Literatura científica selecionada sobre o tema "Estrogen Therapeutic use"
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Artigos de revistas sobre o assunto "Estrogen Therapeutic use"
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Fillit, Howard. "Future Therapeutic Developments of Estrogen Use." Journal of Clinical Pharmacology 35, no. 9S (September 1995): 25S—28S. http://dx.doi.org/10.1002/j.1552-4604.1995.tb04144.x.
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Martin-Jiménez, Cynthia, Diana Milena Gaitán-Vaca, Natalia Areiza, Valentina Echeverria, Ghulam Md Ashraf, Janneth González, Amirhossein Sahebkar, Luis Miguel Garcia-Segura, and George E. Barreto. "Astrocytes Mediate Protective Actions of Estrogenic Compounds after Traumatic Brain Injury." Neuroendocrinology 108, no. 2 (November 4, 2018): 142–60. http://dx.doi.org/10.1159/000495078.
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Traumatic brain injury (TBI) is a serious public health problem. It may result in severe neurological disabilities and in a variety of cellular metabolic alterations for which available therapeutic strategies are limited. In the last decade, the use of estrogenic compounds, which activate protective mechanisms in astrocytes, has been explored as a potential experimental therapeutic approach. Previous works have suggested estradiol (E2) as a neuroprotective hormone that acts in the brain by binding to estrogen receptors (ERs). Several steroidal and nonsteroidal estrogenic compounds can imitate the effects of estradiol on ERs. These include hormonal estrogens, phytoestrogens and synthetic estrogens, such as selective ER modulators or tibolone. Current evidence of the role of astrocytes in mediating protective actions of estrogenic compounds after TBI is reviewed in this paper. We conclude that the use of estrogenic compounds to modulate astrocytic properties is a promising therapeutic approach for the treatment of TBI.
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Santen, Richard J., Risa Kagan, Corrado J. Altomare, Barry Komm, Sebastian Mirkin, and Hugh S. Taylor. "Current and Evolving Approaches to Individualizing Estrogen Receptor-Based Therapy for Menopausal Women." Journal of Clinical Endocrinology & Metabolism 99, no. 3 (March 1, 2014): 733–47. http://dx.doi.org/10.1210/jc.2013-3680.
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Context: Adding progestogens to estrogens changes the risk profile of hormonal therapy for menopausal women, and recent data support the need for progestogen-free options. Several current and evolving approaches to managing estrogen deficiency allow for progestogen omission. We review the mechanisms of estrogen activity and provide an overview of emerging and available estrogen receptor (ER)–based therapies. Evidence Acquisition: PubMed was searched for relevant English-language articles using keywords pertaining to estrogen deficiency, menopause, hormone therapy, and estrogen-only therapy. Pivotal or recent randomized controlled trials, large observational studies, comprehensive meta-analyses, and established therapeutic guidelines were compiled. Evidence Synthesis: Advances in our understanding of ER pharmacology have led to therapies designed to optimize ER activity, including selective ER modulators (SERMs) and tissue-selective estrogen complexes (TSECs). Each estrogen, SERM, and TSEC exhibits a unique profile of tissue-specific activity, spanning the spectrum from ER agonism to antagonism. Systemic estrogens unopposed by progestogens effectively manage menopausal symptoms in hysterectomized postmenopausal women but require progestogen use in postmenopausal women with a uterus. SERMs are effective for managing certain aspects of estrogen deficiency in postmenopausal women, but data suggest that pairing a SERM with estrogens to form a TSEC provides a more optimal therapeutic profile for women with a uterus. Conclusions: Treating signs and symptoms of estrogen deficiency requires an individualized approach based on a woman's goals and the purported risks of different therapies. New and emerging agents have demonstrated efficacy in postmenopausal women with a uterus, while allowing these women to avoid progestogens and their possible adverse effects.
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Macciò, Antonio, and Clelia Madeddu. "Obesity, Inflammation, and Postmenopausal Breast Cancer: Therapeutic Implications." Scientific World JOURNAL 11 (2011): 2020–36. http://dx.doi.org/10.1100/2011/806787.
