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Nathan Goodyear

Comparative Studies of the Estrogen Receptors β and α and the Androgen Recept... - 0 views

ajp.amjpathol.org/...fulltext

ER beta ER-beta AR androgen receptors ER alpha ER-alpha prostate disease cancer estrogen receptor hormone hormones men male

shared by Nathan Goodyear on 21 Jan 14 - No Cached
  • ER-β is predominately immunolocalized in basal cells and to a lesser extent in stromal cells of the morphologically normal human prostate
  • ER-α is detected in stromal cells and rarely in basal cells of the normal gland
  • AR was predominately localized in the nuclei of differentiated secretory cells and variably in basal cells of the normal acinar/duct unit as well as in stromal cells
  • ...9 more annotations...
  • Hall and colleagues44 have reported that ER-β functions as a transdominant inhibitor of ER-α transcription and that it acts to decrease overall cellular sensitivity to estradiol
  • The expression of ER-β was diminished in high-grade dysplasias when compared to normal glands and lower grade lesions.
  • The transition from normal to low/moderate dysplastic glands in the peripheral zone was marked by the appearance of ER-β homogeneously immunostained nuclei in secretory as well as basal cells with no changes in the localization of the other receptors.
  • proliferative signals mediated by AR in basal cells or by ER-α and AR in stromal cells may be opposed by the purported growth-inhibitory action of ER-β25, 26, 27, 28 localized in basal cells.
  • The diminution of ER-β expression in high-grade dysplasias and grade 4/5 cancers may be therefore related to the alteration of DNA methylation pattern in CpG islands of the promoter, resulting in down-regulation of the receptor at the transcriptional level
  • based on the proposed anti-proliferative function of the receptor,25, 26, 27, 28 the presence of ER-β in secretory cells of low/moderate-grade lesions may represent a transient abortive attempt to counter growth of these cells
  • the attrition of receptor-positive basal cells in the high-grade dysplasias may signify a continuing loss of growth inhibitory function mediated by ER-β in these precursor lesions
  • Our findings in prostate therefore differ from those reported for human colon cancer in which Folley and colleagues48 demonstrated that a selective loss of ER-β protein but not receptor message expression occurs in these neoplasms
  • Our findings therefore differed from those of Bonkhoff and colleagues33 who found immunostaining for the receptor in high-grade dysplasias and grade 4/5 carcinomas. Using in situ hybridization these authors also reported that a high percentage of dysplasias and carcinomas in their study contained cells that expressed ER-α message
  • Nathan Goodyear on 21 Jan 14
     
    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.
Nathan Goodyear

Targeting estrogen receptor subtypes (ERα and ERβ) with selective ER modulato... - 0 views

joe.endocrinology-journals.org/...325.abstract

ovarian cancer ER alpha ER beta ER-alpha ER-beta ovary estrogen receptor receptors ER

shared by Nathan Goodyear on 19 May 14 - No Cached
  • Nathan Goodyear on 19 May 14
     
    Studies in breast cancer and prostate cancer have revealed different effects by ER alpha vs ER beta.  It is no surprise that the same effects are found in ovarian cancer.  This study found ER alpha antagonists and ER beta agonists "significantly" suppressed growth in the ovarian cancer cell lines SKOV3 and OV2008.  Also, ER alpha agonist and ER beta antagonist "significantly" increased growth in the same cell lines.  These findings point to in increased proliferation with ER alpha and decreased with ER beta.  This is consistent with breast and prostate cancer also.
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

