2,125 results on '"Estrogen Receptor Modulators"'
Search Results
2. Estrogen deprivation and estrogen receptor α antagonism decrease DSS colitis in female mice.
- Author
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Hjelt, Anja, Anttila, Santeri, Wiklund, Anu, Rokka, Anne, Al‐Ramahi, Darin, Toivola, Diana M., Polari, Lauri, and Määttä, Jorma
- Subjects
- *
ESTROGEN receptors , *ESTRADIOL , *COLITIS , *INFLAMMATORY bowel diseases , *OVARIES , *SLEEP deprivation , *ANIMAL welfare , *ESTROGEN - Abstract
The association of hormonal contraception with increased risk of inflammatory bowel disease (IBD) observed in females suggests involvement of ovarian hormones, such as estradiol, and the estrogen receptors in the progression of intestinal inflammation. Here, we investigated the effects of prophylactic SERM2 and estradiol supplementation in dextran sulfate sodium‐induced colitis using mice with intact ovaries and ovariectomized (OVX) female mice. We found that graded colitis score was threefold reduced in the OVX mice, compared to mice with intact ovaries. Estradiol supplementation, however, aggravated the colitis in OVX mice, increasing the colitis score to a similar level than what was observed in the intact mice. Further, we observed that immune infiltration and gene expression of inflammatory interleukins Il1b, Il6, and Il17a were up to 200‐fold increased in estradiol supplemented OVX colitis mice, while a mild but consistent decrease was observed by SERM2 treatment in intact animals. Additionally, cyclo‐oxygenase 2 induction was increased in the colon of colitis mice, in correlation with increased serum estradiol levels. Measured antagonist properties of SERM2, together with the other results presented here, indicates an exaggerating role of ERα signaling in colitis. Our results contribute to the knowledge of ovarian hormone effects in colitis and encourage further research on the potential use of ER antagonists in the colon, in order to alleviate inflammation. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
3. Estrogen deprivation and estrogen receptor α antagonism decrease DSS colitis in female mice
- Author
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Anja Hjelt, Santeri Anttila, Anu Wiklund, Anne Rokka, Darin Al‐Ramahi, Diana M. Toivola, Lauri Polari, and Jorma Määttä
- Subjects
colitis ,dextran sulfate ,estradiol ,estrogen receptor modulators ,inflammatory bowel diseases ,receptors ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Abstract The association of hormonal contraception with increased risk of inflammatory bowel disease (IBD) observed in females suggests involvement of ovarian hormones, such as estradiol, and the estrogen receptors in the progression of intestinal inflammation. Here, we investigated the effects of prophylactic SERM2 and estradiol supplementation in dextran sulfate sodium‐induced colitis using mice with intact ovaries and ovariectomized (OVX) female mice. We found that graded colitis score was threefold reduced in the OVX mice, compared to mice with intact ovaries. Estradiol supplementation, however, aggravated the colitis in OVX mice, increasing the colitis score to a similar level than what was observed in the intact mice. Further, we observed that immune infiltration and gene expression of inflammatory interleukins Il1b, Il6, and Il17a were up to 200‐fold increased in estradiol supplemented OVX colitis mice, while a mild but consistent decrease was observed by SERM2 treatment in intact animals. Additionally, cyclo‐oxygenase 2 induction was increased in the colon of colitis mice, in correlation with increased serum estradiol levels. Measured antagonist properties of SERM2, together with the other results presented here, indicates an exaggerating role of ERα signaling in colitis. Our results contribute to the knowledge of ovarian hormone effects in colitis and encourage further research on the potential use of ER antagonists in the colon, in order to alleviate inflammation.
- Published
- 2024
- Full Text
- View/download PDF
4. Levels of Circulating Tumor DNA as a Predictive Marker for Early Switch in Treatment for Patients With Metastatic (Stage IV) Breast Cancer
- Author
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Frances Valdes-Albini, Assistant Professor of Clinical Medicine
- Published
- 2023
5. Efficacy Evaluation of Sabizabulin Monotherapy Versus Active Control for Treatment of ER+HER2- Metastatic Breast Cancer
- Published
- 2023
6. Memory-Related Synaptic Plasticity Is Sexually Dimorphic in Rodent Hippocampus
- Author
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Wang, Weisheng, Le, Aliza A, Hou, Bowen, Lauterborn, Julie C, Cox, Conor D, Levin, Ellis R, Lynch, Gary, and Gall, Christine M
- Subjects
Behavioral and Social Science ,Brain Disorders ,Estrogen ,Neurosciences ,Mental Health ,Basic Behavioral and Social Science ,Underpinning research ,1.1 Normal biological development and functioning ,Mental health ,1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine ,Animals ,Enzyme Inhibitors ,Estradiol ,Estrogen Receptor Modulators ,Estrogen Receptor alpha ,Estrogens ,Excitatory Postsynaptic Potentials ,Female ,Hippocampus ,Male ,Memory ,Mice ,Neuronal Plasticity ,Neurons ,Phosphorylation ,Piperidines ,Pyrazoles ,Pyrimidines ,Rats ,Rats ,Sprague-Dawley ,Sex Characteristics ,Spatial Learning ,Synapses ,rho-Associated Kinases ,estrogen ,estrogen receptor alpha ,long-term potentiation ,LTP ,object location memory ,TrkB ,Medical and Health Sciences ,Psychology and Cognitive Sciences ,Neurology & Neurosurgery - Abstract
Men are generally superior to women in remembering spatial relationships, whereas the reverse holds for semantic information, but the neurobiological bases for these differences are not understood. Here we describe striking sexual dimorphism in synaptic mechanisms of memory encoding in hippocampal field CA1, a region critical for spatial learning. Studies of acute hippocampal slices from adult rats and mice show that for excitatory Schaffer-commissural projections, the memory-related long-term potentiation (LTP) effect depends upon endogenous estrogen and membrane estrogen receptor α (ERα) in females but not in males; there was no evident involvement of nuclear ERα in females, or of ERβ or GPER1 (G-protein-coupled estrogen receptor 1) in either sex. Quantitative immunofluorescence showed that stimulation-induced activation of two LTP-related kinases (Src, ERK1/2), and of postsynaptic TrkB, required ERα in females only, and that postsynaptic ERα levels are higher in females than in males. Several downstream signaling events involved in LTP were comparable between the sexes. In contrast to endogenous estrogen effects, infused estradiol facilitated LTP and synaptic signaling in females via both ERα and ERβ. The estrogen dependence of LTP in females was associated with a higher threshold for both inducing potentiation and acquiring spatial information. These results indicate that the observed sexual dimorphism in hippocampal LTP reflects differences in synaptic kinase activation, including both a weaker association with NMDA receptors and a greater ERα-mediated kinase activation in response to locally produced estrogen in females. We propose that male/female differences in mechanisms and threshold for field CA1 LTP contribute to differences in encoding specific types of memories.SIGNIFICANCE STATEMENT There is good evidence for male/female differences in memory-related cognitive function, but the neurobiological basis for this sexual dimorphism is not understood. Here we describe sex differences in synaptic function in a brain area that is critical for learning spatial cues. Our results show that female rodents have higher synaptic levels of estrogen receptor α (ERα) and, in contrast to males, require membrane ERα for the activation of signaling kinases that support long-term potentiation (LTP), a form of synaptic plasticity thought to underlie learning. The additional requirement of estrogen signaling in females resulted in a higher threshold for both LTP and hippocampal field CA1-dependent spatial learning. These results describe a synaptic basis for sexual dimorphism in encoding spatial information.
- Published
- 2018
7. Estrogen receptor-1 is a key regulator of HIV-1 latency that imparts gender-specific restrictions on the latent reservoir
- Author
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Das, Biswajit, Dobrowolski, Curtis, Luttge, Benjamin, Valadkhan, Saba, Chomont, Nicolas, Johnston, Rowena, Bacchetti, Peter, Hoh, Rebecca, Gandhi, Monica, Deeks, Steven G, Scully, Eileen, and Karn, Jonathan
- Subjects
Medical Microbiology ,Biomedical and Clinical Sciences ,Immunology ,Women's Health ,Genetics ,Estrogen ,Infectious Diseases ,Sexually Transmitted Infections ,HIV/AIDS ,Adult ,Estrogen Receptor Modulators ,Estrogen Receptor alpha ,Female ,HIV-1 ,Humans ,Jurkat Cells ,Male ,Receptors ,Antigen ,T-Cell ,Sex Characteristics ,T-Lymphocytes ,Transcription ,Genetic ,Virus Latency ,HIV-1 latency ,HIV-1 reservoir ,estrogen receptor ,latency-reversing agents ,selective estrogen receptor modulators - Abstract
Unbiased shRNA library screens revealed that the estrogen receptor-1 (ESR-1) is a key factor regulating HIV-1 latency. In both Jurkat T cells and a Th17 primary cell model for HIV-1 latency, selective estrogen receptor modulators (SERMs, i.e., fulvestrant, raloxifene, and tamoxifen) are weak proviral activators and sensitize cells to latency-reversing agents (LRAs) including low doses of TNF-α (an NF-κB inducer), the histone deacetylase inhibitor vorinostat (soruberoylanilide hydroxamic acid, SAHA), and IL-15. To probe the physiologic relevance of these observations, leukapheresis samples from a cohort of 12 well-matched reproductive-age women and men on fully suppressive antiretroviral therapy were evaluated by an assay measuring the production of spliced envelope (env) mRNA (the EDITS assay) by next-generation sequencing. The cells were activated by T cell receptor (TCR) stimulation, IL-15, or SAHA in the presence of either β-estradiol or an SERM. β-Estradiol potently inhibited TCR activation of HIV-1 transcription, while SERMs enhanced the activity of most LRAs. Although both sexes responded to SERMs and β-estradiol, females showed much higher levels of inhibition in response to the hormone and higher reactivity in response to ESR-1 modulators than males. Importantly, the total inducible RNA reservoir, as measured by the EDITS assay, was significantly smaller in the women than in the men. We conclude that concurrent exposure to estrogen is likely to limit the efficacy of viral emergence from latency and that ESR-1 is a pharmacologically attractive target that can be exploited in the design of therapeutic strategies for latency reversal.
