TY - JOUR. T1 - MAPK activation predicts poor outcome and the MEK inhibitor, selumetinib, reverses antiestrogen resistance in ER-positive high-grade serous ovarian cancer. AU - Hew, Karina E.. AU - Miller, Philip C.. AU - El-Ashry, Dorraya. AU - Sun, Jun. AU - Besser, Alexandra H.. AU - Ince, Tan A.. AU - Gu, Mengnan. AU - Wei, Zhi. AU - Zhang, Gao. AU - Brafford, Patricia. AU - Gao, Wei. AU - Lu, Yiling. AU - Mills, Gordon B.. AU - Slingerland, Joyce M.. AU - Simpkins, Fiona. PY - 2016/2/15. Y1 - 2016/2/15. N2 - Purpose: Although 67% of high-grade serous ovarian cancers (HGSOC) express the estrogen receptor (ER), most fail antiestrogen therapy. Because MAPK activation is frequent in ovarian cancer, we investigated if estrogen regulates MAPK and if MEK inhibition (MEKi) reverses antiestrogen resistance. Experimental Design: Effects of MEKi (selumetinib), antiestrogen (fulvestrant), or both were assayed in ER-positive HGSOC in vitro and in xenografts. Response biomarkers were investigated by gene ...
Fulvestrant is used to treat certain types of breast cancer. Breast cancer cells need the hormone estrogen in order to grow. Fulvestrant works by blocking the effect of estrogen, slowing tumor cell growth.
Faslodex allergy in children - Are my ankles swollen due to faslodex (fulvestrant)? Probably not. Swelling is not listed as an adverse reaction. But I would discuss it with your prescribing doctor.
Lim, Joanne Siok Liu; Sutiman, Natalia; Muerdter, Thomas E.; Singh, Onkar; Cheung, Yin Bun; Ng, Raymond Chee Hui; Yap, Yoon Sim; Wong, Nan Soon; Ang, Peter Cher Siang; Dent, Rebecca; Schroth, Werner; Schwab, Matthias; Chowbay, Balram ...
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Fulvestrant (ICI 182 780, ICI) has been used in treating patients with hormone-sensitive breast cancer, yet initial or acquired resistance to endocrine therapies frequently arises and, in particular, cancer recurs as metastasis. We demonstrate here that both 17-beta-estradiol (E2) and ICI enhance cell adhesion to matrigel in MCF-7 breast cancer cells, with increased autolysis of calpain 1 (large subunit) and proteolysis of focal adhesion kinase (FAK), indicating calpain activation. Additionally, either E2 or ICI induced down-regulation of estrogen receptor α without affecting G protein coupled estrogen receptor 30 (GPR30) expression. Interestingly, GPR30 agonist G1 triggered calpain 1 autolysis but not calpain 2, whereas ER agonist diethylstilbestrol caused no apparent calpain autolysis. Furthermore, the actions of E2 and ICI on calpain and cell adhesion were tremendously suppressed by G15, or knockdown of GPR30. E2 and ICI also induced phosphorylation of extracellular regulated protein kinases ...
Increased expression of BCL2 and/or BCLW plays a role in antiestrogen resistance by allowing cells to evade apoptosis (35). Using multiple cell lines and different endocrine therapies, we show that GX15-070, a small-molecule pan-inhibitor of antiapoptotic BCL2 family members, potentiates cell death in both antiestrogen-sensitive and -resistant human breast cancer cells. While reports describe apoptosis and autophagy as the major forms of death induced by GX15-070 (14, 18, 19), the downstream mediators of GX15-070-induced autophagy have yet to be elucidated. We show that GX15-070′s anticancer efficacy is due to the blockade of antiapoptotic BCL2 family members and an increase in autophagy initiation without the complete digestion of autolysosomes; perhaps one form of apparent autophagic cell death. Furthermore, GX15-070 inhibits the protein expression of CTSD and CTSL1 that would ultimately limit cells from effectively recycling cargo that could be used to fuel cell metabolism and restore ...
Synonyms for antiestrogen in Free Thesaurus. Antonyms for antiestrogen. 1 synonym for estrogen: oestrogen. What are synonyms for antiestrogen?