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Breast cancer is the female malignant neoplasia with the highest incidence in the industrialized world. Although early diagnosis has contributed to therapeutic success, breast cancer remains a major health issue. In the last few year the hormone therapy for estrogen-dependent breast cancer has evolved achieving significant clinical results; at the same time, it has enabled us to better define the role of estrogens in the etiopathogenesis of this tumour. Weight increase and obesity have been identified as the most important risk and prognostic factors for breast cancer in postmenopausal women. Several hypotheses have been proposed to explain the association of obesity with postmenopausal breast cancer. Specific obesity-associated factors, including leptin, insulin and inflammatory mediators, seem to influence breast cancer growth and prognosis independently of estrogens and at least in part by interacting with estrogen signalling at a cellular level. Therefore, a careful assessment of the nutritional status and body composition is paramount for a proper therapeutic approach for postmenopausal breast carcinoma. The use of antidiabetic and anti-inflammatory drugs associated with conventional hormone therapies and dietary/physical interventions could offer a new therapeutic approach for breast carcinoma that develops in the context of adiposity.
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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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Gérard, Céline, Mélanie Mestdagt, Ekaterine Tskitishvili, Laudine Communal, Anne Gompel, Elisabete Silva, Jean-François Arnal, et al. "Combined Estrogenic and Antiestrogenic Properties of Estetrol on Breast Cancer may provide a Safe Therapeutic Window for the Treatment of Menopausal Symptoms." Journal of SAFOMS 3, no. 1 (2015): 31–33. http://dx.doi.org/10.5005/jsafoms-3-1-31.
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Abstract Increased risk of breast cancer is a critical side-effect associated with the use of a menopausal hormone therapy (MHT). Estetrol (E4) is a natural estrogen produced by the human fetal liver and is a promising compound for clinical use in MHT. However, its impact on breast cancer is controversial and poorly defined. In this preclinical study, we show that E4 acts as a weak estrogen by stimulating the growth of hormone-dependent breast cancer only at concentrations exceeding menopausal therapeutic needs. Estetrol (E4) presents also an antitumor activity by decreasing the strong proliferative effect of estradiol (E2). While estrogen receptor alpha (ERá) is the predominant receptor mediating its effects, the dual weak-estrogenic/antiestrogenic feature of E4 results from differential signaling pathways activation. Both nuclear and rapid extranuclear signaling pathway are necessary for a complete estrogenic effect of E4. However, the antitumor action of E4 is not due to a capacity to antagonize E2-induced nuclear activity. Altogether, our results highlight that E4 has a limited impact on breast cancer and may offer a safe therapeutic window for the treatment of menopausal symptoms.
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Hwang, Wu Jeong, Tae Young Lee, Nahrie Suk Kim, and Jun Soo Kwon. "The Role of Estrogen Receptors and Their Signaling across Psychiatric Disorders." International Journal of Molecular Sciences 22, no. 1 (December 31, 2020): 373. http://dx.doi.org/10.3390/ijms22010373.
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Increasing evidence suggests estrogen and estrogen signaling pathway disturbances across psychiatric disorders. Estrogens are not only crucial in sexual maturation and reproduction but are also highly involved in a wide range of brain functions, such as cognition, memory, neurodevelopment, and neuroplasticity. To add more, the recent findings of its neuroprotective and anti-inflammatory effects have grown interested in investigating its potential therapeutic use to psychiatric disorders. In this review, we analyze the emerging literature on estrogen receptors and psychiatric disorders in cellular, preclinical, and clinical studies. Specifically, we discuss the contribution of estrogen receptor and estrogen signaling to cognition and neuroprotection via mediating multiple neural systems, such as dopaminergic, serotonergic, and glutamatergic systems. Then, we assess their disruptions and their potential implications for pathophysiologies in psychiatric disorders. Further, in this review, current treatment strategies involving estrogen and estrogen signaling are evaluated to suggest a future direction in identifying novel treatment strategies in psychiatric disorders.
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Zhao, Zhuo, Hao Wang, Jewell A. Jessup, Sarah H. Lindsey, Mark C. Chappell, and Leanne Groban. "Role of estrogen in diastolic dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 5 (March 1, 2014): H628—H640. http://dx.doi.org/10.1152/ajpheart.00859.2013.