- Published
- 2018
8. Local delivery of hormonal therapy with silastic tubing for prevention and treatment of breast cancer.
- Author
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Park, Jeenah, Thomas, Scott, Zhong, Allison Y, Wolfe, Alan R, Krings, Gregor, Terranova-Barberio, Manuela, Pawlowska, Nela, Benet, Leslie Z, and Munster, Pamela N
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Cell Line ,Tumor ,Animals ,Humans ,Breast Neoplasms ,Disease Models ,Animal ,Estradiol ,Estrogen Receptor Modulators ,Antineoplastic Agents ,Hormonal ,Chemoprevention ,Chromatography ,Liquid ,Xenograft Model Antitumor Assays ,Cell Proliferation ,Tissue Distribution ,Germ-Line Mutation ,Female ,Tandem Mass Spectrometry ,Biomarkers ,Tumor ,Fulvestrant - Abstract
Broad use of germline testing has identified an increasing number of women at risk for breast cancer with a need for effective chemoprevention. We report a novel method to selectively deliver various anti-estrogens at high drug levels to the breast tissue by implanting a device comprised of silastic tubing. Optimized tubing properties allow elution of otherwise poorly bioavailable anti-estrogens, such as fulvestrant, into mammary tissue in vitro and in vivo with levels sufficient to inhibit estrogen receptor activation and tumor cell proliferation. Implantable silastic tubing delivers fulvestrant selectively to mouse mammary fat tissue for one year with anti-tumor effects similar to those achieved with systemic fulvestrant exposure. Furthermore, local delivery of fulvestrant significantly decreases cell proliferation, as assessed by Ki67 expression, most effectively in tumor sections adjacent to tubing. This approach may thereby introduce a potential paradigm shift and offer a promising alternative to systemic therapy for prevention and early interception of breast cancer.
- Published
- 2018
9. Data from Hainan University Provide New Insights into Thrombocytopenia (Antiviral Activity of Selective Estrogen Receptor Modulators against Severe Fever with Thrombocytopenia Syndrome Virus In Vitro and In Vivo).
- Published
- 2024
10. Research Reports on Breast Cancer from Nicolaus Copernicus University in Torun Provide New Insights [Selective Estrogen Receptor Modulators' (SERMs) Influence on TET3 Expression in Breast Cancer Cell Lines with Distinct Biological Subtypes].
- Abstract
A recent study conducted by researchers at Nicolaus Copernicus University in Torun, Poland, has explored the effects of tamoxifen, a selective estrogen receptor modulator (SERM), on breast cancer cell lines with different biological subtypes. The study found that tamoxifen derivatives, specifically 4-hydroxytamoxifen (4-HT), had a significant impact on DNA methylation patterns and the expression of TET3, a gene involved in epigenetic alterations. The findings suggest that targeting epigenetic modifications could be a promising approach for personalized anti-cancer therapy. This research provides new insights into the role of SERMs in breast cancer treatment and offers potential avenues for improving treatment outcomes. [Extracted from the article]
- Published
- 2024
11. Findings on Breast Cancer Reported by Investigators at Sun Yat-sen University (Different Dosage Forms of Gonadotropin-releasing Hormone Agonist With Endocrine Therapy In Premenopausal Hormone Receptor-positive Breast Cancer).
- Abstract
A recent study conducted at Sun Yat-sen University in Guangzhou, China, explored the effectiveness and safety of different dosage forms of gonadotropin-releasing hormone (GnRH) agonist in premenopausal hormone receptor-positive breast cancer patients. The study included 1109 patients who were treated with GnRH agonist plus selective estrogen receptor modulator or aromatase inhibitor. The results showed that both the 1-month and 3-month GnRH agonist regimens achieved more than 90% estradiol (E2) inhibition within 24 months, confirming the noninferiority of the 3-month regimen. The study concluded that the ovarian function suppression with the 3-month GnRH agonist was not inferior to that with the 1-month regimen, regardless of age or combination with other medications. [Extracted from the article]
- Published
- 2024
12. Autologous Fat Grafting as a Novel Antiestrogen Vehicle for the Treatment of Breast Cancer.
- Author
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Thomas, Scott, Chen, Stephanie, Sbitany, Hani, Kwon, Edwin, Piper, Merisa, Park, Jeenah, Terranova Barberio, Manuela, Pawlowska, Nela, and Munster, Pamela N
- Subjects
Adipose Tissue ,Cells ,Cultured ,Animals ,Humans ,Mice ,Mice ,Nude ,Breast Neoplasms ,Disease Models ,Animal ,Estradiol ,Estrogen Receptor Modulators ,Antineoplastic Agents ,Hormonal ,Chemotherapy ,Adjuvant ,Mammaplasty ,Drug Delivery Systems ,Transplantation ,Autologous ,Female ,Fulvestrant ,Breast Cancer ,Bioengineering ,Biotechnology ,Cancer ,Estrogen ,Development of treatments and therapeutic interventions ,5.2 Cellular and gene therapies ,Clinical Sciences ,Surgery - Abstract
BackgroundAdipose fat transfer is increasingly used for contour corrections of the tumor bed after lumpectomy and breast reconstructions after mastectomy. The lipophilic nature of the fat tissue may render adipocytes an ideal vehicle with which to deliver a high boost of an antiestrogen to the tumor bed to serve as an adjunct systemic hormonal therapy. The authors therefore tested whether adipocytes could safely be loaded with an antiestrogen and allow for release at therapeutic concentrations to treat breast cancer.MethodsAdipose tissue was collected from patients undergoing autologous fat grafting. The influence of adipose tissue on tumorigenesis was determined both in vitro and in vivo using breast cancer cell lines. Ex vivo, adipose tissue was assessed for its ability to depot fulvestrant and inhibit the growth of breast cancer cell lines.ResultsAdipose tissue harvested from patients did not promote breast cancer cell growth in vitro or in an in vivo mouse model. Adipose tissue was successfully loaded with fulvestrant and released at levels sufficient to inhibit estrogen receptor signaling and growth of breast cancer cells.ConclusionsThis work supports the hypothesis that adipose tissue used for autologous fat grafting can serve as a novel method for local drug delivery. As this technique is used to reconstruct a variety of postsurgical defects following cancer resection, this approach for local drug delivery may be an effective alternative in therapeutic settings beyond breast cancer.
- Published
- 2017
13. Estrogens Effects on Excitatory Synaptic Transmission Entail Integrin and TrkB Transactivation and Depend Upon β1-integrin function.
- Author
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Wang, Weisheng, Kantorovich, Svetlana, Babayan, Alex, Hou, Bowen, Gall, Christine, and Lynch, Gary
- Subjects
Animals ,Animals ,Newborn ,Benzodioxoles ,Dipeptides ,Disks Large Homolog 4 Protein ,Estrogen Receptor Modulators ,Estrogens ,Excitatory Postsynaptic Potentials ,Female ,Gene Expression Regulation ,Guanylate Kinases ,Hippocampus ,Integrin beta1 ,Integrins ,Male ,Matrix Metalloproteinase Inhibitors ,Membrane Proteins ,Mice ,Knockout ,Neurons ,Phenylalanine ,Piperidines ,Pyrazoles ,Pyrimidines ,Quinolines ,Rats ,Rats ,Sprague-Dawley ,Receptors ,Estrogen ,Thiophenes - Abstract
Estradiol (E2) perfusion rapidly increases the strength of fast excitatory transmission and facilitates long-term potentiation in the hippocampus, two effects likely related to its memory-enhancing properties. Past studies showed that E2s facilitation of transmission involves activation of RhoA signaling leading to actin polymerization in dendritic spines. Here we report that brief exposure of adult male hippocampal slices to 1 nM E2 increases the percentage of postsynaptic densities associated with high levels of immunoreactivity for activated forms of the BDNF receptor TrkB and β1-integrins, two synaptic receptors that engage actin regulatory RhoA signaling. The effects of E2 on baseline synaptic responses were unaffected by pretreatment with the TrkB-Fc scavenger for extracellular BDNF or TrkB antagonism, but were eliminated by neutralizing antisera for β1-integrins. E2 effects on synaptic responses were also absent in conditional β1-integrin knockouts, and with inhibition of matrix metalloproteinases, extracellular enzymes that generate integrin ligands. We propose that E2, acting through estrogen receptor-β, transactivates synaptic TrkB and β1-integrin, and via mechanisms dependent on integrin activation and signaling, reversibly reorganizes the spine cytoskeleton and thereby enhances synaptic responses in adult hippocampus.
- Published
- 2016
14. In silico screening of potential agonists of a glucagon-like peptide-1 receptor among female sex hormone derivatives.