AstraZeneca (NYSE: AZN) today announced agreement with the US Food and Drug Administration (FDA) on label changes for FASLODEX® (fulvestrant) Injectio
The CDK4/6 inhibitor Kisqali (chemical name: ribociclib) in combination with the hormonal therapy Faslodex (chemical name: fulvestrant) offered better overall survival than Faslodex alone in postmenopausal women diagnosed with advanced-stage, hormone-receptor-positive, HER2-negative breast cancer that either hadnt bee
This phase II clinical trial studies how well fulvestrant and palbociclib works in treating older patients with breast cancer that responds to hormone
We are leading Faslodex Injection distributors, dealers & suppliers in Mumbai. Fulvestrant Medicine is used to treat breast cancer that has spread to other areas of the body in women who have gone through
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Antiestrogens represent the first line of therapy in the treatment of estrogen receptor-positive (ER+) breast cancer patients. Unfortunately, up to 40% of patients develop resistance associated with progression and frequently die for metastatic breast cancer. The molecular events leading to pharmacological resistance are not completely understood. We attempted to verify in an experimental model the role of cytoplasmic clusterin (CLU), a cytoprotective protein found to be up-regulated in antiestrogen-resistant patients, following neoadjuvant treatment with toremifene. The role of cytoplasmic clusterin in modulating response to two antiestrogens (toremifene and tamoxifen) was studied in two ER+ anti-estrogen-sensitive cell lines (MCF-7, 734B) and one ER+ antiestrogen-resistant cell line (T47D) using siRNA strategy. Resistant cells were characterised by higher levels of cytoplasmic clusterin than sensitive cells, and antiestrogen treatments up-regulated clusterin levels in both sensitive and ...
TY - JOUR. T1 - A gene expression signature from human breast cancer cells with acquired hormone independence identifies MYC as a mediator of antiestrogen resistance. AU - Miller, Todd W.. AU - Balko, Justin M.. AU - Ghazoui, Zara. AU - Dunbier, Anita. AU - Anderson, Helen. AU - Dowsett, Mitch. AU - González-Angulo, Ana M.. AU - Mills, Gordon B.. AU - Miller, William R.. AU - Wu, Huiyun. AU - Shyr, Yu. AU - Arteaga, Carlos L.. PY - 2011/4/1. Y1 - 2011/4/1. N2 - Purpose: Although most patients with estrogen receptor α (ER)-positive breast cancer initially respond to endocrine therapy, many ultimately develop resistance to antiestrogens. However, mechanisms of antiestrogen resistance and biomarkers predictive of such resistance are underdeveloped. Experimental Design: We adapted four ER+ human breast cancer cell lines to grow in an estrogen-depleted medium. A gene signature of estrogen independence was developed by comparing expression profiles of long-term estrogen-deprived (LTED) cells to ...
Breast cancer is the most common malignancy in women worldwide. Although the endocrine therapy that targets estrogen receptor α (ERα) signaling has been well established as an effective adjuvant treatment for patients with ERα-positive breast cancers, long-term exposure may eventually lead to the development of acquired resistance to the anti-estrogen drugs, such as fulvestrant and tamoxifen. A better understanding of the mechanisms underlying antiestrogen resistance and identification of the key molecules involved may help in overcoming antiestrogen resistance in breast cancer. The whole-genome gene expression and DNA methylation profilings were performed using fulvestrant-resistant cell line 182R-6 and tamoxifen-resistant cell line TAMR-1 as a model system. In addition, qRT-PCR and Western blot analysis were performed to determine the levels of mRNA and protein molecules. MTT, apoptosis and cell cycle analyses were performed to examine the effect of either guanine nucleotide-binding protein beta-4
Fulvestrant, which degrades ER, is used after aromatase inhibitor (AI) failure in metastatic breast cancer but resistance develops quickly. We hypothesized that using everolimus to inhibit mammalian target of rapamycin (mTOR), a key signaling pathway in endocrine resistance, may delay fulvestrant resistance in patients and thus improve its efficacy. We conducted a phase II trial of combined fulvestrant and everolimus in postmenopausal women with disease progression or relapse after an AI. Primary endpoint was time to progression (TTP) and secondary endpoints included objective response rate, clinical benefit rate (CBR), safety, and biomarker correlates. Tumor blocks were collected and biopsy of accessible tumor was done for future biomarker analysis ...