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The prevalence of left ventricular diastolic dysfunction (LVDD) sharply increases in women after menopause and may lead to heart failure. While evidence suggests that estrogens protect the premenopausal heart from hypertension and ventricular remodeling, the specific mechanisms involved remain elusive. Moreover, whether there is a protective role of estrogens against cardiovascular disease, and specifically LVDD, continues to be controversial. Clinical and basic science have implicated activation of the renin-angiotensin-aldosterone system (RAAS), linked to the loss of ovarian estrogens, in the pathogenesis of postmenopausal diastolic dysfunction. As a consequence of increased tissue ANG II and low estrogen, a maladaptive nitric oxide synthase (NOS) system produces ROS that contribute to female sex-specific hypertensive heart disease. Recent insights from rodent models that mimic the cardiac phenotype of an estrogen-insufficient or -deficient woman (e.g., premature ovarian failure or postmenopausal), including the ovariectomized congenic mRen2.Lewis female rat, provide evidence showing that estrogen modulates the tissue RAAS and NOS system and related intracellular signaling pathways, in part via the membrane G protein-coupled receptor 30 (GPR30; also called G protein-coupled estrogen receptor 1). Complementing the cardiovascular research in this field, the echocardiographic correlates of LVDD as well as inherent limitations to its use in preclinical rodent studies will be briefly presented. Understanding the roles of estrogen and GPR30, their interactions with the local RAAS and NOS system, and the relationship of each of these to LVDD is necessary to identify new therapeutic targets and alternative treatments for diastolic heart failure that achieve the cardiovascular benefits of estrogen replacement without its side effects and contraindications.
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Farkas, Szidónia, Adrienn Szabó, Anita Emőke Hegyi, Bibiána Török, Csilla Lea Fazekas, Dávid Ernszt, Tamás Kovács, and Dóra Zelena. "Estradiol and Estrogen-like Alternative Therapies in Use: The Importance of the Selective and Non-Classical Actions." Biomedicines 10, no. 4 (April 6, 2022): 861. http://dx.doi.org/10.3390/biomedicines10040861.
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Estrogen is one of the most important female sex hormones, and is indispensable for reproduction. However, its role is much wider. Among others, due to its neuroprotective effects, estrogen protects the brain against dementia and complications of traumatic injury. Previously, it was used mainly as a therapeutic option for influencing the menstrual cycle and treating menopausal symptoms. Unfortunately, hormone replacement therapy might be associated with detrimental side effects, such as increased risk of stroke and breast cancer, raising concerns about its safety. Thus, tissue-selective and non-classical estrogen analogues have become the focus of interest. Here, we review the current knowledge about estrogen effects in a broader sense, and the possibility of using selective estrogen-receptor modulators (SERMs), selective estrogen-receptor downregulators (SERDs), phytoestrogens, and activators of non-genomic estrogen-like signaling (ANGELS) molecules as treatment.
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Sulaymanova, R. T. "EXPERIMENTAL MODELS OF TRANSGENERATIONAL EFFECTS OF THE INFLUENCE OF ESTROGENS ON THE MORPHOLOGY OF REPRODUCTIVE ORGANS IN POSTNATAL ONTOGENESIS." Morphological newsletter 27, no. 1 (March 30, 2019): 36–44. http://dx.doi.org/10.20340/mv-mn.19(27).01.36-44.
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In the modern clinical practice there is an increase in the use of hormones, their analogues and substances with hormone-like action in medical practice for the regulation of the menstrual cycle, conception, prevention, maintenance and resolution of pregnancy. According to official reports, in recent years, the number of annual cycles of assisted reproductive technology with hormonal support has increased six times in the country. The purpose of the review is to summarize current data on the effects of experimental and clinical effects of various doses of estrogens and drugs with estrogenic effects during the period of prenatal development on the morphology of the reproductive organs of the offspring in postnatal ontogenesis. The materials for the meta-analysis of the data were the results of relevant studies of domestic and foreign authors and their own published data. The article summarizes current data demonstrating the effects of experimental effects of various doses of estrogen and drugs with an estrogenic effect during the period of prenatal development on the morphology of the reproductive organs of the offspring in postnatal ontogenesis. The data on therapeutic, subtoxic and toxic doses of the effects of estrogen preparations in various experimental models are summarized, causing latent and morphologically manifested changes in the reproductive organs of the offspring.
