Готові списки джерел за темами / Estrogen Receptor - Cancer Therapeutics

Добірка наукової літератури з теми "Estrogen Receptor - Cancer Therapeutics"

Автор: Grafiati
Опубліковано: 7 вересня 2023

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Статті в журналах з теми "Estrogen Receptor - Cancer Therapeutics"

1

Arterburn, Jeffrey B., and Eric R. Prossnitz. "G Protein–Coupled Estrogen Receptor GPER: Molecular Pharmacology and Therapeutic Applications." Annual Review of Pharmacology and Toxicology 63, no. 1 (January 20, 2023): 295–320. http://dx.doi.org/10.1146/annurev-pharmtox-031122-121944.

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Анотація:
The actions of estrogens and related estrogenic molecules are complex and multifaceted in both sexes. A wide array of natural, synthetic, and therapeutic molecules target pathways that produce and respond to estrogens. Multiple receptors promulgate these responses, including the classical estrogen receptors of the nuclear hormone receptor family (estrogen receptors α and β), which function largely as ligand-activated transcription factors, and the 7-transmembrane G protein–coupled estrogen receptor, GPER, which activates a diverse array of signaling pathways. The pharmacology and functional roles of GPER in physiology and disease reveal important roles in responses to both natural and synthetic estrogenic compounds in numerous physiological systems. These functions have implications in the treatment of myriad disease states, including cancer, cardiovascular diseases, and metabolic disorders. This review focuses on the complex pharmacology of GPER and summarizes major physiological functions of GPER and the therapeutic implications and ongoing applications of GPER-targeted compounds.
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2

Mitra, Saikat, Mashia Subha Lami, Avoy Ghosh, Rajib Das, Trina Ekawati Tallei, Fatimawali, Fahadul Islam, et al. "Hormonal Therapy for Gynecological Cancers: How Far Has Science Progressed toward Clinical Applications?" Cancers 14, no. 3 (February 1, 2022): 759. http://dx.doi.org/10.3390/cancers14030759.

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In recent years, hormone therapy has been shown to be a remarkable treatment option for cancer. Hormone treatment for gynecological cancers involves the use of medications that reduce the level of hormones or inhibit their biological activity, thereby stopping or slowing cancer growth. Hormone treatment works by preventing hormones from causing cancer cells to multiply. Aromatase inhibitors, anti-estrogens, progestin, estrogen receptor (ER) antagonists, GnRH agonists, and progestogen are effectively used as therapeutics for vulvar cancer, cervical cancer, vaginal cancer, uterine cancer, and ovarian cancer. Hormone replacement therapy has a high success rate. In particular, progestogen and estrogen replacement are associated with a decreased incidence of gynecological cancers in women infected with human papillomavirus (HPV). The activation of estrogen via the transcriptional functionality of ERα may either be promoted or decreased by gene products of HPV. Hormonal treatment is frequently administered to patients with hormone-sensitive recurring or metastatic gynecologic malignancies, although response rates and therapeutic outcomes are inconsistent. Therefore, this review outlines the use of hormonal therapy for gynecological cancers and identifies the current knowledge gaps.
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3

Monga, Jyoti, Niladry S. Ghosh, Somdutt Mujwar, and Isha Rani. "IN SILICO STUDIES OF SOME NEWLY DESIGNED BENZIMIDAZOLETHIAZOLIDINONE BASED ANTAGONISTS OF HUMAN ESTROGEN RECEPTOR." INDIAN DRUGS 60, no. 08 (August 28, 2023): 15–30. http://dx.doi.org/10.53879/id.60.08.14087.

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Breast cancer is globally associated with majority of the women. Indeed, high estrogen levels are the most common subtype of breast cancer. Three different classes of estrogen receptor antagonists are frequently used to treat such kinds of breast cancers. Each of these interacts directly with the initiation and activation of the estrogen signalling pathway. However, new medicines must be developed because resistance limits the therapeutic effectiveness. In silico studies for drug discovery have become popular in recent years due to their low cost and quick execution. To develop novel therapeutics for breast cancer, three different series of benzimidazole compounds targeting the estrogen receptor were docked. Among these three series, benzimidazole fused with pyrazole showed significant results and the leading compound was 32 based on docking results. The docking data was further validated by executing molecular dynamics (MD) simulations for the stability of designed leads within the macromolecular cavity in relation to time. Therefore, it is proposed that the pyrazole fused benzimidazole nucleus can be a promising pharmacophore for developing novel anticancer therapeutics for breast cancer.
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4

Chang, Minsun, Kuan-wei Peng, Irida Kastrati, Cassia R. Overk, Zhi-Hui Qin, Ping Yao, Judy L. Bolton, and Gregory R. J. Thatcher. "Activation of Estrogen Receptor-Mediated Gene Transcription by the Equine Estrogen Metabolite, 4-Methoxyequilenin, in Human Breast Cancer Cells." Endocrinology 148, no. 10 (October 1, 2007): 4793–802. http://dx.doi.org/10.1210/en.2006-1568.

