shown that the progesterone metabolites, 5α-dihydroprogesterone (5αP) and 3α-dihydroprogesterone (3αHP), respectively, exhibit procancer and anticancer effects on receptor-negative human breast cell lines
  • Onset and growth of ER/PR-negative human breast cell tumors were significantly stimulated by 5αP and inhibited by 3αHP
  • When both hormones were applied simultaneously, the stimulatory effects of 5αP were abrogated by the inhibitory effects of 3αHP and vice versa
  • ...31 more annotations...
  • Treatment with 3αHP subsequent to 5αP-induced tumor initiation resulted in suppression of further tumorigenesis and regression of existing tumors
  • Tumorigenesis of ER/PR-negative breast cells is significantly enhanced by 5αP and suppressed by 3αHP, the outcome depending on the relative concentrations of these two hormones in the microenvironment in the breast regions
  • The findings show that the production of 5αP greatly exceeds that of 3αHP in ER/PR-negative tumors and that treatment with 3αHP can effectively block tumorigenesis and cause existing tumors to regress
  • hypothesis that a high 3αHP-to-5αP concentration ratio in the microenvironment may foster normalcy in noncancerous breast regions.
  • a large proportion (about 30% to 60%) of breast tumors are ER and/or PR negative
  • about 90% of normal proliferating breast epithelial cells are receptor negative
  • Our previous in vitro studies had shown that breast tissues and cell lines readily convert progesterone to 5α-pregnanes, such as 5αP, and delta-4-pregnenes, such as 3αHP (Figure ​(Figure1),1), and that tumorous breast tissues [15] and tumorigenic breast cell lines [16] produce higher levels of 5αP and lower levels of 3αHP than do normal breast tissues and nontumorigenic cell lines
  • The progesterone metabolism studies suggested that increases in 5αP and decreases in 3αHP production accompany the shift toward breast cell neoplasia and tumorigenicity
  • In vitro studies on five different human breast cell lines showed that cell proliferation and detachment are significantly increased by 5αP and decreased by 3αHP
  • the prevailing theory of hormonal regulation of breast cancer, as well as hormone-based therapies, revolves around estrogen and/or progesterone and ER/PR-positive breast cells and tumors.
  • Not only do these "receptor-negative" breast cancers fail to benefit from current hormonal therapies, but they also generally exhibit more-aggressive biologic behaviors and poorer prognosis than the receptor-positive ones
  • The results of the studies reported here show for the first time that the progesterone metabolites, 5αP and 3αHP, act as hormones that regulate ER/PR-negative breast tumor formation, growth, and regression
  • The onset of the ER/PR-negative human breast cell tumors in mice was considerably accelerated, and the growth significantly stimulated, by just one or two applications of 5αP
  • In contrast, 3αHP retarded onset of tumor formation, suppressed tumor growth, and inhibited or regressed existing 5αP-induced tumors
  • When both hormones were administered simultaneously, the effects of one were abrogated by the effects of the other.
  • The 5αPR and 3αHPR (which are associated with the plasma membranes of both ER/PR-positive [19] and ER/PR-negative [29] cells) are distinct from each other and from known ER, PR, androgen, and corticosteroid receptors, and lack affinity for other steroids, such as progesterone, estrogen, androgens, corticosteroids, and other progesterone metabolites
  • Levels of 5αPR are upregulated by 5αP itself and estradiol, and downregulated by 3αHP in both ER/PR-positive and -negative cells
  • ndications are that 5αP acts via the surface receptor-linked mitogen-activated protein kinase (MAPK; Erk1/2) pathway; 5αP significantly stimulates activation of Erk1/2 [30], increases the Bcl-2/Bax expression ratio [18] and actin depolymerization [31], and decreases expression of actin and adhesion plaque-associated vinculin [31], resulting in decreased apoptosis and increased mitosis and cell detachment
  • 3αHP appears to suppress protein kinase C (PKC), phospholipase C (PLC), Ca2+ mobilization (unpublished observations), and the Bcl-2/Bax expression ratio [18], and increases expression of the cell-cycle inhibitor p21 [18], resulting in increased apoptosis and decreased proliferation and detachment of breast cell lines.
  • serum from mice with tumors had significantly more 5αP than 3αHP
  • the tumors, which on average had about threefold higher concentrations of 5αP than the respective sera, and >10-fold higher 5αP than 3αHP levels
  • Previous in vitro metabolism studies showed that human breast tumor tissues convert significantly more progesterone to 5α-pregnanes like 5αP and less to 4-pregnenes like 3αHP than do paired normal (nontumorous) tissues
  • Similar differences in progesterone metabolism and enzyme gene expressions were observed between tumorigenic and nontumorigenic breast cell lines
  • breast carcinomas are able to synthesize progesterone
  • The current findings, along with the previous in vitro studies, suggest that the relative concentrations of 5αP and 3αHP in the breast microenvironment constitute important autocrine/paracrine determinants not only for tumorigenesis but also for potential regression of tumors and the maintenance of normalcy of ER/PR-negative breast cells/tissues.
  • Evidence presented here shows that a high concentration of 5αP, relative to 3αHP in the microenvironment, promotes initiation and growth of tumors, whereas a higher concentration of 3αHP, relative to 5αP, suppresses tumorigenesis and promotes normalcy
  • 5α-reductase and 5αPR levels are upregulated by 5αP
  • in the 3αHP-treated mice, the elevated 3αHP levels, relative to 5αP, in the microenvironment could have opposed progression to xenograft neoplasia by its inherent anticancer actions and the suppression of 5αP synthesis and 5αPR expression
  • the opposing actions of the progesterone metabolites also appear to exert some control over the estrogen-regulated effects on breast cancer by their ability to modulate ER numbers in ER-positive cells
  • because both ER/PR-negative and ER/PR-positive, as well as normal and tumorigenic human breast cell lines, have been shown to respond to 5αP and 3αHP in vitro, it is suggested that these endogenously produced progesterone metabolites may also play regulatory hormonal roles in ER/PR-positive breast cancers, as well as in the maintenance of normalcy in nontumorous breast tissues.
  • The in vivo data provide further evidence that progesterone metabolites, such as 5αP and 3αHP, deserve to be considered as active hormones in their own right, rather than inactive waste products
  • Nathan Goodyear on 28 Jan 14
     
    Progesterone metabolites and breast cancer
Nathan Goodyear

[The Prostate Cancer Prevention Trial (PCPT). Relevance for clinical practice]. - 0 views

www.ncbi.nlm.nih.gov/...17874228

5 alpha reductase inhibitors 5alpha reductase finasteride prostate disease cancer men male hormones PSA

shared by Nathan Goodyear on 14 Oct 15 - No Cached
  • Nathan Goodyear on 14 Oct 15
     
    Finasteride does not increase prostate cancer.
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