Teses / dissertações sobre o assunto "Estrogen Therapeutic use"
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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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Dennis, Maxine Elizabeth. "Oestrogen and atherosclerosis." University of Western Australia. School of Pathology and Laboratory Medicine, 2009. http://theses.library.uwa.edu.au/adt-WU2009.0134.
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[Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a negative effect of hormone replacement therapy (HRT) on cardiovascular disease (CVD) risk amongst postmenopausal women. It is important to determine how a hormone with numerous positive effects on intermediate pathways of atherosclerosis fails to offer cardioprotection. Further investigation into the actions of oestrogen in the vasculature may add to our current understanding of the pathogenesis of atherosclerosis and oestrogen biology. The primary aim of this thesis was to investigate involvement of the oestrogen receptors (ERs) in atherosclerotic CVD and to provide further insight into the actions of oestrogen on the vasculature by studying the actions of oestrogen on the regulation of an oestrogen-responsive gene within human vascular cells. Following confirmation of ERa and ERß expression at the RNA and protein level in human aorta sections, correlations of receptor expression with age and atherosclerosis were examined. Significantly strong negative relationships of ERa, androgen receptor (AR), and progesterone receptor (PR) with age in both males and females were detected. No trend was detected between ERß expression and age. These findings suggest that the receptor-mediated actions of hormones in the vasculature may change with age. Further, this thesis compared for the first time sex hormone receptor expression in normal and adjacent atherosclerotic aortic tissue providing a critical assessment of receptor differences due to atherosclerosis. Results revealed reductions of all hormone receptors in early atherosclerotic versus normal aorta tissue. ... These results suggest that the 3'-UTR SNPS may have more of an influence on carotid thickening when oestrogen levels are lower, suggesting the importance of both genetic variation of the ERß gene and oestrogen status on carotid thickening. Finally, this was the first study to investigate oestrogen-induced regulation of angiotensinogen (AGT), a candidate gene for CVD, in human vascular cells. Oestrogen influenced AGT transcription in a cell specific manner. The overall influence of oestrogen on AGT transcription in the vasculature is unknown. This thesis adds to the knowledge of oestrogen and atherosclerosis by suggesting the involvement of the sex hormone receptors (ERa, ERß, PR and AR) in atherosclerosis, presenting ERß as a potentially important candidate gene for atherosclerosis, revealing interactions between estrogen status and associations of ERß SNPs with carotid thickening, and demonstrating vascular cell-specific actions of oestrogen on the regulation of a candidate gene for CVD. These factors may have contributed to the lack of cardio-protection following HRT, as revealed by large clinical trials.
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Benz, David James. "Estrogenic and androgenic regulation of human osteoblast-like cells is mediated by specific steroid receptors." Diss., The University of Arizona, 1991. http://hdl.handle.net/10150/185442.
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The effectiveness of estrogen replacement therapy in the prevention of postmenopausal osteoporosis has led to its current widespread use throughout the United States and much of Western Europe, and recently, clinical correlations between circulating androgen levels and structural bone integrity have been presented. Nevertheless, the biochemical mechanism through which estrogens and androgens act to protect and maintain bone has remained unclear. One possibility is that these hormones directly modulate the activity of cells responsible for bone formation. Therefore, studies were conducted to examine the effects of sex steroids on human osteoblast-like cells. In the first set of experiments, a finite human cell line was established from trabecular bone explants obtained from a 48 year-old woman. These cells, designated BG688, were characterized as osteoblast-like in phenotype using several independent criteria. In addition to classical osteoblast markers, BG688 cells also possess approximately 2400 high affinity (K(d) = 0.45nM) 17-β estradiol (E₂) binding sites per cell. The binding of E₂ to a subset of these sites was specific. BG688 cells were also shown to respond to a physiological concentration (10nM) of E₂, which elicits pleiotropic changes in several mRNA levels including a 2-fold increase in the steady state concentration of α₁(I)-procollagen mRNA. These results indicate that human osteoblast-like cells respond to E₂ via a receptor mediated mechanism, but that, unlike the reproductive tissues, osteoblasts are a less sensitive target. In the second series of experiments, the effects of androgenic hormones on the osteoblast-like, human osteosarcoma cell line, HOS TE85 were evaluated. Employing radiolabelled dihydrotestosterone (DHT), 2800 saturable, high-affinity (K(d) = 0.66nM) androgen binding sites were detected per HOS TE85 cell. Androgen binding was specific. The expression of androgen receptors in HOS TE85 cells was further substantiated by Northern analysis. Physiological concentrations of DHT and testosterone decreased HOS TE85 cell proliferation. This finding suggests that androgens may also play a role in osteoblast differentiation. In support of this hypothesis, treatment with testosterone enhanced the abundance of both α₁ (I)-procollagen mRNA and transforming growth factor- β mRNA. The non-aromatizable androgen DHT also elicited an increase in the steady state concentration of α₁(I)-procollagen mRNA. The findings presented herein are significant within the field of bone cell biology in that they demonstrate that osteoblasts are a target cell for the action of sex steroids, via their cognate, high-affinity receptors. These results also have important implications within the broader context of bone pathophysiology in that they suggest a direct modulation of bone forming and bone remodeling activity by sex steroids.