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4-Methoxyequilenin (4-MeOEN) is an O-methylated metabolite in equine estrogen metabolism. O-methylation of catechol estrogens is considered as a protective mechanism; however, comparison of the properties of 4-MeOEN with estradiol (E2) in human breast cancer cells showed that 4-MeOEN is a proliferative, estrogenic agent that may contribute to carcinogenesis. 4-MeOEN results from O-methylation of 4-hydroxyequilenin, a major catechol metabolite of the equine estrogens present in hormone replacement therapeutics, which causes DNA damage via quinone formation, raising the possibility of synergistic hormonal and chemical carcinogenesis. 4-MeOEN induced cell proliferation with nanomolar potency and induced estrogen response element (ERE)-mediated gene transcription of an ERE-luciferase reporter and the endogenous estrogen-responsive genes pS2 and TGF-α. These estrogenic actions were blocked by the antiestrogen ICI 182,780. In the standard radioligand estrogen receptor (ER) binding assay, 4-MeOEN showed very weak binding. To test for alternate ligand-ER-independent mechanisms, the possibility of aryl hydrocarbon receptor (AhR) binding and ER-AhR cross talk was examined using a xenobiotic response element-luciferase reporter and using AhR small interfering RNA silencing in the ERE-luciferase reporter assay. The results negated the possibility of AhR-mediated estrogenic activity. Comparison of gene transcription time course, ER degradation, and rapid activation of MAPK/ERK in MCF-7 cells demonstrated that the actions of 4-MeOEN mirrored those of E2 with potency for classical and nonclassical estrogenic pathways bracketing that of E2. Methylation of 4-OHEN may not represent a detoxification pathway because 4-MeOEN is a full, potent estrogen agonist.
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5

Shete, Nivida, Jordan Calabrese, and Debra A. Tonetti. "Revisiting Estrogen for the Treatment of Endocrine-Resistant Breast Cancer: Novel Therapeutic Approaches." Cancers 15, no. 14 (July 17, 2023): 3647. http://dx.doi.org/10.3390/cancers15143647.

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Анотація:
Estrogen receptor (ER)-positive breast cancer is the most common subtype, representing 70–75% of all breast cancers. Several ER-targeted drugs commonly used include the selective estrogen receptor modulator (SERM), tamoxifen (TAM), aromatase inhibitors (AIs) and selective estrogen receptor degraders (SERDs). Through different mechanisms of action, all three drug classes reduce estrogen receptor signaling. Inevitably, resistance occurs, resulting in disease progression. The counterintuitive action of estrogen to inhibit ER-positive breast cancer was first observed over 80 years ago. High-dose estrogen and diethylstilbestrol (DES) were used to treat metastatic breast cancer accompanied by harsh side effects until the approval of TAM in the 1970s. After the development of TAM, randomized trials comparing TAM to estrogen found similar or slightly inferior efficacy but much better tolerability. After decades of research, it was learned that estrogen induces tumor regression only after a period of long-term estrogen deprivation, and the mechanisms of tumor regression were described. Despite the long history of breast cancer treatment with estrogen, this therapeutic modality is now revitalized due to the development of novel estrogenic compounds with improved side effect profiles, newly discovered predictive biomarkers, the development of non-estrogen small molecules and new combination therapeutic approaches.
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6

Petrie, Whitney K., Megan K. Dennis, Chelin Hu, Donghai Dai, Jeffrey B. Arterburn, Harriet O. Smith, Helen J. Hathaway, and Eric R. Prossnitz. "G Protein-Coupled Estrogen Receptor-Selective Ligands Modulate Endometrial Tumor Growth." Obstetrics and Gynecology International 2013 (2013): 1–17. http://dx.doi.org/10.1155/2013/472720.