- Author
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Nedyalkova M, Robeva R, Romanova J, Yovcheva K, Lattuada M, and Simeonov V
- Abstract
Glucagon-like peptide-1 (GLP-1) is an intestinal hormone that exerts its pleiotropic effects through a specific GLP-1 receptor (GLP-1R). The hormone-receptor complex might regulate glucose-dependent insulin secretion, and energy homeostasis; moreover, it could decrease inflammation and provide cardio- and neuroprotection. Additionally, the beneficial influence of GLP-1 on obesity in women might lead to improvement of their ovarian function. The links between metabolism and reproduction are tightly connected, and it is not surprising that different estrogen derivatives, estrogen-receptor modulator (SERM) and progestins used for gonadal and oncological disorders might influence carbohydrate and lipid metabolism. However, their possible influence on the GLP-1R has not been studied. The docking scores and top-ranked poses of raloxifene were much higher than those observed for other investigated SERMs and estradiol per se. Among different studied progestins, drospirenone showed slightly higher affinity to GLP-1R. Herein, the same data set of the drugs is evaluated by molecular dynamics (MD) simulations and compared with the obtained docking result. Notably, it is demonstrated that the used docking protocol and the applied MD calculations ranked the same ligand (raloxifene) as the best one. In the present study, raloxifene might exert an allosteric influence on GLP-1R signaling, which might contribute to potential beneficial effects on metabolism and weight regulation. However, further experimental and clinical studies are needed to reveal if the GLP-1R modulation has a real biological impact.Communicated by Ramaswamy H. Sarma.
- Published
- 2024
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15. Selective ER-β agonists alleviate neuronal deficits in insulin-resistant estrogen-deficient rats.
- Author
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Bansal, S. and Chopra, K.
- Subjects
- *
RATS , *BRAIN-derived neurotrophic factor , *ESTROGEN receptors , *HIGH-fat diet , *MEMORY loss - Abstract
The present study aimed to determine the effect of estrogen receptor (ER) agonists on depression and memory impairment in insulin-resistant ovariectomized (OVX) rats. Rats underwent bilateral ovariectomy, and low-dose streptozotocin (STZ) and a high-fat diet (58% fat, 25% protein, and 17% carbohydrates as a percentage of kilocalories) were administered to induce an estrogen-deficient insulin-resistant state. After 1 week of STZ administration, rats were treated with 17β-estradiol (17βE2) and selective ER-α (propylpyrazoletriol) and ER-β (diarylpropionitrile) agonists (10 μg/kg subcutaneously). Memory was evaluated using the Morris water maze and depression using the forced swim test. Treatment with selective ER-β agonist and 17βE2 but not with selective ER-α agonist significantly modulated the neurobehavioral deficits in insulin-resistant OVX rats. These neurobehavioral parameters were further correlated with brain-derived neurotrophic factor (BDNF) levels and acetylcholinesterase (AChE) activity. Selective ER-β agonist and 17βE2 significantly modulated BDNF levels and AChE activity in insulin-resistant OVX rats. Significant increases in estradiol and uterine weight were observed in 17βE2-treated rats, but selective ER agonists did not show any effect. ER-β agonist can be an effective strategy for the mitigation of memory loss and depression in an estrogen-deficient insulin-resistant state without all of the deleterious feminizing effects that occur with the use of 17βE2. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
16. Patent Issued for Method of treating cancer using selective estrogen receptor modulators (USPTO 11951080).
- Abstract
A patent has been issued to Duke University for a method of treating estrogen receptor positive cancers of the brain. The method involves administering a compound that is represented by a specific chemical formula. The patent also mentions the challenges of treating breast cancer brain metastases due to the blood brain barrier, as well as the need for safe and effective treatments for climacteric conditions associated with estrogen deprivation. The inventors propose the use of selective estrogen receptor modulators (SERMs) as a potential treatment option. [Extracted from the article]
- Published
- 2024
17. A Pilot Study of Chemoprevention With Tamoxifen in Patients With Pre-Invasive Pancreas Mucinous Cystic Neoplasms Who Will Not Undergo Immediate Resection.
- Abstract
This document provides information about a pilot study conducted by the University of Nebraska that aims to investigate the use of tamoxifen as a chemoprevention treatment for patients with pre-invasive pancreas mucinous cystic neoplasms (MCN). The study plans to enroll up to 15 subjects who will take tamoxifen orally daily for 24 weeks. The primary goals of the study are to assess the feasibility of tamoxifen as a chemoprevention treatment and to evaluate the objective response rate using MRI. The document also includes keywords related to the study and outlines the eligibility criteria for participants. [Extracted from the article]
- Published
- 2024
18. Phase III Study of Atamestane Plus Toremifene Versus Letrozole in Advanced Breast Cancer
- Published
- 2015
19. Synthesis, biological evaluation, and stability studies of raloxifene mono- and bis-sulfamates as dual-targeting agents.
- Author
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Zaraei SO, Dohle W, Anbar HS, El-Gamal R, Leblond B, Foster PA, Al-Tel TH, Potter BVL, and El-Gamal MI
- Subjects
- Humans, Female, Estrogen Receptor alpha, Cell Line, Tumor, Enzyme Inhibitors chemistry, Steryl-Sulfatase, Estrogen Receptor Modulators, Raloxifene Hydrochloride pharmacology, Breast Neoplasms drug therapy, Sulfonic Acids
- Abstract
All three possible sulfamate derivatives of the selective estrogen receptor modulator Raloxifene (bis-sulfamate 7 and two mono-sulfamates 8-9) were synthesized and evaluated as inhibitors of the clinical drug target steroid sulfatase (STS), both in cell-free and in cell-based assays, and also as estrogen receptor (ER) modulators. Bis-sulfamate 7 was the most potent STS inhibitor with an IC
50 of 12.2 nM in a whole JEG3 cell-based assay, with the two mono-sulfamates significantly weaker. The estrogen receptor-modulating activities of 7-9 showed generally lower affinities compared to Raloxifene HCl, diethylstilbestrol and other known ligands, with mono-sulfamate 8 being the best ligand (Ki of 1.5 nM) for ERα binding, although 7 had a Ki of 13 nM and both showed desirable antagonist activity. The antiproliferative activities of the sulfamate derivatives against the T-47D breast cancer cell line showed 7 as most potent (GI50 = 7.12 µM), comparable to that of Raloxifene. Compound 7 also showed good antiproliferative potency in the NCI-60 cell line panel with a GI50 of 1.34 µM against MDA-MB-231 breast cancer cells. Stability testing of 7-9 showed that bis-sulfamate 7 hydrolyzed by desulfamoylation at a surprisingly rapid rate, initially leading selectively to 8 and finally to Raloxifene 3 without formation of 9. The mechanisms of these hydrolysis reactions could be extensively rationalized. Conversion of Raloxifene (3) into its bis-sulfamate (7) thus produced a promising drug lead with nanomolar dual activity as an STS inhibitor and ERα antagonist, as a potential candidate for treatment of estrogen-dependent breast cancer., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)- Published
- 2024
- Full Text
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20. Investigation of the potential effects of estrogen receptor modulators on immune checkpoint molecules.
- Author
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Abramenko N, Vellieux F, Veselá K, Kejík Z, Hajduch J, Masařík M, Babula P, Hoskovec D, Pacák K, Martásek P, Smetana K Jr, and Jakubek M
- Subjects
- Humans, CTLA-4 Antigen, B7-H1 Antigen, Selective Estrogen Receptor Modulators pharmacology, Programmed Cell Death 1 Receptor, Estrogen Receptor Modulators, Quercetin, Immunotherapy, Immune Checkpoint Proteins, Neoplasms therapy
- Abstract
Immune checkpoints regulate the immune system response. Recent studies suggest that flavonoids, known as phytoestrogens, may inhibit the PD-1/PD-L1 axis. We explored the potential of estrogens and 17 Selective Estrogen Receptor Modulators (SERMs) as inhibiting ligands for immune checkpoint proteins (CTLA-4, PD-L1, PD-1, and CD80). Our docking studies revealed strong binding energy values for quinestrol, quercetin, and bazedoxifene, indicating their potential to inhibit PD-1 and CTLA-4. Quercetin and bazedoxifene, known to modulate EGFR and IL-6R alongside estrogen receptors, can influence the immune checkpoint functionality. We discuss the impact of SERMs on PD-1 and CTLA-4, suggesting that these SERMs could have therapeutic effects through immune checkpoint inhibition. This study highlights the potential of SERMs as inhibitory ligands for immune checkpoint proteins, emphasizing the importance of considering PD-1 and CTLA-4 inhibition when evaluating SERMs as therapeutic agents. Our findings open new avenues for cancer immunotherapy by exploring the interaction between various SERMs and immune checkpoint pathways., (© 2024. The Author(s).)
- Published
- 2024
- Full Text
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21. Antiestrogen agents could be associated with a form of polyarticular osteoarthritis.
- Author
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Cañas CA, Varela MJ, Posso-Osorio I, Esquivel JD, Nieto-Aristizábal I, Rivera-Londoño R, Bolaños JD, and Bonilla-Abadía F
- Subjects
- Humans, Estrogen Receptor Modulators, Osteoarthritis
- Published
- 2024
- Full Text
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22. Patent Application Titled "Oral Octreotide Administered In Combination With Other Therapeutic Agents" Published Online (USPTO 20240041973).