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Amaral, Sandra Margarida Caldas. "Estrogen receptor dependent genetic and epigenetic factors of tamoxifen resistance." Doctoral thesis, Faculdade de Ciências Médicas. Universidade Nova de Lisboa, 2009. http://hdl.handle.net/10362/5038.
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Resumo: A decisão da terapêutica hormonal no tratamento do cancro da mama baseiase
na determinação do receptor de estrogénio alfa por imunohistoquímica (IHC). Contudo, a presença deste receptor não prediz a resposta em todas as situações, em parte devido a limitações do método IHC. Investigámos se a expressão dos genes ESR1 e ESR2, bem como a metilação dos respectivos
promotores, pode estar relacionada com a evolução desfavorável de uma proporção de doentes tratados com tamoxifeno assim como com a perda dos receptores de estrogénio alfa (ERα) e beta (ERß). Amostras de 211 doentes com cancro da mama diagnosticado entre 1988 e 2004, fixadas em formalina
e preservadas em parafina, foram utilizadas para a determinação por IHC da presença dos receptores ERα e ERß. O mRNA total do gene ESR1 e os níveis específicos do transcrito derivado do promotor C (ESR1_C), bem como
dos transcritos ESR2_ß1, ESR2_ß2/cx, and ESR2_ß5 foram avaliados por Real-time PCR. Os promotores A e C do gene ESR1 e os promotores 0K e 0N do gene ESR2 foram investigados por análise de metilação dos
dinucleotidos CpG usando bisulfite-PCR para análise com enzimas de restrição, ou para methylation specific PCR. Atendendo aos resultados promissores relacionados com a metilação do promotor do gene ESR1,
complementamos o estudo com um método quantitativo por matrix-assisted
laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS)
suportado pelo software Epityper para a medição da metilação nos promotores A e C. Fez-se a avaliação da estabilidade do mRNA nas linhas celulares de cancro da mama MCF-7 e MDA-MB-231 tratadas com actinomicina D. Baixos níveis do transcrito ESR1_C associaram-se a uma melhor sobrevivência global (p = 0.017). Níveis elevados do transcrito ESR1_C associaram-se a uma resposta inferior ao tamoxifeno (HR = 2.48; CI 95% 1.24-4.99), um efeito mais pronunciado em doentes com tumores de
fenótipo ERα/PgR duplamente positivo (HR = 3.41; CI 95% 1.45-8.04). A isoforma ESR1_C mostrou ter uma semi-vida prolongada, bem como uma estrutura secundária da região 5’UTR muito mais relaxada em comparação
com a isoforma ESR1_A. A análise por Western-blot mostrou que ao nível da 21 proteína, a selectividade de promotores é indistinguivel. Não se detectou qualquer correlação entre os níveis das isoformas do gene ESR2 ou entre a metilação dos promotores do gene ESR2, e a detecção da proteína ERß. A metilação do promotor C do gene ESR1, e não do promotor A, foi
responsável pela perda do receptor ERα. Estes resultados sugerem que os níveis do transcrito ESR1_C sejam usados como um novo potencial marcador para o prognóstico e predição de resposta ao tratamento com
tamoxifeno em doentes com cancro da mama. Abstract: The decision of endocrine breast cancer treatment relies on ERα IHC-based
assessment. However, ER positivity does not predict response in all cases in part due to IHC methodological limitations. We investigated whether ESR1 and ESR2 gene expression and respective promoter methylation may be related to non-favorable outcome of a proportion of tamoxifen treated patients as well as to ERα and ERß loss. Formalin-fixed paraffin-embedded breast