Tamoxifen is currently the endocrine therapy of choice for early and advanced breast cancer. Attempts to improve the therapeutic efficacy have included altering the triphenylethylene ring structure of tamoxifen, forming new nonsteroidal ring structures or creating steroidal estradiol analogs with greater antiestrogenic activity. There are now six nonsteroidal compounds either on the market or in clinical development and one steroidal pure antiestrogen has entered clinical trials. A number of these agents show improved estrogen-receptor binding affinity, antiestrogenic activity, and/or antitumor activity compared with tamoxifen. Preclinical and clinical data on these compounds are discussed and compared with tamoxifen when possible ...
Patients with HR-positive, HER2-negative advanced or metastatic breast cancer who have had disease progression on or after prior adjuvant or metastatic endocrine therapy. The safety of IBRANCE (125 mg/day) plus fulvestrant (500 mg) versus placebo plus fulvestrant was evaluated in Study 2 (PALOMA-3). The data described below reflect exposure to IBRANCE in 345 out of 517 patients with HR-positive, HER2-negative advanced or metastatic breast cancer who received at least 1 dose of IBRANCE plus fulvestrant in Study 2. The median duration of treatment for IBRANCE plus fulvestrant was 10.8 months while the median duration of treatment for placebo plus fulvestrant arm was 4.8 months.. Dose reductions due to an adverse reaction of any grade occurred in 36% of patients receiving IBRANCE plus fulvestrant. No dose reduction was allowed for fulvestrant in Study 2.. Permanent discontinuation associated with an adverse reaction occurred in 19 of 345 (6%) patients receiving IBRANCE plus fulvestrant, and in 6 of ...
The T47D/S2 Cell line is the control cell line for the tamoxifen resistant T47D/TR-1 and T47D/TR-2 lines. Antiestrogen resistance is
The primary objective of this study is to determine if estrogen receptor-targeted therapy with fulvestrant used in combination with RAD001 (Everolimus)
Breast cancer can be divided into 4 major subtypes using molecular and genetic information from the tumors. Each subtype is associated with different prognosis and should be taken into consideration when making treatment ...
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4-OHT is believed to exert antiestrogenic activity by silencing the transcriptional activity of AF2 by repositioning helix 12 to block the coactivator binding site (Fig. 8B) ⇓ . The agonist activity of 4-OHT is believed to be mediated through AF1 in a cell- and promoter-dependent manner (5 , 6) . 4-OHT induced TGF-α gene expression in wild-type ERα cells (Fig. 3) ⇓ without inducing coactivator binding to GST-HBD3 (Fig. 5) ⇓ , suggesting that 4-OHT can activate TGF-α gene expression through the AF1 domain. This was confirmed because 4-OHT did not induce TGF-α mRNA when liganded to D351ΔAF1, which does not contain the AF1 domain (Fig. 3) ⇓ . However, 4-OHT also failed to enhance the TGF-α mRNA level in D351-3m cells (Fig. 3) ⇓ , which is consistent with a previous report that AF2 is required for agonist activity of 4-OHT (49) . These results indicated that the agonist activity of 4-OHT was not simply estrogen like, because E2 can induce the TGF-α mRNA level through both D351ΔAF1 ...
Anti-Estrogen Formulas list and information including what is Anti-Estrogen Formulas, health benefits and usage indications. Find articles and product list for other top low-carb products, fat-burners, nutrition bars and shakes.
Anti-Estrogen Formulas list and information including what is Anti-Estrogen Formulas, health benefits and usage indications. Find articles and product list for other top low-carb products, fat-burners, nutrition bars and shakes.
Anti-Estrogens: mATD overview and facts This is the 17aMethyl version of ATD. It could, in theory, have androgenic effects and we have no way of knowing if it actually reduces estrogen.