- Subjects
PATENT applications ,INVENTORS ,NERVE tissue proteins ,SELECTIVE estrogen receptor modulators ,SOMATOTROPIN receptors ,INTERNET publishing - Abstract
The patent application titled "Oral Octreotide Administered In Combination With Other Therapeutic Agents" discusses the use of oral octreotide, a medication used to treat acromegaly, in combination with other therapeutic agents. The application provides specific dosages and formulations for the combination therapy, as well as a method of treatment that involves adjusting the dosage of oral octreotide based on blood levels of IGF-1 and clinical symptoms. The inventors support their claims with various publications and patents. This document provides detailed information on the dosages and combinations of medications used in the treatment of acromegaly. [Extracted from the article]
- Published
- 2024
23. Phase 2 Study of Low Dose Tamoxifen +/- High Dose Omega-3 Fatty Acids in Overweight Postmenopausal Women at Increased Risk for Breast Cancer.
- Abstract
The document provides information about a clinical trial, NCT06195306, which aims to evaluate the effectiveness of tamoxifen, with or without omega-3 fatty acids, in reducing the risk of breast cancer in postmenopausal women who are overweight or obese and at increased risk of developing breast cancer. The trial will investigate the effects of low dose tamoxifen and high dose omega-3 fatty acids on serum adiponectin levels, insulin resistance, insulin sensitivity, insulin secretory function, and benign breast tissue estrogen response gene index (ERGI). The study is currently in the recruitment phase and aims to enroll 66 participants. The trial is being conducted by the National Cancer Institute (NCI) and data will be shared in accordance with NIH policy. [Extracted from the article]
- Published
- 2024
24. Refining Tamoxifen Dose for Premenopausal Breast Cancer Risk Reduction (RENAISSANCE): A Phase II Single Arm Trial.
- Abstract
A clinical trial, NCT06184750, is set to begin in June 2024 and aims to evaluate the effectiveness of low-dose tamoxifen in reducing breast density in premenopausal women at higher risk for breast cancer. Tamoxifen, a selective estrogen receptor modulator, has been shown to reduce breast density and is approved for breast cancer prevention. The trial will assess the response rate to tamoxifen, changes in biomarkers, patient-reported symptoms, adherence to medication, and breast tissue-based biomarkers. It will also explore genetic factors related to tamoxifen response and breast cancer risk. The trial is estimated to enroll 200 participants and is expected to be completed by July 2027. The document provides eligibility criteria for the trial, including age, hormonal status, breast conditions, and risk eligibility for preventive medication. Exclusion criteria include certain medical conditions, medication use, and pregnancy. The trial is overseen by the National Cancer Institute in the United States. [Extracted from the article]
- Published
- 2024
25. Patent Issued for Method for the diagnosis, prognosis and treatment of prostate cancer metastasis (USPTO 11840740).
- Abstract
A patent has been issued to Inbiomotion S.L. for a method related to the diagnosis, prognosis, and treatment of prostate cancer metastasis. The invention involves determining the expression level or amplification of the c-MAF gene in a tumor sample and comparing it to a control sample. If the expression level is increased, it indicates a positive diagnosis for metastasis, relapse, or recurrence. The patent also discusses the use of various therapies, such as bisphosphonates and RANKL inhibitors, for preventing or inhibiting bone degradation in prostate cancer patients with bone metastasis. [Extracted from the article]
- Published
- 2024
26. Effect of Systemic Adjuvant Treatment on Risk for Contralateral Breast Cancer in the Women's Environment, Cancer and Radiation Epidemiology Study
- Author
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Bertelsen, Lisbeth, Bernstein, Leslie, Olsen, Jørgen H, Mellemkjær, Lene, Haile, Robert W, Lynch, Charles F, Malone, Kathleen E, Anton-Culver, Hoda, Christensen, Jane, Langholz, Bryan, Thomas, Duncan C, Begg, Colin B, Capanu, Marinela, Ejlertsen, Bent, Stovall, Marilyn, Boice, John D, Shore, Roy E, and Bernstein, Jonine L
- Subjects
Prevention ,Clinical Research ,Aging ,Breast Cancer ,Cancer ,Evaluation of treatments and therapeutic interventions ,6.1 Pharmaceuticals ,Adult ,Antineoplastic Agents ,Hormonal ,Antineoplastic Combined Chemotherapy Protocols ,Breast Neoplasms ,Case-Control Studies ,Chemotherapy ,Adjuvant ,Confounding Factors ,Epidemiologic ,Cyclophosphamide ,Doxorubicin ,Estrogen Receptor Modulators ,Female ,Fluorouracil ,Humans ,Menopause ,Methotrexate ,Middle Aged ,Multivariate Analysis ,Neoplasms ,Second Primary ,Ovary ,Radiotherapy ,Adjuvant ,Research Design ,Risk Assessment ,Tamoxifen ,Treatment Outcome ,Women's Environment ,Cancer and Radiation Epidemiology Study Collaborative Group ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
BackgroundResults from randomized trials indicate that treatment with tamoxifen or chemotherapy for primary breast cancer reduces the risk for contralateral breast cancer. However, less is known about how long the risk is reduced and the impact of factors such as age and menopausal status.MethodsThe study included 634 women with contralateral breast cancer (case patients) and 1158 women with unilateral breast cancer (control subjects) from the Women's Environment, Cancer and Radiation Epidemiology Study. The women were younger than age 55 when they were first diagnosed with breast cancer during 1985-1999. Rate ratios (RRs) and 95% confidence intervals (CIs) for contralateral breast cancer after treatment with chemotherapy or tamoxifen were assessed by multivariable adjusted conditional logistic regression analyses.ResultsChemotherapy was associated with a lower risk for contralateral breast cancer (RR = 0.57, 95% CI = 0.42 to 0.75) than no chemotherapy. A statistically significant association between chemotherapy and reduced risk for contralateral breast cancer persisted up to 10 years after the first breast cancer diagnosis and was stronger among women who became postmenopausal within 1 year of the first breast cancer diagnosis (RR = 0.28, 95% CI = 0.11 to 0.76). Tamoxifen use was also associated with reduced risk for contralateral breast cancer (RR = 0.66, 95% CI = 0.50 to 0.88) compared with no use, and the association was statistically significant for 5 years after the first diagnosis.ConclusionThe associations between chemotherapy and tamoxifen treatment and reduced risk for contralateral breast cancer appear to continue for 10 and 5 years, respectively, after the initial breast cancer is diagnosed. Ovarian suppression may have a role in the association between chemotherapy and reduced risk for contralateral breast cancer.
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- 2008
27. A combined treatment with selective androgen and estrogen receptor modulators prevents bone loss in orchiectomized rats
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M. Komrakova, G. Büchler, K. O. Böker, W. Lehmann, A. F. Schilling, P. J. Roch, S. Taudien, D. B. Hoffmann, and S. Sehmisch
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Male ,Rats, Sprague-Dawley ,Selective Estrogen Receptor Modulators ,Lumbar Vertebrae ,Endocrinology ,Estrogen Receptor Modulators ,Bone Density ,Raloxifene Hydrochloride ,Endocrinology, Diabetes and Metabolism ,Androgens ,Animals ,Orchiectomy ,Rats - Abstract
Purpose Enobosarm (EN), a selective androgen receptor modulator and raloxifene (RAL), a selective estrogen receptor modulator, have been shown to improve bone tissue in osteoporotic males. The present study evaluated the effects of a combination therapy of EN and RAL on bone properties in orchiectomized rats compared to the respective single treatments. Methods Eight-month-old male Sprague–Dawley rats were either left intact (Non-Orx) or orchiectomized (Orx). The Orx rats were divided into four groups (n = 15 each): 1) Orx, 2) EN treatment (Orx + EN), 3) RAL treatment (Orx + RAL), 4) combined treatment (Orx + EN + RAL). EN and RAL (0.4 mg and 7 mg/kg body weight/day) were applied immediately after Orx with a soy-free pelleted diet for up to 18 weeks. The lumbar spine and femora were examined by micro-CT, biomechanical, histomorphological, ashing, and gene expression analyses. Results EN exhibited an anabolic effect on bone, improving some of its parameters in Orx rats, but did not affect biomechanical properties. RAL exhibited antiresorptive activity, maintaining the biomechanical and trabecular parameters of Orx rats at the levels of Non-Orx rats. EN + RAL exerted a stronger effect than the single treatments, improving most of the bone parameters. Liver weight increased after all treatments; the kidney, prostate, and levator ani muscle weights increased after EN and EN + RAL treatments. BW was reduced due to a decreased food intake in the Orx + RAL group and due a reduced visceral fat weight in the Orx + EN + RAL group. Conclusion The EN + RAL treatment appeared to be promising in preventing male osteoporosis, but given the observed side effects on liver, kidney, and prostate weights, it requires further investigation.