cancer samples from 211 patients diagnosed between 1988 and 2004 were submitted to IHC-based ERα and ERß protein determination. ESR1
whole mRNA and promoter C specific transcript levels, as well as ESR2_ß1,
ESR2_ß2/cx, and ESR2_ß5 transcripts were assessed by real-time PCR. ESR1 promoters A and C, and ESR2 promoters 0N and 0K were investigated by CpG methylation analysis using bisulfite-PCR for restriction analysis, or methylation specific PCR. Due to the promising results related to ESR1
promoter methylation, we have used a quantification method by matrixassisted
laser desorption/ionization time-of-flight mass spectrometry (MALDITOF MS) together with Epityper software to measure methylation at promoters A and C. mRNA stability was assessed in actinomycin D treated MCF-7 and MDA-MB-231 cells. ERα protein was quantified using transiently
transfected breast cancer cells. Low ESR1_C transcript levels were associated with better overall survival (p = 0.017). High levels of ESR1_C transcript were associated with non-favorable response in tamoxifen treated patients (HR = 2.48; CI 95% 1.24-4.99), an effect that was more pronounced
in patients with ERα/PgR double-positive tumors (HR = 3.41; CI 95% 1.45-8.04). The ESR1_C isoform had a prolonged mRNA half-life and a more relaxed 5’UTR structure compared to ESR1_A isoform. Western-blot analysis showed that at protein level, the promoter selectivity is undistinguishable.
There was no correlation between levels of ESR2 isoforms or ESR2 promoter
methylation and ERß protein staining. ESR1 promoter C CpG methylation and not promoter A was responsible for ERα loss. We propose ESR1_C levels as a putative novel marker for breast cancer prognosis and prediction of
tamoxifen response.
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Papich, Sandra G. (Sandra Gene). "Estrogen Replacement Therapy and its Association with Life Satisfaction of Women over Fifty." Thesis, University of North Texas, 1991. https://digital.library.unt.edu/ark:/67531/metadc500948/.
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This study analyzed the effects of estrogen replacement therapy (ERT), ethnicity, marital status, education level, maternal status and financial security on the perceived life satisfaction of women over fifty. Information was collected from 125 subjects at an independent school district. The instrument was adapted from a life satisfaction scale originally developed by B. Neugarten. Eight demographic items included ERT use, age, menopause status, marital status, educational level, ethnicity and perception of financial security. Statistical analysis consisting of one way analysis of variance, Student Newman-Keuls ad hoc procedure and multiple regression indicated an independent correlation between financial security and education level to life satisfaction scores. Neither ERT nor menopause status was correlated with perceived life satisfaction score of respondents.
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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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Visser, Jacobus Albertus Koch. "Phytoestrogenic extracts of Cyclopia modulate molecular targets involved in the prevention and treatment of breast cancer." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86718.