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Endometrial carcinoma is the most common cancer of the female reproductive tract. GPER/GPR30 is a 7-transmembrane spanning G protein-coupled receptor that has been identified as the third estrogen receptor, in addition to ERαand ERβ. High GPER expression is predictive of poor survival in endometrial and ovarian cancer, but despite this, the estrogen-mediated signaling pathways and specific estrogen receptors involved in endometrial cancer remain unclear. Here, employing ERα-negative Hec50 endometrial cancer cells, we demonstrate that GPER mediates estrogen-stimulated activation of ERK and PI3K via matrix metalloproteinase activation and subsequent transactivation of the EGFR and that ER-targeted therapeutic agents (4-hydroxytamoxifen, ICI182,780/fulvestrant, and Raloxifene), the phytoestrogen genistein, and the “ERα-selective” agonist propylpyrazole triol also function as GPER agonists. Furthermore, xenograft tumors of Hec50 cells yield enhanced growth with G-1 and estrogen, the latter being inhibited by GPER-selective pharmacologic antagonism with G36. These results have important implications with respect to the use of putatively ER-selective ligands and particularly for the widespread long-term use of “ER-targeted” therapeutics. Moreover, our findings shed light on the potential mechanisms of SERM/SERD side effects reported in many clinical studies. Finally, our results provide the first demonstration that pharmacological inhibition of GPER activityin vivoprevents estrogen-mediated tumor growth.
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7

Medina, Mauricio A., Goldie Oza, Ashutosh Sharma, L. G. Arriaga, José Manuel Hernández Hernández, Vincent M. Rotello, and Jose Tapia Ramirez. "Triple-Negative Breast Cancer: A Review of Conventional and Advanced Therapeutic Strategies." International Journal of Environmental Research and Public Health 17, no. 6 (March 20, 2020): 2078. http://dx.doi.org/10.3390/ijerph17062078.

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Triple-negative breast cancer (TNBC) cells are deficient in estrogen, progesterone and ERBB2 receptor expression, presenting a particularly challenging therapeutic target due to their highly invasive nature and relatively low response to therapeutics. There is an absence of specific treatment strategies for this tumor subgroup, and hence TNBC is managed with conventional therapeutics, often leading to systemic relapse. In terms of histology and transcription profile these cancers have similarities to BRCA-1-linked breast cancers, and it is hypothesized that BRCA1 pathway is non-functional in this type of breast cancer. In this review article, we discuss the different receptors expressed by TNBC as well as the diversity of different signaling pathways targeted by TNBC therapeutics, for example, Notch, Hedgehog, Wnt/b-Catenin as well as TGF-beta signaling pathways. Additionally, many epidermal growth factor receptor (EGFR), poly (ADP-ribose) polymerase (PARP) and mammalian target of rapamycin (mTOR) inhibitors effectively inhibit the TNBCs, but they face challenges of either resistance to drugs or relapse. The resistance of TNBC to conventional therapeutic agents has helped in the advancement of advanced TNBC therapeutic approaches including hyperthermia, photodynamic therapy, as well as nanomedicine-based targeted therapeutics of drugs, miRNA, siRNA, and aptamers, which will also be discussed. Artificial intelligence is another tool that is presented to enhance the diagnosis of TNBC.
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8

Ide, Hiroki, and Hiroshi Miyamoto. "Sex Hormone Receptor Signaling in Bladder Cancer: A Potential Target for Enhancing the Efficacy of Conventional Non-Surgical Therapy." Cells 10, no. 5 (May 11, 2021): 1169. http://dx.doi.org/10.3390/cells10051169.

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There have been critical problems in the non-surgical treatment for bladder cancer, especially residence to intravesical pharmacotherapy, including BCG immunotherapy, cisplatin-based chemotherapy, and radiotherapy. Recent preclinical and clinical evidence has suggested a vital role of sex steroid hormone-mediated signaling in the progression of urothelial cancer. Moreover, activation of the androgen receptor and estrogen receptor pathways has been implicated in modulating sensitivity to conventional non-surgical therapy for bladder cancer. This may indicate the possibility of anti-androgenic and anti-estrogenic drugs, apart from their direct anti-tumor activity, to function as sensitizers of such conventional treatment. This article summarizes available data suggesting the involvement of sex hormone receptors, such as androgen receptor, estrogen receptor-α, and estrogen receptor-β, in the progression of urothelial cancer, focusing on their modulation for the efficacy of conventional therapy, and discusses their potential of overcoming therapeutic resistance.
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9

Lucà, Rossella, Giorgia di Blasio, Daniela Gallo, Valentina Monteleone, Isabella Manni, Laura Fici, Marianna Buttarelli, et al. "Estrogens Counteract Platinum-Chemosensitivity by Modifying the Subcellular Localization of MDM4." Cancers 11, no. 9 (September 12, 2019): 1349. http://dx.doi.org/10.3390/cancers11091349.