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- 2022
28. Effect of Environmental Tobacco Smoke on Levels of Urinary Hormone Markers
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Chen, Changzhong, Wang, Xiaobin, Wang, Lihua, Yang, Fan, Tang, Genfu, Xing, Houxun, Ryan, Louise, Lasley, Bill, Overstreet, James W, Stanford, Joseph B, and Xu, Xiping
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Reproductive Medicine ,Biomedical and Clinical Sciences ,Tobacco Smoke and Health ,Estrogen ,Clinical Research ,Tobacco ,Prevention ,Contraception/Reproduction ,Aetiology ,2.2 Factors relating to the physical environment ,Reproductive health and childbirth ,Good Health and Well Being ,Adult ,China ,Chorionic Gonadotropin ,Environmental Exposure ,Estrogen Receptor Modulators ,Estrone ,Female ,Humans ,Longitudinal Studies ,Pregnanediol ,Tobacco Smoke Pollution ,Environmental Sciences ,Medical and Health Sciences ,Toxicology ,Biomedical and clinical sciences ,Environmental sciences ,Health sciences - Abstract
Our recent study showed a dose-response relationship between environmental tobacco smoke (ETS) and the risk of early pregnancy loss. Smoking is known to affect female reproductive hormones. We explored whether ETS affects reproductive hormone profiles as characterized by urinary pregnanediol-3-glucuronide (PdG) and estrone conjugate (E1C) levels. We prospectively studied 371 healthy newly married nonsmoking women in China who intended to conceive and had stopped contraception. Daily records of vaginal bleeding, active and passive cigarette smoking, and daily first-morning urine specimens were collected for up to 1 year or until a clinical pregnancy was achieved. We determined the day of ovulation for each menstrual cycle. The effects of ETS exposure on daily urinary PdG and E1C levels in a +/-10 day window around the day of ovulation were analyzed for conception and nonconception cycles, respectively. Our analysis included 344 nonconception cycles and 329 conception cycles. In nonconception cycles, cycles with ETS exposure had significantly lower urinary E1C levels (beta = -0.43, SE = 0.08, p < 0.001 in log scale) compared with the cycles without ETS exposure. There was no significant difference in urinary PdG levels in cycles having ETS exposure (beta = -0.07, SE = 0.15, p = 0.637 in log scale) compared with no ETS exposure. Among conception cycles, there were no significant differences in E1C and PdG levels between ETS exposure and nonexposure. In conclusion, ETS exposure was associated with significantly lower urinary E1C levels among nonconception cycles, suggesting that the adverse reproductive effect of ETS may act partly through its antiestrogen effects.
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- 2005
29. Advances in breast cancer treatment and prevention: preclinical studies on aromatase inhibitors and new selective estrogen receptor modulators (SERMs)
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Schiff, Rachel, Chamness, Gary C, and Brown, Powel H
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Breast Cancer ,Estrogen ,Aging ,Cancer ,Prevention ,6.1 Pharmaceuticals ,5.1 Pharmaceuticals ,Development of treatments and therapeutic interventions ,Evaluation of treatments and therapeutic interventions ,Animals ,Antineoplastic Combined Chemotherapy Protocols ,Aromatase Inhibitors ,Breast Neoplasms ,Drug Evaluation ,Preclinical ,Drugs ,Investigational ,Estrogen Receptor Modulators ,Humans ,Mammary Neoplasms ,Experimental ,Mice ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
Intensive basic and clinical research over the past 20 years has yielded crucial molecular understanding into how estrogen and the estrogen receptor act to regulate breast cancer and has led to the development of more effective, less toxic, and safer hormonal therapy agents for breast cancer management and prevention. Selective potent aromatase inhibitors are now challenging the hitherto gold standard of hormonal therapy, the selective estrogen-receptor modulator tamoxifen. Furthermore, new selective estrogen-receptor modulators such as arzoxifene, currently under clinical development, offer the possibility of selecting one with a more ideal pharmacological profile for treatment and prevention of breast cancer. Two recent studies in preclinical model systems that evaluate mechanisms of action of these new drugs and suggestions about their optimal clinical use are discussed.
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- 2003
30. Effects of estrogen receptor modulators on cytoskeletal proteins in the central nervous system
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Julia J Segura-Uribe, Rodolfo Pinto-Almazán, Angélica Coyoy-Salgado, Claudia E Fuentes-Venado, and Christian Guerra-Araiza
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estrogen receptor modulators ,selective estrogen receptor modulators ,microtubules ,neurofilaments ,tibolone ,tamoxifen ,raloxifene ,Neurology. Diseases of the nervous system ,RC346-429 - Abstract
Estrogen receptor modulators are compounds of interest because of their estrogenic agonistic/antagonistic effects and tissue specificity. These compounds have many clinical applications, particularly for breast cancer treatment and osteoporosis in postmenopausal women, as well as for the treatment of climacteric symptoms. Similar to estrogens, neuroprotective effects of estrogen receptor modulators have been described in different models. However, the mechanisms of action of these compounds in the central nervous system have not been fully described. We conducted a systematic search to investigate the effects of estrogen receptor modulators in the central nervous system, focusing on the modulation of cytoskeletal proteins. We found that raloxifene, tamoxifen, and tibolone modulate some cytoskeletal proteins such as tau, microtuble-associated protein 1 (MAP1), MAP2, neurofilament 38 (NF38) by different mechanisms of action and at different levels: neuronal microfilaments, intermediate filaments, and microtubule-associated proteins. Finally, we emphasize the importance of the study of these compounds in the treatment of neurodegenerative diseases since they present the benefits of estrogens without their side effects.
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- 2017
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31. Patient and Provider Web-Based Decision Support for Breast Cancer Chemoprevention: A Randomized Controlled Trial
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Katherine D. Crew, Gauri Bhatkhande, Thomas Silverman, Jacquelyn Amenta, Tarsha Jones, Julia E. McGuinness, Jennie Mata, Ashlee Guzman, Ting He, Jill Dimond, Wei-Yann Tsai, and Rita Kukafka
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Adult ,Internet ,Cancer Research ,Estrogen Receptor Modulators ,Oncology ,Humans ,Breast Neoplasms ,Female ,Middle Aged ,Chemoprevention ,Article ,Aged ,Decision Support Techniques - Abstract
Significant underutilization of breast cancer chemoprevention remains, despite guidelines stating that physicians should recommend chemoprevention with antiestrogen therapy to high-risk women. We randomized women, ages 35 to 75 years, who met high-risk criteria for breast cancer, without a personal history of breast cancer or prior chemoprevention use, to standard educational materials alone or combined with a web-based decision aid. All healthcare providers, including primary care providers and breast specialists, were given access to a web-based decision support tool. The primary endpoint was chemoprevention uptake at 6 months. Secondary outcomes included decision antecedents (perceived breast cancer risk/worry, chemoprevention knowledge, self-efficacy) and decision quality (decision conflict, chemoprevention informed choice) based upon patient surveys administered at baseline, 1 and 6 months after randomization. Among 282 evaluable high-risk women enrolled from November 2016 to March 2020, mean age was 57 years (SD, 9.9) and mean 5-year invasive breast cancer risk was 2.98% (SD, 1.42). There was no significant difference in chemoprevention uptake at 6 months between the intervention and control groups (2.1% vs. 3.5%). Comparing the intervention and control arms at 1 month, there were significant differences among high-risk women in accurate breast cancer risk perceptions (56% vs. 39%, P = 0.017), adequate chemoprevention knowledge (49% vs. 27%, P < 0.001), mean decision conflict (34.0 vs. 47.0, P < 0.001), and informed choice (41% vs. 23%, P = 0.003). These differences were no longer significant at 6 months. Although our decision support tools did not result in a significant increase in chemoprevention uptake, we did observe improvements in decision antecedents and decision quality measures. Prevention Relevance: In this randomized controlled trial of decision support for 300 high-risk women and 50 healthcare providers, we did not observe a significant increase in chemoprevention uptake, which remained low at under 5%. However, these decision support tools may increase knowledge and informed choice about breast cancer chemoprevention.
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- 2022
32. Contribution of the unfolded protein response to breast and prostate tissue homeostasis and its significance to cancer endocrine response.
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Direito, Inês, Fardilha, Margarida, and Helguero, Luisa A
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PROSTATE , *BREAST , *PROSTATE cancer , *HOMEOSTASIS , *CANCER - Abstract
Resistant breast and prostate cancers remain a major clinical problem, new therapeutic approaches and better predictors of therapeutic response are clearly needed. Because of the involvement of the unfolded protein response (UPR) in cell proliferation and apoptosis evasion, an increasing number of publications support the hypothesis that impairments in this network trigger and/or exacerbate cancer. Moreover, UPR activation could contribute to the development of drug resistance phenotypes in both breast and prostate cancers. Therefore, targeting this pathway has recently emerged as a promising strategy in anticancer therapy. This review addresses the contribution of UPR to breast and prostate tissues homeostasis and its significance to cancer endocrine response with focus on the current progress on UPR research related to cancer biology, detection, prognosis and treatment. [ABSTRACT FROM AUTHOR]
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- 2019
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33. Study Findings from University College London (UCL) Broaden Understanding of Breast Cancer (A systematic review of randomised clinical trials - The safety of vaginal hormones and selective estrogen receptor modulators for the treatment of...).