Verzenio (abemaciclib) is a dual CDK4/6 inhibitor, which inhibits Rb1 protein phosphorylation and may induce cell cycle arrest and prevent growth in cancer cells (PMID: 24919854). Verzenio (abemaciclib) is FDA approved as a monotherapy and in combination with Faslodex (fulvestrant) in patients with hormone receptor-positive (ESR, PGR) and ERBB2 (HER2) receptor-negative advanced or metastatic breast cancer (FDA.gov).. ...
Hello guys i am thinking of staking natadrol with anadraulic.Should i take an anti-estrogen with them or w8 to take formadrol for post cycle?What you
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Nolvadex is perhaps the most popular anti-estrogen available due to the fact that it essentially was the first of its kind developed almost 50 years ago
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Faslodex (chemical name: fulvestrant) is an estrogen receptor downregulator (ERD), a type of hormonal therapy. Faslodex blocks the effect of estrogen on breast tissue by sitting in the estrogen receptor in breast cells. Faslodex is a liquid given as an injection into a muscle. On Aug. 28, 2017, the U. S. Food and Drug Administration (FDA) approved a broader use of Faslodex to treat breast cancer. Faslodex can now be used alone as the first treatment for postmenopausal women diagnosed with hormone-receptor-positive, HER2-negative, advanced-stage breast cancer that hasnt been treated with hormonal therapy. Before this, Faslodex was approved to treat postmenopausal women diagnosed with metastatic, hormone-receptor-positive breast cancer that had stopped responding to other hormonal therapy medicines. The new FDA approval is based on results from the 2016 FALCON trial. The FALCON trial found that postmenopausal women diagnosed with hormone-receptor-positive, locally advanced or metastatic breast ...
PRIMARY OBJECTIVES:. I. To determine the maximum tolerated dose (MTD) of BKM120 (PI3K inhibitor BKM120) in combination with fulvestrant.. II. To evaluate the toxicity profile of BKM120 in combination with fulvestrant.. SECONDARY OBJECTIVES:. I. To evaluate the toxicity profile of BKM120 in combination with fulvestrant when administered for at least 3 months.. II. To determine the steady state blood concentrations of BKM120 when combined with fulvestrant.. III. To evaluate the anti-tumor effect (partial response [PR], complete response [CR], stable disease [SD], and progressive disease [PD]) of BKM120 in combination with fulvestrant in patients with ER+ metastatic breast cancer.. TERTIARY OBJECTIVES:. I. To examine baseline tumor specimens for phosphatidylinositol 3-kinase (PI3K) pathway abnormalities, and to correlate with treatment response.. II. To examine the PIK3 catalytic alpha polypeptide (PIK3CA) mutation status in circulating deoxyribonucleic acid (DNA) at baseline and following study ...
... overall survival of ER positive breast cancer patients. ADAM12 in breast tumor cell proliferation and as potential mediators of endocrine resistance. Methods Using stable clones of ADAM12-overexpressing MCF-7 cells, we analyzed proliferation rates of these ER+ breast tumor cells both in estrogen-depleted medium and in the presence of the antiestrogens, tamoxifen and ICI 182,780. Acquired estrogen resistance in these cells was analyzed using phosphoRTK analysis. Upregulation and phosphorylation of proteins were detected via immunoprecipitation and immunoblotting. EGFR and MAPK inhibitors were used to explore the mechanism of acquired estrogen resistance in breast tumor cells. Results We observed that overexpression of the two isoforms, transmembrane ADAM12-L and secreted ADAM12-S, in breast tumor cells promoted estrogen-independent growth. In ADAM12-L-expressing cells, estrogen-independence was a immediate result ...
Background: Preclinical data suggest that patients with ER+ Breast Cancer become less sensitive to hormonal therapy by upregulation of the mTOR pathway. BOLERO-2 demonstrated that the combination of an allosteric mTOR inhibitor and an aromatase inhibitor improves progression-free survival in postmenopausal women with hormone resistant advanced breast cancer (NEJM 2012; 366:520-529). AZD2014 is a selective dual mTORC1 and mTORC2 inhibitor whilst fulvestrant is an estrogen receptor antagonist that is approved for the treatment of postmenopausal women with disease progression following antiestrogen therapy. This phase I trial assessed the safety, tolerability, pharmacokinetics, and preliminary efficacy of AZD2014 administered in combination with fulvestrant.. Methods: Continuous BID or QD dosing of AZD2014 was administered in combination with fulvestrant 500 mg intramuscularly on day 1 of each 28 day cycle. An additional 500 mg dose of fulvestrant was administered on day 15 of cycle 1 as per the ...