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Estrogen activity towards cancer-related pathways can impact therapeutic intervention. Recent omics data suggest possible crosstalk between estrogens/gender and MDM4, a key regulator of p53. Since MDM4 can either promote cell transformation or enhance DNA damage-sensitivity, we analysed in vivo impact of estrogens on both MDM4 activities. In Mdm4 transgenic mouse, Mdm4 accelerates the formation of fibrosarcoma and increases tumor sensitivity to cisplatin as well, thus confirming in vivo Mdm4 dual mode of action. Noteworthy, Mdm4 enhances chemo- and radio-sensitivity in male but not in female animals, whereas its tumor-promoting activity is not affected by mouse gender. Combination therapy of transgenic females with cisplatin and fulvestrant, a selective estrogen receptor degrader, was able to recover tumor cisplatin-sensitivity, demonstrating the relevance of estrogens in the observed sexual dimorphism. Molecularly, estrogen receptor-α alters intracellular localization of MDM4 by increasing its nuclear fraction correlated to decreased cell death, in a p53-independent manner. Importantly, MDM4 nuclear localization and intra-tumor estrogen availability correlate with decreased platinum-sensitivity and apoptosis and predicts poor disease-free survival in high-grade serous ovarian carcinoma. These data demonstrate estrogen ability to modulate chemo-sensitivity of MDM4-expressing tumors and to impinge on intracellular trafficking. They support potential usefulness of combination therapy involving anti-estrogenic drugs.
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10

Di Zazzo, Galasso, Giovannelli, Di Donato, Bilancio, Perillo, Sinisi, Migliaccio, and Castoria. "Estrogen Receptors in Epithelial-Mesenchymal Transition of Prostate Cancer." Cancers 11, no. 10 (September 23, 2019): 1418. http://dx.doi.org/10.3390/cancers11101418.

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Prostate cancer (PC) remains a widespread malignancy in men. Since the androgen/androgen receptor (AR) axis is associated with the pathogenesis of prostate cancer, suppression of AR-dependent signaling by androgen deprivation therapy (ADT) still represents the primary intervention for this disease. Despite the initial response, prostate cancer frequently develops resistance to ADT and progresses. As such, the disease becomes metastatic and few therapeutic options are available at this stage. Although the majority of studies are focused on the role of AR signaling, compelling evidence has shown that estrogens and their receptors control prostate cancer initiation and progression through a still debated mechanism. Epithelial versus mesenchymal transition (EMT) is involved in metastatic spread as well as drug-resistance of human cancers, and many studies on the role of this process in prostate cancer progression have been reported. We discuss here the findings on the role of estrogen/estrogen receptor (ER) axis in epithelial versus mesenchymal transition of prostate cancer cells. The pending questions concerning this issue are presented, together with the impact of the available data in clinical management of prostate cancer patients.
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Дисертації з теми "Estrogen Receptor - Cancer Therapeutics"

1

Jackson, Alexander. "Estradiol based steroid reagents : potential estrogen receptor targeted breast cancer therapeutics and diagnostics." Thesis, University of Warwick, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248833.

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2

Jetson, Rachael Rene. "Design and Development of Potential Therapeutic Agents for Use in Hormone Responsive Cancers." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1384270219.

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3

Hatchell, Esme Claire. "Insight into estrogen action in breast cancer via the study of a novel nuclear receptor corepressor : SLIRP." University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0206.