Circulating 2-hydroxy and 16-α hydroxy estrone levels and risk of breast canc... - 1 views

www.ncbi.nlm.nih.gov/...PMC2562592

estrogen metabolism menopause post-menopause post menopause estrogen metabolite 2-OH-estrone 16-alpha-OH-estrone 2:16alpha-OH estrone breast cancer risk hormone hormones

shared by Nathan Goodyear on 21 Aug 14 - No Cached
  • 2-OH estrogens bind to the estrogen receptor (ER) with affinity equivalent to or greater than estradiol
  • previous prospective studies have not observed any significant associations with either 2-OH or 16α-OH estrone or the ratio of the two metabolites and breast cancer risk overall.
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      whether that risk is increased or decreased
  • it has been hypothesized that metabolism favoring the 2-OH over the 16α-OH pathway may be inversely associated with breast cancer risk (28).
  • ...24 more annotations...
  • they may act as only weak mitogens (14, 15), or as inhibitors of proliferation
  • No significant associations have been observed between 2-OH estrone and breast cancer risk
  • While 16α-OH estrone binds to the ER with lower affinity than estradiol, it binds covalently (18-20) and once bound, fails to down-regulate the receptor (21). Thus, 16α-OH estrone stimulates cell proliferation in a manner comparable to estradiol in ER+ breast cancer cell lines
  • In this large prospective study of 2-OH and 16α-OH estrone metabolites and breast cancer risk, we did not observe any significant associations overall with either individual metabolite or with the ratio of the two metabolites
  • we observed positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with lower BMI and women with ER-/PR-tumors,
  • To date, several epidemiologic studies have examined the association between the 2-OH and 16α-OH estrogen metabolites and breast cancer risk with inconclusive results.
  • circulating estrogen levels have been associated more strongly with ER+/PR+ tumors than with ER-/PR- tumors
  • our results do not support the hypothesis that metabolism favoring the 2-OH estrone pathway is more beneficial to breast cancer risk than that favoring the 16α-OH estrone pathway
  • we observed significant positive associations of both 2-OH estrone and the 2:16α-OH estrone ratio with ER-/PR-tumors
  • Three (30, 32, 33) of four (30-33) studies observed RRs above 1 for the association between 16α-OH estrone and breast cancer risk (range of RRs=1.23-2.47); none of the point estimates was statistically significant though one trend was suggestive
  • based on animal studies, 2-OH estrone and the 2:16α-OH estrone ratio have been hypothesized to be inversely associated with breast cancer risk
  • No significant associations have been observed between 2-OH estrone, 16α-OH estrone, or the 2:16α-OH estrone ratio and breast cancer risk and the direction of the estimates is not consistent across studies.
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      better worded is no consistent, significant associations.   There are some studies that point to the 16 catecholestrogen and increased cancer risk; limited studies show negative effects of 2 catecholestrogens on cancer risk and prospective studies available pretty much dispel the idea that the 2:16 ratio has an risk predictability.
  • we observed a suggestive inverse association with 16α-OH estrone and a significant positive association with the 2:16α-OH estrone ratio among lean women, suggesting possible associations in a low estrogen environment.
  • 16α-OH estrone increases unscheduled DNA synthesis in mouse mammary cells (27) and hence also may be genotoxic
  • Although 2-OH estrogens are capable of redox cycling, the semiquinones and quinones (i.e., the oxidized forms) form stable DNA adducts that are reversible without DNA destruction
  • In our population of PMH nonusers, we observed no associations with ER+/PR+ tumors, but significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with ER-/PR- tumors
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      one of the few studies to find this association between 2 catecholestrogens and the 2:16 ratio and ER-/PR-tumors
  • Animal and in vitro studies have shown that hydroxy estrogens can induce DNA damage either directly, through the formation of quinones and DNA adducts, or indirectly, through redox cycling and the generation of reactive oxygen species
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      genotoxic via directe DNA adducts and indirectly via ROS; this is in addition to the proliferative effect
  • we observed a significant positive association between the 2:16α-OH estrone ratio and breast cancer risk among lean women
  • No significant associations have been observed with the 2:16α-OH estrone ratio
  • In the Danish study, no associations were observed with either ER+ or ER- tumors among PMH nonusers
  • significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio were observed among PMH users with ER+, but not ER-, tumors
  • it is possible that the genotoxicity of 2-OH estrone plays a role in hormone receptor negative tumors
  • 4-OH estrogens have a greater estrogenic potential than 2-OH estrogens, given the lower dissociation rate from estrogen receptors compared with estradiol (61), and are potentially more genotoxic since the quinones form unstable adducts, leading to depurination and mutation in vitro and in vivo
  • the balance between the catechol (i.e., 2-OH and 4-OH) and methoxy (i.e., 2-Me and 4-Me) estrogens may impact risk
  • Nathan Goodyear on 21 Aug 14
     