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Thesis (PhD)--Stellenbosch University, 2014.<br>ENGLISH ABSTRACT: Phytoestrogen containing extracts of Cyclopia, an indigenous South African fynbos plant used to prepare honeybush tea, may serve as a source of new estrogen analogues. It would be of great benefit if these new analogues would not only prevent the development and progression of breast cancer which, globally, is responsible for the highest number of cancer associated deaths among females, but also have a reduced side-effect profile when compared to current treatments and, in addition, also alleviate menopause associated symptoms. In this study three extracts, P104, SM6Met, and cup-of-tea, from two species of Cyclopia, C. genistoides and C. subternata, were evaluated for their potential to modulate molecular targets involved in prevention and treatment of breast cancer. We show that the phytoestrogenic extracts of Cyclopia antagonise estrogen-induced cell proliferation both in vitro as well as in vivo. Furthermore, our study presents various molecular mechanisms whereby the Cyclopia extracts may be eliciting this effect. Importantly, we show, for the first time, that the Cyclopia extracts behave as ERα antagonists and ERβ agonists which, with respect to the known role of the ER subtypes in breast cancer, where the ERα subtype is associated with the stimulation of cell proliferation and the occurrence of breast cancer, while ERβ ameliorates the action of ERα in breast cancer and could act as an inhibitor of breast cancer development, may be beneficial for the prevention or treatment of breast cancer. In addition, we also show that the extracts of Cyclopia behave as selective estrogen receptor degraders by down-regulating ERα protein levels while stabilising ERβ protein levels, which not only provides a possible molecular explanation for the observed ERα antagonism and ERβ agonism, but, in addition, may be beneficial as higher ERα levels are associated with malignant breast cancer tumours, while higher ERβ levels are associated with benign tumours. Furthermore, we show that the Cyclopia extracts affect the nuclear localization and distribution of both ER subtypes in a manner that provides an additional molecular explanation for the observed ERα antagonism and ERβ agonism. Investigation of the molecular processes involved in the promotion and progression of breast cancer, such as the distribution of cells between the phases of the cell cycle, cancer cell invasion, and the regulation of genes governing these processes provides evidence that the Cyclopia extracts are not as proliferative as estrogen. In addition, Cyclopia extracts display anti-inflammatory properties, which may be beneficial as inflammation is an enabling characteristic in cancer development and progression. Furthermore, this study, for the first time, shows that the phytoestrogenic extracts of Cyclopia are absorbed, are not toxic, and display biological ERα antagonist activity in vivo by retarding uterine growth. Thus, we propose that the Cyclopia extracts act as selective estrogen receptor subtype modulators with potential to be developed as a nutraceutical for the treatment or prevention of breast cancer.<br>AFRIKAANSE OPSOMMING: Fitoëstrogeen-bevattende ekstrakte van Cyclopia, ‘n inheemse Suid Afrikaanse fynbosplant wat gebruik word vir die voorbereiding van heuningbostee, mag as ‘n bron van nuwe estrogeen-analoë dien. Dit sal baie voordelig wees indien hierdie nuwe analoë nie net die ontwikkeling en progressie van borskanker sal voorkom nie, aangesien borskanker wêreldwyd verantwoordelik is vir die grootste getal kankerverwante sterftes onder vroue, maar ook ‘n verminderde newe-effek profiel vertoon in vergelyking met huidige behandelings en ook, boonop, simptome wat met menopouse geassosieer word, sal verlig. In hierdie studie is drie ekstrakte, P104, SM6Met, en cup-of-tea, vanaf twee spesies van Cyclopia, C. genistoides en C. subternata, geëvalueer vir hul potensiaal om die molekulêre teikens betrokke by die voorkoming en behandeling van borskanker te moduleer. Ons wys dat die fitoëstrogeniese ekstrakte van Cyclopia antagoniseer estrogeen-geïnduseerde selproliferasie beide in vitro as ook in vivo. Verder bied ons studie ook verkskeie molekulêre meganismes aan oor hoe die Cyclopia ekstrakte hierdie effek mag ontlok. ‘n Belangrike bevinding is dat ons vir die eerste keer wys dat die Cyclopia ekstrakte hulself as ERα -antagoniste en ERβ-agoniste gedra wat, met betrekking tot die erkende rol van die ER-subtipes in borskanker, waar die ERα-subtipe geassosieer word met die stimulasie van selproliferasie en die gebeurtenis van borskanker, terwyl ERβ die aksie van ERα onderdruk en as ‘n inhibeerder van borskankerontwikkeling kan dien, voordelig mag wees vir die voorkoming of behandeling van borskanker. Ons