- Abstract
Keywords: Breast Cancer; Cancer; Clinical Research; Clinical Trials and Studies; DNA-Binding Proteins; Drugs and Therapies; Estrogen Receptor Modulators; Estrogen Receptors; Health and Medicine; Hormone Antagonists; Hormones; Oncology; Proteins; Risk and Prevention; Selective Estrogen Receptor Modulators; Steroid Receptors; Transcription Factors; Women's Health EN Breast Cancer Cancer Clinical Research Clinical Trials and Studies DNA-Binding Proteins Drugs and Therapies Estrogen Receptor Modulators Estrogen Receptors Health and Medicine Hormone Antagonists Hormones Oncology Proteins Risk and Prevention Selective Estrogen Receptor Modulators Steroid Receptors Transcription Factors Women's Health 1481 1481 1 10/30/23 20231103 NES 231103 2023 OCT 31 (NewsRx) -- By a News Reporter-Staff News Editor at Women's Health Weekly -- New research on breast cancer is the subject of a new report. For more information on this research see: A systematic review of randomised clinical trials - The safety of vaginal hormones and selective estrogen receptor modulators for the treatment of genitourinary menopausal symptoms in breast cancer survivors. [Extracted from the article]
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- 2023
34. The CAT Study: Atamestane Plus Toremifene Versus Letrozole in Advanced Breast Cancer
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- 2007
35. Effect of a Smart Pill Bottle Reminder Intervention on Medication Adherence, Self-efficacy, and Depression in Breast Cancer Survivors
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Hyang Rang Park, Savitri Singh-Carlson, Soo-Hyun Kim, and Hee Sun Kang
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medicine.medical_specialty ,Breast Neoplasms ,Medication Adherence ,law.invention ,Breast cancer ,Cancer Survivors ,Estrogen Receptor Modulators ,Randomized controlled trial ,law ,Internal medicine ,Intervention (counseling) ,medicine ,Humans ,Depression (differential diagnoses) ,Aromatase Inhibitors ,Depression ,Oncology (nursing) ,business.industry ,Cancer ,Antiestrogen ,medicine.disease ,Self Efficacy ,Tamoxifen ,Oncology ,Pill ,Female ,business ,medicine.drug - Abstract
BACKGROUND Globally, breast cancer has been identified as the most common cancer among women. The clinical efficacy of adjuvant oral antiestrogen therapy-including tamoxifen and aromatase inhibitors-has been proven to be clinically efficacious for breast cancer survivors. However, medication adherence for these therapies remains suboptimal among breast cancer survivors. OBJECTIVE The aim of this study was to evaluate the effect of a reminder intervention-a smart pill bottle paired with the Pillsy mobile application-on medication adherence, medication self-efficacy, and depression, among breast cancer survivors who were undergoing oral antiestrogen therapy. METHODS This study is a randomized controlled trial. Sixty-one women were allocated to an experimental group (n = 31) and the control group (n = 30). The experimental group received the reminder intervention of a smart pill bottle for 4 weeks. Study outcomes were identified as medication adherence, medication self-efficacy, and depression. RESULTS Fifty-seven women completed the follow-up measurement. Significant differences in favor of the experimental group were noted for medication adherence (P = .004) and medication self-efficacy (P = .004). There was no statistically significant difference between the 2 groups with regard to depression (P = .057). CONCLUSIONS Reminder intervention using smart pill bottles was effective in improving medication adherence and medication self-efficacy among breast cancer survivors undergoing oral antiestrogen therapy. IMPLICATIONS FOR PRACTICE A smart pill bottle method of intervention can be a useful reminder strategy to improve medication adherence among breast cancer survivors.
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- 2021
36. Endocrine resistance in breast cancer: from molecular mechanisms to therapeutic strategies
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Ozgur Sahin, Ozge Saatci, and Kim-Tuyen Huynh-Dam
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Antineoplastic Agents ,Breast Neoplasms ,P110α ,Article ,Breast cancer ,Estrogen Receptor Modulators ,Drug Discovery ,Animals ,Humans ,Medicine ,Endocrine system ,Epidermal growth factor receptor ,Mechanistic target of rapamycin ,Genetics (clinical) ,PI3K/AKT/mTOR pathway ,Tumor microenvironment ,biology ,Aromatase Inhibitors ,business.industry ,Cancer ,medicine.disease ,Receptors, Estrogen ,Drug Resistance, Neoplasm ,Cancer research ,biology.protein ,Molecular Medicine ,Female ,Neoplasm Recurrence, Local ,business - Abstract
Estrogen receptor-positive (ER+) breast cancer accounts for approximately 75% of all breast cancers. Endocrine therapies, including selective ER modulators (SERMs), aromatase inhibitors (AIs) and selective ER down-regulators (SERDs) provide substantial clinical benefit by reducing the risk of disease recurrence and mortality. However, resistance to endocrine therapies represents a major challenge, limiting the success of ER+ breast cancer treatment. Mechanisms of endocrine resistance involve alterations in ER signaling via modulation of ER (e.g., ER downregulation, ESR1 mutations or fusions); alterations in ER coactivators/corepressors, transcription factors (TFs), nuclear receptors and epigenetic modulators; regulation of signaling pathways; modulation of cell cycle regulators; stress signaling; alterations in tumor microenvironment, nutrient stress and metabolic regulation. Current therapeutic strategies to improve outcome of endocrine resistant patients in clinics include inhibitors against mechanistic target of rapamycin (mTOR), cyclin-dependent kinase (CDK) 4/6 and the Phosphoinositide 3-kinase (PI3K) subunit, p110α. Preclinical studies reveal novel therapeutic targets, some of which are currently tested in clinical trials as single agents or in combination with endocrine therapies, such as ER partial agonists, ER proteolysis targeting chimeras (PROTACs), next-generation selective estrogen receptor modulators (SERDs), AKT inhibitors, epidermal growth factor receptor 1 &2 (EGFR/HER2) dual inhibitors, HER2 targeting antibody-drug conjugates and histone deacetylase (HDAC) inhibitors. In this review, we summarize the established and emerging mechanisms of endocrine resistance, alterations during metastatic recurrence, and discuss the approved therapies and on-going clinical trials testing the combination of novel targeted therapies with endocrine therapy in endocrine-resistant ER+ breast cancer patients.
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- 2021
37. A Nursing Educational Intervention to Improve Antiestrogen Adherence and Self-Management of Side Effects
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Kaitlyn, Fishman, Brittany, Rosenthal, Mimi, Oupravanh, and Emily L, Davenport Alonso
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Estrogen Receptor Modulators ,Drug-Related Side Effects and Adverse Reactions ,Self-Management ,Humans ,Female ,Breast Neoplasms - Abstract
Antiestrogens prescribed to reduce breast cancer risk or recurrence can have undesirable musculoskeletal side effects that may lead to early discontinuation of therapy. Previous studies have not focused on nurse-led assessmen.
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- 2022
38. Role of calcium in hormone‐independent and ‐resistant breast cancer
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Mudit Kaushal, Qiaochu Wang, William Yeguech, Zeina Sharawi, Mary Beth Martin, John B Psaltis, Bassem R. Haddad, Glyn Noguchi, Kedra Cyrus, Fatima Gibrel, Tiffany Chang, and William Rydzewski
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Cancer Research ,medicine.drug_class ,Estrogen receptor ,chemistry.chemical_element ,Breast Neoplasms ,Calcium channel blocker ,Calcium ,Article ,Calcium in biology ,Estrogen Receptor Modulators ,Epidermal growth factor ,medicine ,Humans ,Cell Proliferation ,Estradiol ,Voltage-dependent calcium channel ,Chemistry ,Calcium channel ,Estrogen Receptor alpha ,Estrogens ,Calcium Channel Blockers ,Antiestrogen ,Gene Expression Regulation, Neoplastic ,Oncology ,Drug Resistance, Neoplasm ,MCF-7 Cells ,Cancer research ,Female ,Calcium Channels ,Receptors, Progesterone - Abstract
Approximately one-third of estrogen receptor (ER) positive breast tumors fail to respond to or become resistant to hormonal therapy. Although the mechanisms responsible for hormone resistance are not completely understood, resistance is associated with alterations in ERα; overexpression of proteins that interact with the receptor; and hormone-independent activation of the receptor by growth factor signal transduction pathways. Our previous studies show that in estrogen dependent breast cancer cells, activation of the epidermal growth factor signaling pathway increases intracellular calcium which binds to and activates ERα through sites in the ligand-binding domain of the receptor and that treatment with extracellular calcium increases the concentration of intracellular calcium which activates ERα and induces hormone-independent cell growth. The present study asked whether overexpression of calcium channels contributes to the hormone-independent and -resistant phenotype of breast cancer cells and whether clinically used calcium channel blockers reverse hormone independence and resistance. The results show that hormone-independent and -resistant cells overexpress calcium channels, have high concentrations of intracellular calcium, overexpress estrogen responsive genes and, as expected, grow in the absence of estradiol and that treatment with calcium channel blockers decreased the concentration of intracellular calcium, the expression of estrogen responsive genes and cell growth. More importantly, in hormone-resistant cells, treatment that combined a calcium channel blocker with an antiestrogen reversed resistance to the antiestrogen.
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- 2021
39. Gingival cell growth with antiresorptive treatment combined with corticosteroids or antiestrogen
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Tero Soukka, Eliisa Löyttyniemi, Heidi M. Ekholm, Jaana Rautava, Department of Oral and Maxillofacial Diseases, Clinicum, Faculty of Medicine, University of Helsinki, and Helsinki University Hospital Area
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bisphosphonate ,corticosteroid ,medicine.medical_treatment ,03 medical and health sciences ,0302 clinical medicine ,Estrogen Receptor Modulators ,Adrenal Cortex Hormones ,medicine ,Humans ,Viability assay ,Fibroblast ,General Dentistry ,Cell Proliferation ,Diphosphonates ,oral mucosa ,Cell growth ,business.industry ,denosumab ,RK1-715 ,Original Articles ,030206 dentistry ,Bisphosphonate ,Antiestrogen ,313 Dentistry ,3. Good health ,Denosumab ,medicine.anatomical_structure ,Cell culture ,030220 oncology & carcinogenesis ,Dentistry ,Cancer research ,antiestrogen ,Original Article ,Keratinocyte ,business ,hormones, hormone substitutes, and hormone antagonists ,medicine.drug - Abstract
Objectives: Antiresorptive treatment has been shown to impair mucosal cell proliferation, migration, and viability. However, in the clinic, antiresorptives are often used in combination with other drugs. We studied the effect of antiresorptives combined with a corticosteroid or antiestrogen on oral mucosal keratinocytes and fibroblasts. Material and methods: Human gingival keratinocyte and fibroblast cell lines were exposed to bisphosphonates (BPs) and denosumab in different concentrations and durations together with an antiestrogen or corticosteroid. Changes in cell viability, proliferation and migration after exposures were measured. Data were evaluated with hierarchical linear mixed model for repeated measurements. Results: Bisphosphonate exposure suppressed keratinocyte and fibroblast cell viability, proliferation, and migration in a time-dependent manner. Combining a corticosteroid or antiestrogen with BPs further increased this negative effect. Denosumab alone had a mild positive effect on keratinocyte and fibroblast growth. When denosumab was combined with a corticosteroid or antiestrogen, cell growth was suppressed. Conclusions: Our results show that coexisting medications may increase the negative impact of BPs or denosumab on oral mucosal cells.