    The risks of estrogen metabolism are not clear cut.  Likely never will be due to the complexity of individual metabolism.  This study found no correlation between 2OH-Estrone and 2OH:16alpha-Estrone and breast cancer risk in ER+/PR+ breast cancer.  Translated: no benefit in breast cancer risk in 2OH-Estrone metabolism or increased 2OH:16alpha estrone metabolism.  There was a positive association between 2OH-Estrone and 2:16alpha-Estrone in women with ER-/PR- tumors and low BMI.
  • anonymous on 28 Oct 15
     
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Nathan Goodyear

Oestrogen receptor α and β mRNA expression in human endometrium throughout th... - 0 views

molehr.oxfordjournals.org/...559.full

endometrium ER-alpha ER-beta estrogen receptor alpha estrogen receptor beta estrogen receptor estrogen receptors estrogen receptor receptors alpha beta menstrual cycle human

shared by Nathan Goodyear on 07 Dec 12 - No Cached
  • Nathan Goodyear on 07 Dec 12
     
    Estrogen receptors alpha and beta show dominance in the proliferative phases, with alpha isoform predominating.  In the secretory phase, less expression of ER was present. ER alpha was predominantly expressed in the epithelial and stromal cells in the proliferative phase.  ER beta was predominantly expressed in glandular cells in the same proliferative phase.   in the luteal phase, ER alpha expression declined in the funtionalis layers.  ER alpha in the basalis remained unchanged.  ER beta in the functionalis layers also declined in the luteal phase.   No relative change was found in the weak expression of ER alpha/beta in the myometrium.
Nathan Goodyear

Estrogen receptor (ER) β, a modulator of ERα in the uterus - 0 views

www.pnas.org/...5936.full

receptors ER-alpha ER-beta hormones hormone

shared by Nathan Goodyear on 16 Aug 12 - No Cached
  • induction of PR is an ERα-mediated event and repression of epithelial PR is ERβ mediated.
  • Nathan Goodyear on 16 Aug 12
     
    ER alpha and ER beta have different effects on the uterus in this mice model.  ER beta modulates ER alpha.  ER beta decreases PR, whereas ER alpha increases PR.
Nathan Goodyear

Opposing Action of Estrogen Receptors α and β on Cyclin D1 Gene Expression - 0 views

www.jbc.org/24353

ER beta ER-beta ER estrogen receptor beta estrogen receptor estrogen receptors cancer ER-alpha ER alpha estrogen

shared by Nathan Goodyear on 09 Jun 14 - No Cached
  • Nathan Goodyear on 09 Jun 14
     
    ER-beta inhibits ER-alpha activation of cell proliferation via cyclin D1 gene expression.  This points to ER-beta as a counter regulatory receptor to ER-alpha.  This explains how a loss of ER-beta expression is found to be associated with increased cancers.  
Nathan Goodyear

Estrogen receptor acts as a dominant regulator of estrogen signaling - 0 views

www.nature.com/...1203828a.html

ER beta ER-beta ER alpha ER-alpha ER estrogen receptor estrogen receptors estrogen

shared by Nathan Goodyear on 09 Jun 14 - No Cached
  • Nathan Goodyear on 09 Jun 14
     
    ER-beta expression appears to regulate estrogenic activity through ER-alpha expression.  Co-expression of ER-alpha and ER-beta is associated with reduced estrogenic signaling, indicating a significant counter regulatory role for ER-beta.
Nathan Goodyear