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[Truncated abstract] Breast cancer is the cause of significant suffering and death in our community. It is now estimated that the risk of developing breast cancer for an Australian woman before the age of 85 is 1 in 8, with this risk rising for unknown reasons. While mortality rates from breast cancer are falling due to increased awareness and early detection, few new treatments have been developed from an advanced understanding of the molecular basis of the disease. From decades of scientific research it is clear that estrogen (E2) has a large role to play in breast cancer. However, the basic mechanism behind E2 action in breast cancer remains unclear. E2 plays a fundamental role in breast cancer cell proliferation and is highly expressed in breast cancers, thus, it is important to understand both E2 and its receptor, the estrogen receptor (ER). The ER is a member of the nuclear receptor (NR) superfamily. The NR superfamily consists of a large group of proteins which regulate a large number of homeostatic proteins together with regulator proteins termed coregulators and corepressors. SRA (steroid receptor RNA activator) is the only known RNA coactivator and augments transactivation by NRs. SRA has been demonstrated to play an important role in mediating E2 action (Lanz et al., 1999; Lanz et al., 2003) and its expression is aberrant in many human breast tumors, suggesting a potential role in breast tumorigenesis (Murphy et al., 2000). Despite evidence that an alternative splice variant of SRA exists as a protein (Chooniedass-Kothari et al., 2004), it has been conclusively shown that SRA can function as an RNA transcript to coactivate NR transcription (Lanz et al., 1999; Lanz et al., 2002; Lanz et al., 2003). The precise mechanism by which SRA augments ER activity remains unknown. However, it is currently hypothesized that SRA acts as an RNA scaffold for other coregulators at the transcription initiation site. Several SRA stem loops have been identified as important for SRA function, including structure (STR) 1, 5 and 7 (Lanz et al., 2002; Zhao et al., 2007). Previously, I sought to identify SRA-binding proteins using a specific stem-loop structure of SRA (STR7) that was identified as both important for its coactivator function (Lanz et al., 2002) and also as a target for proteins from breast cancer cell extracts (Hatchell, 2002). From a yeast E. Hatchell Abstract iii III hybrid screen using STR7 as bait, I identified a novel protein which was named SLIRP (Patent Number: WO/2007/009194): SRA stem-Loop Interacting RNA-binding Protein (Hatchell, 2002; Hatchell et al., 2006). '...' This thesis demonstrates that SLIRP modulates NR transactivation, provides mechanistic insight into interactions between SRA, SRC-1, HSP-60 and NCoR and suggests that SLIRP may regulate mitochondrial function. These studies contribute significantly to the growing field of NR biology, and contribute more specifically to the elucidation of estrogen action in breast cancer. Furthermore, it lays a strong and exciting foundation for further studies to evaluate SLIRP as a biomarker and potential therapeutic target in hormone dependent cancers.
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4

Wei, Na. "Oestrogen receptor subtypes in ovarian cancer." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/HKUTO/record/B39558058.

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5

Stewart, Ceri Elisabeth. "Estrogen receptor beta and estrogen response in breast cancer cell lines." Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491371.

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Ced Stewart: Estrogen receptor beta and estrogen response in breast cancer cell lines Breast cancer affects 1 in 9 women in Britain and its development and treatment are greatly influenced by hormonal status, such as exposure to endogenous estrogen and expression of estrogen receptors (ERs). ERa is an established prognostic marker in breast cancer, but the role of ERp is less certain. The ERs act to regulate gene transcription via a highly complex variety of mechanisms in response to stimuli such as estrogen, tamoxifen or fulvestrant. In order to further define the role of ERp isoforms in breast cancer, their role in the estrogen response must be characterised. This thesis has used a set of four breast cancer cell lines, as well as an MCF7 cell line engineered to over-express ERpl mRNA (MCF7PIx), to investigate the role of ERp in estrogen response. Cells were - treated with a variety of stimuli (estrogen, tamoxifen, fulvestrant, epidermal growth factor and fibroblast growth factor-2) and expression of a panel of ER isoforms, estrogen responsive genes and housekeeping genes was measured using real-time, quantitative PCR. Estrogen response is cell line specific, both in terms of the genes affected and the level of response. These responses can be partly, but not fully, related to the levels of ERa expressed by the cell lines. Expression of individual ER isoforms varies in response to treatment in a time, stimulus and cell line specific manner. Different cell lines vary expression of different subsets of ER isoforms and MCF7pIx, which constitutively over-expresses ERpl mRNA, shows down-regulation of ERpl mRNA expression in response to estrogen. Together these data suggest that regulation may occur at the level of splicing and mRNA stability, as well as at the transcription level. MCF7 and MCF7P Ix showed.remarkably similar responses to treatments. In both cell lines, similar sets of genes were both up- and down-regulated by estrogenic and growth factor treatments. Most -genes showed a similar pattern of transcriptional activation at 0 to 8 h as at 24 h, except for ERpl and ERp2, indicating the importance of control of ERp expression. It was not possible to measure the levels of ERpl protein in the cells, therefore the similarity in responses in MCF7 and MCF7pIx may indicate that, despite the higher levels of ERpl rnRNA, MCF7pIx cells do not overexpress ERPI protein. Measurement of endogenous expression of a set of estrogen responsive genes in a panel of breast cancer cell lines in response to various stimuli has afforded new insights into the levelS and variation in the response achieved in this system. Expression of ERp mRNA was shown to be controlled in a cell line and treatment specific manner, as has previously been shown for ERa. Additionally, it was shown that this regulation was isofonn specific and was maintained when the ERp was overexpressed under the control of an exogenous promoter. This is particularly interesting, as it suggests various levels of regulation, indicating the important role of ERp in downstream estrogen responses. - Supplied by The British Library - 'The world's knowledge'
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6

Curran, Edward M. "Regulation of the estrogen receptor in human breast cancer cells /." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9901231.