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- 2021
40. First-line Treatment with Ribociclib plus Endocrine Therapy for Premenopausal Women with Hormone-receptor-positive Advanced Breast Cancer: A Cost-effectiveness Analysis
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Xin Rao, Xiaoting Huang, Hang Wang, Dayong Zeng, Shen Lin, Xiuhua Weng, and Pinfang Huang
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0301 basic medicine ,Oncology ,China ,Cancer Research ,medicine.medical_specialty ,Antineoplastic Agents, Hormonal ,Receptor, ErbB-2 ,Cost effectiveness ,Cost-Benefit Analysis ,Aminopyridines ,Breast Neoplasms ,Ribociclib ,Drug Costs ,03 medical and health sciences ,0302 clinical medicine ,Breast cancer ,Estrogen Receptor Modulators ,Internal medicine ,medicine ,Humans ,Endocrine system ,health care economics and organizations ,business.industry ,Estrogen Antagonists ,Cancer ,Cost-effectiveness analysis ,medicine.disease ,Markov Chains ,United States ,Clinical trial ,030104 developmental biology ,Premenopause ,Purines ,Hormone receptor ,030220 oncology & carcinogenesis ,Drug Therapy, Combination ,Female ,Quality-Adjusted Life Years ,business - Abstract
Background We conducted a cost-effectiveness analysis incorporating recent phase III clinical trial (MONALEESA-7) data to evaluate the cost-effectiveness of ribociclib (RIB) as a first-line treatment for premenopausal women with hormone receptor (HR)-positive and human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer (ABC) from the United States healthcare payer perspective. In addition, because RIB has not been marketed in China, we identified the range of drug costs for which RIB could be considered cost effective from a Chinese healthcare system perspective. Patients and Methods A Markov model was developed to evaluate the cost-effectiveness of adding RIB to endocrine therapy over a lifetime. The clinical outcomes and utility data were obtained from published literature. Costs data were obtained from United States and Chinese official websites, and we determined the potential price for RIB in China based on its price in the United States. The main outcomes of this study were the incremental cost-effectiveness ratio (ICER) and quality-adjusted life-years (QALYs). Results The model projected that mean outcome was better with RIB and endocrine combined (3.83366 QALYs) than with endocrine therapy alone (2.71203 QALYs). In the United States, RIB and endocrine therapy cost an additional $604,960.06, resulting in an ICER of $539,357.95/QALY compared with endocrine monotherapy. Subgroup analyses indicated that, in China, the projected mean outcomes were better for RIB and endocrine therapy (6.37 QALYs) than for endocrine monotherapy (2.71 QALYs). The corresponding incremental costs were $224,731.88943. Thus, the ICER comparing RIB and endocrine therapy with endocrine therapy alone represented a $61,454.96/QALY gain. Conclusion Additional use of RIB is estimated to not be cost effective as a first-line treatment for premenopausal women with HR-positive, HER2-negative ABC in the United States. A value-based price for the cost of RIB is less than $31.74/200 mg for China.
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- 2021
41. Glucose starvation greatly enhances antiproliferative and antiestrogenic potency of oligomycin A in MCF-7 breast cancer cells
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Mikhail A. Krasil'nikov, Danila V. Sorokin, Andrey E. Shchekotikhin, Olga A. Omelchuk, and Alexander M. Scherbakov
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Oligomycin ,Chemistry ,fungi ,AMPK ,Estrogen receptor ,Breast Neoplasms ,General Medicine ,Oxidative phosphorylation ,Biochemistry ,chemistry.chemical_compound ,Glucose ,Estrogen Receptor Modulators ,MCF-7 ,MCF-7 Cells ,Cancer research ,Humans ,Female ,Oligomycins ,Viability assay ,skin and connective tissue diseases ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Cell Proliferation - Abstract
Energy imbalance is one of the key properties of tumour cells, which in certain cases supports fast cancer progression and resistance to therapy. The simultaneous blocking of glycolytic processes and oxidative phosphorylation pathways seems to be a promising strategy for antitumor therapies. The study aimed to evaluate the effect of glucose starvation on the antiproliferative and antiestrogenic potency of oligomycin A against hormone-dependent breast cancer cells. Cell viability was assessed by the MTT test. Estrogen receptor alpha (ERα) activity was evaluated by reporter assay. mTOR, AMPK, Akt, and S6 kinase expression was assessed by immunoblotting. Glucose starvation caused multiple increases in the antiproliferative potency of oligomycin A in the hormone-dependent breast cancer MCF-7 cells, while its effect on the sensitivity of the second hormone-dependent cancer cell line, named T47D, was weak and limited. Glycolytic inhibitors, 3-bromopyruvate and 2-deoxyglucose, greatly enhanced the antiproliferative potency of oligomycin A in MCF-7 cells. Glucose starvation leads to remarkable activation of Akt in MCF-7 cells, whereas oligomycin A enhances its effect. The mTOR, S6 kinase, and AMPK signalling pathways are significantly modulated by oligomycin A under glucose starvation. Oligomycin A demonstrates more pronounced antiestrogenic effects under glucose starvation. Thus, glucose starvation and pharmacological inhibition of glycolysis are of interest for revealing the antitumor potential of macrolide oligomycin A against hormone-dependent breast cancers.
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- 2021
42. Benign Conditions Associated with a Risk for the Subsequent Development of Cancer
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Thomas, Patricia A. and Thomas, Patricia A., editor
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- 2011
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43. Clinical Translation: Targeting the Estrogen Receptor
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Ciara, Metcalfe and Jennifer O, Lauchle
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Tamoxifen ,Estradiol ,Estrogen Receptor Modulators ,Receptors, Estrogen ,Aromatase Inhibitors ,Estrogen Receptor alpha ,Humans ,Breast Neoplasms ,Female ,Neoplasm Recurrence, Local ,Fulvestrant - Abstract
Estrogen Receptor alpha (ERα) stands as one of the most successfully prosecuted drug targets in oncology, beginning with the approval of tamoxifen for women with ERα positive (ER+) breast cancer over 40 years ago. The field continued to advance with the development of aromatase inhibitors and the pure antiestrogen fulvestrant. With multiple endocrine therapies approved for the treatment of ER+ breast cancer, efforts to generate novel ERα-targeted therapeutics somewhat diminished in the early 2000s. Today however, there are at least eight new molecular entities targeting ERα under active clinical investigation, each with the aim of bringing further benefit to patients. This remarkable re-energizing of the field was spurred in part by the discovery of highly prevalent ERα mutations as a mechanism of resistance to standard-of-care therapies, which provided unequivocal evidence of the continued, and broad, dependence of tumors on ERα, despite relapsing after earlier lines of endocrine therapy. Re-engagement of the pharmaceutical and biotechnology industries with ERα as a drug target has been further underpinned by the impressive advances made in medicinal chemistry, enabling desirable mechanistic features - high potency full ERα antagonism - to be combined with improved drug-like properties - oral bioavailability and optimized pharmacokinetics. In this chapter, we describe the rich history and science behind the currently evolving landscape of ERα targeting in breast cancer.
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- 2022
44. A kinase inhibitor screen reveals MEK1/2 as a novel therapeutic target to antagonize IGF1R-mediated antiestrogen resistance in ERα-positive luminal breast cancer
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Wester, L., Venneker, S., Hazenoot, M., Pont, C.M., Koedoot, E., Timmermans, A.M., Martens, J.W.M., Jansen, M.P.H.M., Kockx, C.E.M., IJcken, W.F.J. van, Meerman, J.H.N., Zhang, Y., Water, B. van de, Medical Oncology, and Cell biology
- Subjects
Selumetinib ,EGFR ,Breast Neoplasms ,Biochemistry ,Receptor, IGF Type 1 ,Estrogen Receptor Modulators ,SDG 3 - Good Health and Well-being ,IGF1R ,Cell Line, Tumor ,Breast Cancer ,Humans ,Anaplastic Lymphoma Kinase ,Insulin-Like Growth Factor I ,Protein Kinase Inhibitors ,Pharmacology ,Mitogen-Activated Protein Kinase Kinases ,Diphenylamine ,Estrogen Antagonists ,Estrogen Receptor alpha ,MEK Inhibitors ,ErbB Receptors ,Tamoxifen ,Drug Resistance, Neoplasm ,Benzamides ,Female ,Tamoxifen Resistance - Abstract
Antiestrogen resistance of breast cancer has been related to enhanced growth factor receptor expression and activation. We have previously shown that ectopic expression and subsequent activation of the insulin-like growth factor-1 receptor (IGF1R) or the epidermal growth factor receptor (EGFR) in MCF7 or T47D breast cancer cells results in antiestrogen resistance. In order to identify novel therapeutic targets to prevent this antiestrogen resistance, we performed kinase inhibitor screens with 273 different inhibitors in MCF7 cells overexpressing IGF1R or EGFR. Kinase inhibitors that antagonized antiestrogen resistance but are not directly involved in IGF1R or EGFR signaling were prioritized for further analyses. Various ALK (anaplastic lymphoma receptor tyrosine kinase) inhibitors inhibited cell proliferation in IGF1R expressing cells under normal and antiestrogen resistance conditions by preventing IGF1R activation and subsequent downstream signaling; the ALK inhibitors did not affect EGFR signaling. On the other hand, MEK (mitogen-activated protein kinase kinase)1/2 inhibitors, including PD0325901, selumetinib, trametinib and TAK-733, selectively antagonized IGF1R signaling-mediated antiestrogen resistance but did not affect cell proliferation under normal growth conditions. RNAseq analysis revealed that MEK inhibitors PD0325901 and selumetinib drastically altered cell cycle progression and cell migration networks under IGF1R signaling-mediated antiestrogen resistance. In a group of 219 patients with metastasized ER + breast cancer, strong pMEK staining showed a significant correlation with no clinical benefit of first-line tamoxifen treatment. We propose a critical role for MEK activation in IGF1R signaling-mediated antiestrogen resistance and anticipate that dual-targeted therapy with a MEK inhibitor and antiestrogen could improve treatment outcome.