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors i... - 0 views

advances.sciencemag.org/...e1501924.full

progesterone PR progesterone receptors progesterone receptor cancer breast cancer hormones

shared by Nathan Goodyear on 29 Jun 16 - No Cached
  • The presence and activity of PR significantly affect the prognostic value of ER.
  • The observed loss of PR protein expression in a subset of ER+/PR+ breast cancers, because of hypermethylation or deletion of the PR gene locus, results in the loss of ER prognostic value
  • These findings emphasize the clinical value of assessing both PR and ER expression in breast cancer samples
  • ...7 more annotations...
  • PR is an essential modulator of ER-regulated genes but also that it significantly contributes to the prognostic value of ER in ER+/PR+ breast cancers
  • PR-regulated genes have independent prognostic value, and the presence of PR correlates with favorable clinicopathological outcomes
  • this study demonstrates that progestin-activated PR redirects ER chromatin binding and functions as a genomic estrogen agonist and as a phenotypic estrogen antagonist in ER+/PR+ breast cancer cells and human tumors
  • Approximately 80% of ER+ breast cancers are also positive for PR,
  • In isolation, both hormones activate or inhibit cellular processes in similar directions, although the magnitude of these effects is less for progestin alone than for estrogen alone
  • PR-mediated antagonism of estrogenic phenotypes is well documented
  • joint activation of ER and PR antagonized ER-regulated oncogenic processes
  • Nathan Goodyear on 29 Jun 16
     
    WOW!!  study finds that progesterone through PR activity antagonizes ER protein expression by the cell.  This has huge implications in breast cancer and possible prostate cancer.  But then again, women don't need progesterone; only estrogen.  The presence of PR correlates with improved clinicopathological outcomes.  The authors do seem to get confused about progesterone and progestins.  They are not one in the same.
Nathan Goodyear

Associations between ERα, ERβ, and AR Genotypes and Colon and Rectal Cancer - 0 views

cebp.aacrjournals.org/...2936.full.pdf+html

colon cancer colorectal cancer ER ER alpha ER-alpha ER beta ER-beta HRT estrogen receptors

shared by Nathan Goodyear on 19 Nov 14 - No Cached
  • Nathan Goodyear on 19 Nov 14
     
    Study finds ER-beta plays more significant role in the development of Colon cancer than ER-alpha in women.  HRT in women reduces colon cancer risk in comparison to breast, which is increased.  Shows the different tissue expression of ER-alpha and ER-beta, as well as the HRT itself.
Nathan Goodyear

Estrogen Receptor β in Prostate Cancer: Brake Pedal or Accelerator? - 0 views

ajp.amjpathol.org/...fulltext

prostate cancer ER beta ER-beta ER alpha ER-alpha estrogen receptor receptors men male hormone hormones

shared by Nathan Goodyear on 21 Jan 14 - No Cached
  • Nathan Goodyear on 21 Jan 14
     
    Great article on ER beta and the prostate.  ER alpha expression is very important in the development of the prostate.  IN that instance, ER beta is down regulated.  In prostate cancer generation, ER beta expression in the epithelium is lost.
Nathan Goodyear

Estrogen Receptor β Expression Is Associated with Tamoxifen Response in ERα-N... - 0 views

clincancerres.aacrjournals.org/...1987.long

ER beta ER-beta estrogen receptors breast cancer tamoxifen estrogen receptor estrogen receptor women hormone hormones

shared by Nathan Goodyear on 08 Oct 14 - No Cached
  • Nathan Goodyear on 08 Oct 14
     
    Increased survival in those with ER beta + and ER alpha -.  Early relapse was associated with lack of ER beta expression.  ER beta is transcribed from a different genomic location than ER alpha.  
Nathan Goodyear

Impact of Estrogen Receptor β on Gene Networks Regulated by Estrogen Receptor... - 0 views

endo.endojournals.org/...4831.long

estrogen receptors receptor hormone hormones ER-alpha ER-beta ER cancer breast

shared by Nathan Goodyear on 16 Oct 12 - No Cached
  • ERβ acts as a tumor-suppressive protein
  • E2 may promote cell proliferation by inhibiting TGFβ production
  • ERβ modulated ERα regulation of TGFβ
  • Nathan Goodyear on 16 Oct 12
     