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7

Zhang, Qiu-Xia. "Estrogen receptor gene alterations in human breast cancer." Lund : Jubileumsinstitutionen, Dept. of Oncology,Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39738537.html.

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8

Wei, Na, and 魏娜. "Oestrogen receptor subtypes in ovarian cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B39558058.

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9

Chiu, Shih-Jiuan. "Receptor-mediated DNA-based therapeutics delivery." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1127403022.

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10

Stuart, Emma, and n/a. "Therapeutic potential of SERM and EGCG drug combinations for the treatment of basal-like breast cancer." University of Otago. Department of Pharmacology & Toxicology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090708.090405.

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Basal-like breast cancer represents a subgroup of mammary cancers associated with a particularly poor prognosis, as they are refractory to current targeted therapies employed for the treatment of breast cancer. In this work I aimed to explore the therapeutic potential of selective estrogen receptor modulators (SERMs), a targeted breast cancer treatment, in combination with epigallocatechin gallate (EGCG), for the treatment of basal-like breast cancer, using MDA-MB-231 cell as an in vitro model of the disease. A significant reduction in MDA-MB-231 cell number and a significant increase in cytotoxicity was observed following treatment with 25 [mu]M of EGCG in combination with 1 [mu]M of 4-hydroxytamoxifen (4-OHT) (EGCG+4-OHT) or 4 [mu]M of raloxifene (EGCG+Ral) over a 36 h time course. However, these effects were not resolved in time, with an increase in G₁-phase cell cycle arrest. Changes in the metabolism of EGCG were dismissed as a possible mechanism through which the combination treatments may be eliciting the cytotoxicity. Changes in the expression and phosphorylation of various signaling proteins, important for the proliferation and survival of basal-like breast cancer, were investigated through Western blotting. Interestingly, the two combination treatments produced very similar results; reductions in the phosphorylation of EGFR and AKT occurred after 6, 12, and 18 h with EGCG+4-OHT and 6, 12, 18 and 24 h with EGCG+Ral, while a reduction in S6K phosphorylation was observed following 6, 12, 18 and 24 h of both combination treatments. Interestingly, both SERMs contributed significantly to the net reduction in S6K phosphorylation, induced by the combination treatments. Both combination treatments were also associated with a significant increase in the phosphorylation and total expression of stress activated protein kinases, p38 and JNK1/2 following 12, 18 and 24 h of treatment. As changes were observed at an intracellular signaling level, the effect of the combination treatments were investigated at the transcriptomic level after 18 h of treatment, using human oligonucleotide microarrays. This transcriptomic analysis revealed that both combination treatments reduced the transcript expression of five enzymes involved with cholesterol synthesis, which was confirmed through qRT-PCR. Cholesterol is an important component of the plasma membrane and is critical for the transduction of extracellular signals. Furthermore, both combination treatments induced the transcriptomic expression of the zinc coordinating metallothionein (MT) proteins. This was associated with an increased nuclear localization of MTF-1, the transcription factor responsible for MT expression, after 6, 12 and 18 h of both combination treatments. Finally, nuclear Western blotting of the NF-[kappa]B subunit, p65, revealed that both combination treatments reduced the nuclear localization of NF-[kappa]B following 6, 12 and 18 h. In collating this data, it appears that the combination treatments of EGCG+4-OHT and EGCG+Ral are inducing cytotoxicity through various mechanisms, including reduced cellular signaling through EGFR, AKT and S6K, increased stress signaling through JNK1/2 and p38 and altered gene expression of MTs and enzymes involved with cholesterol synthesis. Therefore, the combination treatment of EGCG+SERMs exhibits therapeutic potential in MDA-MB-231 cells, a model of basal-like breast cancer.
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Книги з теми "Estrogen Receptor - Cancer Therapeutics"

1

Craig, Jordan V., and Furr B. J. A, eds. Hormone therapy in breast and prostate cancer. Totowa, N.J: Humana Press, 2002.