- Published
- 2022
45. Upregulation of the EGFR/MEK1/MAPK1/2 signaling axis as a mechanism of resistance to antiestrogen‑induced BimEL dependent apoptosis in ER
- Author
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Mackenzie L, Hagan, Suchreet, Mander, Carol, Joseph, Michael, McGrath, Amanda, Barrett, Allison, Lewis, William D, Hill, Darren, Browning, Meghan E, McGee-Lawrence, Haifeng, Cai, Kebin, Liu, John T, Barrett, David A, Gewirtz, Muthusamy, Thangaraju, and Patricia V, Schoenlein
- Subjects
ErbB Receptors ,Mitogen-Activated Protein Kinase 1 ,Estrogen Receptor Modulators ,Bcl-2-Like Protein 11 ,Drug Resistance, Neoplasm ,Cell Line, Tumor ,Humans ,Female ,Breast Neoplasms ,Apoptosis ,Up-Regulation - Abstract
The epidermal growth factor receptor (EGFR) is commonly upregulated in multiple cancer types, including breast cancer. In the present study, evidence is provided in support of the premise that upregulation of the EGFR/MEK1/MAPK1/2 signaling axis during antiestrogen treatment facilitates the escape of breast cancer cells from BimEL‑dependent apoptosis, conferring resistance to therapy. This conclusion is based on the findings that ectopic BimEL cDNA overexpression and confocal imaging studies confirm the pro‑apoptotic role of BimEL in ERα expressing breast cancer cells and that upregulated EGFR/MEK1/MAPK1/2 signaling blocks BimEL pro‑apoptotic action in an antiestrogen‑resistant breast cancer cell model. In addition, the present study identified a pro‑survival role for autophagy in antiestrogen resistance while EGFR inhibitor studies demonstrated that a significant percentage of antiestrogen‑resistant breast cancer cells survive EGFR targeting by pro‑survival autophagy. These pre‑clinical studies establish the possibility that targeting both the MEK1/MAPK1/2 signaling axis and pro‑survival autophagy may be required to eradicate breast cancer cell survival and prevent the development of antiestrogen resistance following hormone treatments. The present study uniquely identified EGFR upregulation as one of the mechanisms breast cancer cells utilize to evade the cytotoxic effects of antiestrogens mediated through BimEL‑dependent apoptosis.
- Published
- 2022
46. Analysis of advanced non-small cell lung cancer course during high dose antiestrogen therapy use in complex chemoradiotherapy treatment of patients
- Author
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A. V. Kadzhoian
- Subjects
Lung Neoplasms ,Tamoxifen ,Estrogen Receptor Modulators ,Pathology ,RB1-214 - Abstract
Aim. To analyze the advanced non-small cell lung cancer course during high dose antiestrogen therapy use in complex chemoradiotherapy treatment of patients. Methods and results. With the help of immunohistochemcial method the low expression of estrogen α and progesteron (1.7%) receptors but rather high expression of estrogen β receptors (50.8%) were established. Separation of patients into the groups with the presence or absence of estrogen β receptors allowed to show in clinical terms different mechanisms of action and the possibility of antiestrogen therapy use in the treatment of advanced non-small cell lung cancer. Conclusion. Effectiveness of treatment and overall survival were shown to be statistically better in patients who received high doses of tamoxifen in addition to standard treatment regimens (one-year and median survival – 48.9% and 12 months, respectively) than in patients who received only standard conservative anticancer treatment (one-year and median survival – 28.2% and 9 months, respectively), which was caused by the antiestrogenic effect of tamoxifen and its non-hormonal mechanisms of antitumor action.
- Published
- 2014
- Full Text
- View/download PDF
47. Estrogen Receptor Modulators
- Author
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Gregory R. J. Thatcher, Lauren M. Gutgesell, Kiira Ratia, and Carlo I. Rosales
- Subjects
Breast cancer ,Nuclear receptor ,business.industry ,Estrogen ,medicine.drug_class ,medicine ,Cancer research ,Endocrine therapy ,Estrogen Receptor Modulators ,medicine.disease ,business - Published
- 2021
48. New Melanoma Study Results Reported from Technical University Dresden (TU Dresden) (Therapeutic Potential of Nitric Oxide-releasing Selective Estrogen Receptor Modulators In Malignant Melanoma).
- Abstract
An ER beta-selective ER modulator with nitric oxide-releasing moiety (nitric oxide-releasing selective ER modulator 4d [NO-SERM 4d]) significantly reduced the prometastatic behavior of two melanoma cell lines (A2058 and MEL-JUSO). Keywords: Dresden; Germany; Europe; Cancer; Chemicals; DNA-Binding Proteins; Drugs and Therapies; Estrogen Receptor Modulators; Estrogen Receptors; Genetics; Health and Medicine; Hormone Antagonists; Melanoma; Nitric Oxide; Nitrogen Oxides; Oncology; Pharmaceuticals; Proteins; Reactive Nitrogen Species; Steroid Receptors; Transcription Factors EN Dresden Germany Europe Cancer Chemicals DNA-Binding Proteins Drugs and Therapies Estrogen Receptor Modulators Estrogen Receptors Genetics Health and Medicine Hormone Antagonists Melanoma Nitric Oxide Nitrogen Oxides Oncology Pharmaceuticals Proteins Reactive Nitrogen Species Steroid Receptors Transcription Factors 1219 1219 1 09/25/23 20230929 NES 230929 2023 SEP 29 (NewsRx) -- By a News Reporter-Staff News Editor at Genomics & Genetics Weekly -- Current study results on Oncology - Melanoma have been published. [Extracted from the article]
- Published
- 2023
49. Findings from Laboratorio Virtual NANOCOSMOS Provides New Data on Breast Cancer [Cdft-based Chemical Reactivity Properties Analysis of the Fluorine Substitution In the Selective Estrogen Receptor Modulator (Serm) Tamoxifen].
- Abstract
Keywords: Chihuahua; Mexico; North and Central America; Antineoplastics; Benzene Derivatives; Breast Cancer; Cancer; DNA-Binding Proteins; Drugs and Therapies; Endocrinology; Estrogen; Estrogen Receptor Modulators; Estrogen Receptors; Fluorine; Halogens; Health and Medicine; Hormone Antagonists; Hormones; Oncology; Pharmaceuticals; Pharmacokinetics; Pharmacology; Proteins; Risk and Prevention; Selective Estrogen Receptor Modulators; Steroid Receptors; Stilbenes; Tamoxifen; Tamoxifen Therapy; Transcription Factors; Women's Health EN Chihuahua Mexico North and Central America Antineoplastics Benzene Derivatives Breast Cancer Cancer DNA-Binding Proteins Drugs and Therapies Endocrinology Estrogen Estrogen Receptor Modulators Estrogen Receptors Fluorine Halogens Health and Medicine Hormone Antagonists Hormones Oncology Pharmaceuticals Pharmacokinetics Pharmacology Proteins Risk and Prevention Selective Estrogen Receptor Modulators Steroid Receptors Stilbenes Tamoxifen Tamoxifen Therapy Transcription Factors Women's Health 334 334 1 09/11/23 20230912 NES 230912 2023 SEP 12 (NewsRx) -- By a News Reporter-Staff News Editor at Women's Health Weekly -- Fresh data on Oncology - Breast Cancer are presented in a new report. Chihuahua, Mexico, North and Central America, Antineoplastics, Benzene Derivatives, Breast Cancer, Cancer, DNA-Binding Proteins, Drugs and Therapies, Endocrinology, Estrogen, Estrogen Receptors, Fluorine, Halogens, Health and Medicine, Hormone Antagonists, Estrogen Receptor Modulators, Hormones, Oncology, Pharmaceuticals, Pharmacokinetics, Pharmacology, Proteins, Risk and Prevention, Selective Estrogen Receptor Modulators, Steroid Receptors, Stilbenes, Tamoxifen, Tamoxifen Therapy, Transcription Factors, Women's Health. [Extracted from the article]
- Published
- 2023
50. The TRADE Study: A Phase 2 Trial to Assess the ToleRability of Abemaciclib Dose Escalation in Patients With Early-Stage HR-positive and HER2-negative Breast Cancer.
- Published
- 2023
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