In vivo administration of estradiol benzoate (E2B) or parathyroid hormone (PTH) stimulates in vitro renal conversion of 25-hydroxyvitamin D3 [25-(OH)D3] to 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] in birds. In the present investigation, the effect of PTH on 1,25-(OH)2D3 production was studied in female Japanese quail pretreated with the antiestrogen, tamoxifen citrate (30 mg/kg) daily for 7 days. PTH was injected at two different doses (92 and 275 U.S.P. units/kg) every 8 hours during the last two days of tamoxifen treatment. E2B (0.1 and 1.0 mg/kg) was injected 24 hours before sacrifice. Control groups received vehicle only. All injections were given intramuscularly. Kidney homogenates were prepared and incubated with tritiated 25-(OH)D3. E2B-induced stimulation of 1,25-(OH)2D3 production was completely blocked by prior treatment with tamoxifen, but PTH-induced stimulation of 1,25-(OH)2D3 production was unaffected by antiestrogen treatment. When PTH and E2B were injected together, no additive ...
A Phase II Trial Assessing the Tolerability of Palbociclib in Combination With Letrozole or Fulvestrant in Patients Aged 70 and Older With Estrogen Receptor-Positive, HER2-Negative Metastatic Breast ...
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Tibolone is an analogue of the progestin, norethynodrel. After ingestion, it is converted to three metabolites, namely 3 alpha and 3 beta hydroxytibolone which have oestrogenic effects, and delta 4 isomerase, which has progestogenic and androgenic properties. Both the oestrogenic metabolites bind to the alpha oestrogen receptor, but not the beta oestrogen receptor, whilst the delta 4 isomer binds to the alpha and beta oestrogen, the progestogen and the androgen receptors. Tibolone also is a sulphatase inhibiter, blocking conversion of oestrone sulphate to oestrone, as well as stimulating local sulphotransferase activity. In contrast to other forms of postmenopausal hormonal therapy, it decreases sex hormone binding globulin and hence increases circulating free testosterone, and thereby further adding to its androgenicity. Tibolone significantly decreases vasomotor symptoms, mood disorders, insomnia, bone loss, vaginal atrophy. It has a favourable impact on the cardiovascular system and minimal impact on
In approximately two-thirds of cases, ER-positive breast cancer is characterized by the sustained expression of the ER-α (ESR1), making this receptor the most frequently utilized biomarker and therapeutic target for ER-positive disease.. Genetic mutations fuelling ESR1 expression in ER-positive breast cancer have been studied extensively, therefore, in this study the team aimed to look beyond genetic mutations. Utilizing epigenetics, the team observed a significant number of somatic mutations in a set of regulatory elements that have previously been demonstrated to regulate ESR1 expression in 7% of ER-positive breast cancers.. Lead author Mathieu Lupien (Princess Margaret Cancer Centre) commented: "By investigating acquired mutations found outside of genes through the power of epigenetics, we have identified that functional regulatory components can be altered to impact the expression of genes to promote breast cancer development.". Lupien believes that this research highlights the importance ...
The BCPT, part of the National Surgical Adjuvant Breast and Bowel Project (NSABP), began in April 1992 to determine whether the nonsteroidal anti-estrogen drug tamoxifen could reduce the incidence of breast cancer in women who were at high risk for development of the disease. Only women who were at increased risk for developing breast cancer participated in the study. They were chosen based on their breast cancer risk as determined by a computer calculation that included specific factors.. By September 1997, more than 13,000 women had participated in the study. Data showed the results of tamoxifen treatment to be highly significant with a 49 percent reduction in the number of invasive breast cancers seen across all age groups. These results were confirmed in the final report issued in 2005.. The data were then turned over to the Endpoint Review, Safety Monitoring, and Advisory Committee for review of toxicity, adverse side effects, and effectiveness of tamoxifen. This independent committee ...