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2

1944-, Miller William R., and Ingle James N. 1944-, eds. Endocrine therapy in breast cancer. New York: Marcel Dekker, 2002.

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3

Zhang, Xiaoting, ed. Estrogen Receptor and Breast Cancer. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99350-8.

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4

Power, Krista Anne. Selective estrogen receptor modulators in breast cancer. Ottawa: National Library of Canada, 2002.

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5

M, Berstein Lev, and Santen Richard J, eds. Innovative endocrinology of cancer. New York: Springer Science+Business Media, 2008.

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6

Moelleken, Brent Roderick Wilfred. Tamoxifen - 5-fluorouracil synergy in human breast cancer cell lines: Correlating in vitro synergy with the current estrogen receptor model. [New Haven: s.n.], 1985.

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7

Yarden, Yosef, and Moshe Elkabets, eds. Resistance to Anti-Cancer Therapeutics Targeting Receptor Tyrosine Kinases and Downstream Pathways. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67932-7.

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8

MIller/Ingle. Endocrine Therapy in Breast Cancer. Informa Healthcare, 2002.

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9

(Editor), James N. Ingle, and Mitchell Dowsett (Editor), eds. Endocrine Therapy for Breast Cancer. Informa Healthcare, 2004.

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10

Estrogen/antiestrogen action and breast cancer therapy. Madison, Wis: University of Wisconsin Press, 1986.

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Частини книг з теми "Estrogen Receptor - Cancer Therapeutics"

1

Leonard, Marissa, Juan Tan, Yongguang Yang, Mahmoud Charif, Elyse E. Lower, and Xiaoting Zhang. "Emerging Therapeutic Approaches to Overcome Breast Cancer Endocrine Resistance." In Estrogen Receptor and Breast Cancer, 379–403. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99350-8_14.

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2

McBryan, Jean, and Leonie S. Young. "Ligand-Independent Signalling Through Estrogen Receptor Pathways in Breast Cancer." In Resistance to Targeted Anti-Cancer Therapeutics, 115–44. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17972-8_7.

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3

Mir, Manzoor Ahmad, and Ulfat Jan. "Cdk4/Cdk6 Dysregulation in Estrogen-Positive Receptor Breast Cancers." In Therapeutic potential of Cell Cycle Kinases in Breast Cancer, 211–32. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-8911-7_10.

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4

Klinge, C. M. "Selective Estrogen Receptor Modulators as Therapeutic Agents in Breast Cancer Treatment." In Transcription Factors, 455–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_15.

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5

Lazennec, Gwendal. "Estrogen Receptor." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_2014-2.

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Lazennec, Gwendal. "Estrogen Receptor." In Encyclopedia of Cancer, 1633–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_2014.

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7

Lazennec, Gwendal. "Estrogen Receptor." In Encyclopedia of Cancer, 1327–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2014.

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8

Chang, Jenny, and C. Kent Osborne. "SERMs and Breast Cancer Prevention." In Selective Estrogen Receptor Modulators, 267–78. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-157-2_16.

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9

Hansen, R. K., and S. A. W. Fuqua. "The Estrogen Receptor and Breast Cancer." In Breast Cancer, 1–30. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-456-6_1.

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10

Encarnacion, Carlos A., and Suzanne A. W. Fuqua. "Estrogen receptor variants in breast cancer." In Cancer Treatment and Research, 97–109. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2592-9_6.

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Тези доповідей конференцій з теми "Estrogen Receptor - Cancer Therapeutics"

1

Price, Meghan, Catherine Lavau, Cesar Baeta, Jovita Byemerwa, Suzanne Wardell, Olivia Brueckner, Debarati Mukherjee, et al. "Abstract P131: The role of UDP-6 glucose dehydrogenase (UGDH) in estrogen-mediated phenotypes in both estrogen receptor positive and estrogen receptor negative breast cancer." In Abstracts: AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; October 7-10, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1535-7163.targ-21-p131.

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2

Cherian, Mathew, Jharna Datta, Mahmoud Kassem, Natalie Willingham, Jasmine Manouchehri, Joel David, Mirisha Sheth та ін. "Abstract 5158: Estrogen receptor β agonists: A novel therapeutic strategy for breast cancer". У Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5158.