    Good discussion of the different effects of ER-alpha and ER-beta in breast cancer.  ER-beta inhibits growth in contrast to ER-alpha.
Nathan Goodyear

PLOS ONE: Alternate Estrogen Receptors Promote Invasion of Inflammatory Breast Cancer C... - 0 views

www.plosone.org/...journal.pone.0030725

ER-alpha ER-beta estrogen receptors ER inflammatory breast cancer hormone hormones

shared by Nathan Goodyear on 10 Oct 12 - No Cached
  • Nathan Goodyear on 10 Oct 12
     
    This study looked at estrogen receptors and inflammatory breast cancer.  ER-alpha36 varian and ER-beta were found to be present in non-genomic signaling in this disease.  ER-alpha is regular absent in this disease.  There is both genomic and non-genomic pathways with regards to signaling with ER
Nathan Goodyear

ERβ Has Nongenomic Action in Caveolae: Molecular Endocrinology: Vol 16, No 5 - 0 views

press.endocrine.org/...mend.16.5.0827

ER estrogen receptor estrogen receptors ER-alpha ER alpha ER beta ER-beta hormone hormones

shared by Nathan Goodyear on 09 Jun 14 - No Cached
  • Nathan Goodyear on 09 Jun 14
     
    Estrogen receptors are primarily located inside the nucleus and in the cytoplasm; not on the cell membrane surface. This article specifically focus' on the non-genomic action of ER-beta.  ER-alpha and ER-beta are classic transcription factors.
Nathan Goodyear

Immunohistochemical Expression of Estrogen and Progesterone Receptors in Human Colorect... - 0 views

www.ncbi.nlm.nih.gov/...PMC3215447

estrogen progesterone ER estrogen receptor estrogen receptors ER alpha ER beta ER-alpha ER-beta PR progesterone receptor progesterone receptors

shared by Nathan Goodyear on 09 Jun 14 - No Cached
  • Nathan Goodyear on 09 Jun 14
     
    Study finds ER and PR increase along the timeline of tumor initiation.  The authors point to likely association that ER and PR expression is associated with and key to initiating colorectal transformation.  A lot to be determined from this study.  IF this were entirely true, then what to explain the 35% lower colorectal cancer risk in women vs men?  Likely ER and PR pertubance plays a significant role is likely, but the mere expression--yet to be determined.
Nathan Goodyear

BMC Cancer | Full text | Estrogen receptor alpha/beta ratio and estrogen rece... - 0 views

www.biomedcentral.com/...425

breast cancer ER alpha ER-alpha ER beta ER-beta SERM tamoxifen anastrazole women hormone hormones female

shared by Nathan Goodyear on 08 Oct 14 - No Cached
  • 75% of human BCs express estrogen receptors (ERs)
  • Nathan Goodyear on 08 Oct 14
     
    ER beta expression and the ratio of ER alpha/ER beta is important in prognosis and effectiveness of SERM therapy like tamoxifen.  This study looked at the aromatase inhibitor anastrazole as well.
Nathan Goodyear

Expression of estrogen receptors-α and -β in bladder cancer cell lines and hu... - 0 views

onlinelibrary.wiley.com/...full

ER ER beta ER-beta bladder cancer bladder cancer

shared by Nathan Goodyear on 04 Jan 15 - No Cached
  • Nathan Goodyear on 04 Jan 15
     
    ER-beta is commonly expressed versus ER-alpha in bladder cancer.  There was a positive correlation between ER-beta expression and invasion and grade of cancer.  This study also found that blockade of the ER resulted in a decrease in growth.
Nathan Goodyear

Exposure to the environmental estrogen bisphenol A ... [Life Sci. 2003] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12505546

Bisphenol-A ER alpha ER beta estrogen receptor estrogen receptor alpha estrogen receptor beta hormone hormones

shared by Nathan Goodyear on 14 May 13 - No Cached
  • Nathan Goodyear on 14 May 13
     
    Bisphenol A causes shift in ER-beta to ER-alpha through increase ER alpha transcription in the testis.  This only looked at ER expression in the testis.
Nathan Goodyear