Purpose: FGFR1 amplification occurs in ~15% of ER+ human breast cancers. We investigated mechanisms by which FGFR1 amplification confers antiestrogen resistance to ER+ breast cancer.,br /,,br /,Experimental Design: ER+ tumors from patients treated with letrozole before surgery were subjected to Ki67 immunohistochemistry, FGFR1 FISH, and RNA-sequencing. ER+/FGFR1 amplified breast cancer cells and patient-derived xenografts (PDXs) were treated with FGFR1 siRNA or the FGFR tyrosine kinase inhibitor lucitanib. Endpoints were cell/xenograft growth, FGFR1/ERα association by co-immunoprecipitation and proximity ligation, ER genomic activity by ChIP-sequencing, and gene expression by RT-PCR.,br /,,br /,Results: ER+/FGFR1 amplified tumors in patients treated with letrozole maintained cell proliferation (Ki67). Estrogen deprivation increased total and nuclear FGFR1 and FGF ligands expression in ER+/FGFR1-amplified primary tumors and breast cancer cells. In estrogen-free conditions, FGFR1 associated with ...
Currently, ERa is the main therapeutic and prognostic marker for breast cancer but about 30% do not respond to the antiestrogens. Some studies have shown that ERb isoforms are predictive marker to antiestrogens. ERb isoforms also are significantly expressed in ERa negative tumors. Thus, ERb may be the potential targeted therapy in some ERa and ERa negative breast cancers. ERb isoforms mRNA by qPCR and protein expression by immunohistochemistry will be tested in both ERa positive and ERa negative breast cancer tissues, and also breast cancer cell lines (BCC). Then BCC will be subjected to estrogens and different antiestrogens to determine their responses, and their effects and analyzed for their potential therapeutic effects. We hypothesize that ERß will eventually play an important role in controlling growth of breast cancers. We believe that ERb isoforms may be new potential therapeutic targets to the patients with non-responder to the current available ERa targeted antiestrogen therapy, and ...
Purpose: Determine the roles of the PI3K isoforms p110α and p110β in PTEN-deficient, estrogen receptor α (ER)-positive breast cancer, and the therapeutic potential of isoform-selective inhibitors.. Experimental Design: Anti-estrogen-sensitive and -resistant PTEN-deficient, ER+ human breast cancer cell lines, and mice bearing anti-estrogen-resistant xenografts were treated with the anti-estrogen fulvestrant, the p110α inhibitor BYL719, the p110β inhibitor GSK2636771, or combinations. Temporal response to growth factor receptor-initiated signaling, growth, apoptosis, predictive biomarkers, and tumor volumes were measured.. Results: p110β primed cells for response to growth factor stimulation. Although p110β inhibition suppressed cell and tumor growth, dual targeting of p110α/β enhanced apoptosis and provided sustained tumor response. The growth of anti-estrogen-sensitive cells was inhibited by fulvestrant, but fulvestrant inconsistently provided additional therapeutic effects beyond PI3K ...
In women with aromatase inhibitor-resistant, advanced or metastatic breast cancer positive for both estrogen receptor (ER) and progesterone receptor (PR), adding pictilisib (previously GDC-0941) to the endocrine therapeutic fulvestrant increased survival.
The mechanisms of antisteroid action have been extensively studied in recent years, mostly because of the clinical importance of these compounds. One question that was addressed was whether these drugs display a partial agonist activity under certain conditions. This question is important because of its implications for the efficacy of the drug as well as for understanding the molecular mechanisms of the inhibition of the hormone action. These studies were made possible by the availability of expression vectors for the various steroid receptors and by the use of transfection assays. Using such approaches, it was shown that the antiprogestin and antiglucocorticoid RU 486 (27,28) and the antiestrogen tamoxifen (29) display agonist activity under certain conditions. In fact, antiestrogens can be grouped into several classes distinguished by their relative agonist activity, reflecting their differential effect on the receptor conformation (30). Much less is known about the properties of the ...
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