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3

Parashar, Deepak, Anjali Geethadevi, Jyotsna Mishra, Bindu Nair, Bindu Santhamma, Klaus Nickisch, and Pradeep Chaluvally-Raghavan. "Abstract A195: A novel selective estrogen receptor degrader, EC-372, inhibits tumor growth and metastasis of breast cancer cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a195.

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4

Barlaam, Bernard, Jason Breed, Rodrigo J. Carbajo, Eric Gangl, Samantha Hughes, Christopher J. Morrow, Thomas A. Moss, et al. "Abstract A107: Small Molecule Degraders of the Estrogen Receptor (SERDs): Optimization of the tricyclic indole scaffold beyond AZD9496." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-a107.

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5

Singh, Kriti, Ravi SN Munuganti, Miriam Butler, Artem Cherkasov та Paul S. Rennie. "Abstract PD6-7: In-silico discovery of novel estrogen receptor-α inhibitors as potential therapeutics for tamoxifen resistant breast cancer". У Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-pd6-7.

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6

Darimont, Beatrice, Steven Govek, James Joseph, Katherine Grillot, Eric Bischoff, Anna Aparicio, Celine Bonnefous, et al. "Abstract A133: A novel class of selective estrogen receptor degraders regresses tumors in preclinical models of endocrine-resistant breast cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a133.

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7

Okuhira, Keiichiro, Yosuke Demizu, Takayuki Hattori, Nobumichi Ohoka, Norihito Shibata, Tomoko Nishimaki-Mogami, Haruhiro Okuda, Masaaki Kurihara, and Mikihiko Naito. "Abstract B255: Development of hybrid small molecules that induce degradation of estrogen receptor-alpha and necrotic cell death in breast cancer cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b255.

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8

Samayoa, C., NK Krishnegowda, R. Vadlamudi та RR Tekmal. "Abstract P3-04-03: Investigating the therapeutic use of estrogen receptor β agonists in breast cancer". У Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p3-04-03.

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9

Liang, Yayun, and Salman Hyder. "Abstract P139: An estrogen receptor beta agonist liquiritigenin potentiates inhibition of hormone-dependent breast-cancer growth by cholesterol biosynthesis inhibitor RO 48-8071." In Abstracts: AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; October 7-10, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1535-7163.targ-21-p139.

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10

Meng, Ran, Heng Yuan Tang, Shaker A. Mousa, Mary K. Luidens, Faith B. Davis, Paul J. Davis, Hung Yun Lin та Aleck A. Hercbergs. "Abstract C146: In human lung carcinoma cells that contain estrogen receptor-α(ER), thyroid hormone-induced proliferation initiated at an integrin requires ER." У Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c146.

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Звіти організацій з теми "Estrogen Receptor - Cancer Therapeutics"

1

Wuttke, Deborah S. Breast Cancer Therapeutics, Environmental Estrogens, and the Estrogen Receptor (ER); Characterization of the Diverse Ligand Binding Properties of the ER. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408777.

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2

Wuttke, Deborah S. Breast Cancer Therapeutics, Environmental Estrogens, and the Estrogen Receptor (ER); Characterization of the Diverse Ligand Binding Properties of the ER. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada420485.

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3

Burgess, Richard R. Estrogen-Related Receptor Alpha (ERRa)-Coactivator Interactions as Targets for Discovery of New Anti-Breast Cancer Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada452545.

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4

Burgess, Richard R. Estrogen-related Receptor alpha (ERR (alpha))-Coactivator Interactions as Targets for Discovery of New Anti-breast Cancer Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada572642.

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5

Burgess, Richard R. Estrogen-Related Receptor alpha (ERR (alpha))-Coactivator Interactions as Targets for Discovery of New Anti-Breast Cancer Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada469959.

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6

Greene, Geoffrey. Multidomain Assembly of Nuclear Estrogen Receptors: Structural Insights into ER-Positive Breast Cancer Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada562255.

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7

Greene, Geoffrey. Multi-Domain Assembly of Nuclear Estrogen Receptors: Structural Insights into ER-Positive Breast Cancer Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580416.

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8

Wuttke, Deborah S. Breast Cancer Therapeutics, Environmental Estrogens, and the Estrogens Receptor (ER); Characterization of the Diverse Ligand Binding Properties of the ER. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada398995.

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9

Greene, Geoffrey L. Estrogen Receptor Accessory Factors in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359619.

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10

Adami, Hans-Olov G., and Landegran. Estrogen Receptor Gene Polymorphisms and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, December 2000. http://dx.doi.org/10.21236/ada392392.

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