ScienceDirect.com - Cell Metabolism - Estrogen Receptors and the Metabolic Network - 0 views

www.sciencedirect.com/...S1550413111003123

ER-alpha ER-beta estrogen receptor receptors metabolic syndrome MetS hormone hormones

shared by Nathan Goodyear on 11 Oct 12 - No Cached
  • The pro-opiomelanocortin (POMC) neurons have an anorexigenic action and, when activated, reduce food intake through the release of two peptides, α-melanocyte-stimulating hormone (α-MSH) and cocaine-and-amphetamine-regulated transcripts (CART). The neuropeptide Y (NPY) neurons, on the other hand, release NPY hormone and agouti gene-related protein (AgRP), which prevent the binding of α-MSH to MC3R and MC4R, increasing food intake
  • This suggests that the central anorexic effects of E2 may occur via ERβ
  • The main hypothalamic areas involved in food intake and satiety are the arcuate nucleus (ARC), the lateral hypothalamus (LH), the paraventricular nucleus (PVN), the ventromedial hypothalamus (VMH), and the dorsomedial hypothalamus (DMH)
  • ...22 more annotations...
  • Leptin is a potent anorexigenic and catabolic hormone secreted by adipose cells that reduces food intake and increases energy expenditure
  • E2 not only modulates leptin receptor mRNA in the ARC and VMH, but also increases hypothalamic sensitivity to leptin, altering peripheral fat distribution
  • ghrelin. It acts on growth hormone secretagogue receptors (GHSR1a) located in the ARC and is a potent stimulator of food intake
  • It thus appears that of the two ERs, ERα plays a predominant role in the CNS regulation of lipid and carbohydrate homeostasis.
  • Both ERs have been identified in the ARC
  • Stimulation of MCH neurons increases food intake and fat accumulation while its inhibition leads to decreased food intake and reduced fat accumulation.
  • Both ERs have been identified in the LH
  • both ERs have been identified in this nucleus
  • The PVN is the region of the hypothalamus with the highest expression of ERβ and is reported to be weakly ERα positive
  • The VMH is ERα regulated
  • Skeletal muscle is responsible for 75% of the insulin-induced glucose uptake in the body
  • GLUT4 is highly expressed in muscle and represents a rate-limiting step in the insulin-induced glucose uptake
  • data suggest that in the physiological range, E2 is beneficial for insulin sensitivity, whereas hypo- or hyperestrogenism is related to insulin resistance
  • In aging female rats, E2 treatment improves glucose homeostasis mainly through its ability to increase muscle GLUT4 content on the cell membrane
  • It is evident that ERα and ERβ have distinct actions and that much more research is needed to clearly identify the function of each receptor in muscle.
  • E2 prevents accumulation of visceral fat, increases central sensitivity to leptin, increases the expression of insulin receptors in adipocytes, and decreases the lipogenic activity of lipoprotein lipase in adipose tissue
  • In rats, ovariectomy increases body weight, intra-abdominal fat, fasting glucose and insulin levels, and insulin resistance followed by decreased phosphorylation of AMPK and its substrate acetyl-CoA carboxylase in adipose tissue
  • decreased adiponectin, PPARγ coactivator-1α (PGC-1α), and uncoupling protein 2 (UCP2) and increased resistin
  • Men with aromatase deficiency have truncal obesity, elevated blood lipids, and severe insulin resistance
  • Although not all studies are in agreement, polymorphisms of ERα in humans have been associated with risk factors for CVDs
  • Human subcutaneous and visceral adipose tissues express both ERα and ERβ, whereas only ERα mRNA has been identified in brown adipose tissue
  • suggesting that ERα is the main regulator of GLUT4 expression in adipose tissue
  • Nathan Goodyear on 11 Oct 12
     
    very nice article that looks at the balance of ER-alpha/ER-beta and their role in metabolic syndrome.  This article discusses the balance of  these receptors are tissue dependent in their effect.  I like their conclusion: "...but these mechanisms will never be completely understood if they are not considered in the context of a whole system.
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