wys boonop ook dat die ekstrakte van Cyclopia hulself soos selektiewe estrogeen- reseptor-degradeerders gedra deurdat hul ERα-proteïnvlakke verlaag terwyl hul ERβ-proteïnvlakke stabiliseer. Dit verksaf nie net ‘n moontlike molekulêre verduideliking vir die waargeneemde ERα-antagonisme en ERβ-agonisme nie, maar mag ook voordelig wees in borskanker aangesien hoër ERα-vlakke geasosieer word met kwaadaardige borskankertumors en hoër ERβ-vlakke met nie-kwaadaardige tumors. Verder wys ons dat die Cyclopia ekstrakte die lokalisering en verspreiding van beide ER-subtipes in die selkern op so ‘n wyse beïnvloed dat dit ‘n addisionele molekulêre verduideliking bied vir die ERα-antagonisme en ERβ-agonisme wat waargeneem is. Verdere ondersoek van die molekulêre prosesse betrokke by die promosie en progressie van borskanker, soos die verspreiding van selle tussen die fases van die selsiklus, die beweging van kankerselle na omliggende weefsels, en die regulering van gene wat hierdie prosesse beheer, verskaf bewyse dat die Cyclopia-ekstrakte nie so proliferatief is soos estrogeen nie. Die ekstrakte van Cyclopia vertoon boonop ook anti-inflamatoriese eienskappe, wat voordelig mag wees aangesien inflammasie ‘n bydraende eienskap in kankerontwikkeling en -progressie is. Verder wys hierdie studie vir die eerste keer dat die fitoëstrogeniese ekstrakte van Cyclopia geabsorbeer word, nie toksies is nie, en dat hulle biologiese ERα-antagonis aktiwiteit vertoon deurdat hulle uterus-groei vertraag in vivo. Dus stel ons voor dat die Cyclopia-ekstrakte optree soos selektiewe-estrogeen-reseptor-subtipe-moduleerders met die potensiaal om ontwikkel te word as ‘n nutraseutiese middel vir die behandeling of voorkoming van borskanker.
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Wu, Wing Man. "An investigation into the neuroprotective effects of estrogen and progesterone in a model of homocysteine-induced neurodegeration." Thesis, Rhodes University, 2006. http://hdl.handle.net/10962/d1003284.
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Homocysteine (Hcy) is a sulfur containing amino acid and is a potent neurotoxin. It has been shown that elevated levels of Hcy, termed hyperhomocysteinemia, plays a role in the pathologies of Alzheimer’s disease (AD) and age-related cognitive decline. Hcy is a glutamate agonist, which causes in increase in Ca[superscript (2+)] influx via the activation of NMDA class of excitatory amino acid receptors, which results in neuronal cell death and apoptosis. Estrogen and progesterone are female hormones that are responsible for reproduction and maternal behaviour. However, in the last decade, it is evident that both female hormones have neuroprotective properties in many animal models of neurodegeneration. Collectively, both estrogen and progesterone reduce the consequences of the oxidative stress by enhancing the antioxidant defence mechanisms, reducing excitotoxicity by altering glutamate receptor activity and reducing the damage caused by lipid peroxidation. However, the mechanisms by which estrogen and progesterone provide such neuroprotection probably depend on the type and concentration of hormone present. Moreover, numerous studies have shown that hormone replacement therapy (HRT, estrogen and progestins) or estrogen-only replacement therapy (ERT) may prevent or delay the onset of AD and improve cognition for women with AD. Clinical trials have also shown that women taking HRT may modify the effects of Hcy levels on cognitive functioning. Oxidative stress increases in the aging brain and thus has a powerful effect on enhanced susceptibility to neurodegenerative disease. The detection and measurement of lipid peroxidation and superoxide anion radicals in the brain tissue supports the involvement of free radical reactions in neurotoxicity and in neurodegenerative disorders. The hippocampus is an important region of the brain responsible for the formation of memory. However, agents that induce stress in this area have harmful effects and could lead to dementia. This study aims to investigate and clarify the neuroprotective effects of estrogen and progesterone, using Hcy-induced neurodegenerative models. The initial studies demonstrate that estrogen and progesterone have the ability to scavenge potent free radicals. Histological studies undertaken reveal that both estrogen and progesterone protect against Hcy-induced neuronal cell death. In addition, immunohistochemical investigations show that Hcy-induced apoptosis in the hippocampus can be inhibited by both estrogen and progesterone. However, estrogen also acts at the NMDA receptor as an agonist, while progesterone blocks at the NMDA receptor. These mechanisms reduce the ability of Hcy to cause damage to neurons, since Hcy-induced neurotoxicity is dependent on the overstimulation of the NMDA receptor. SOD and GPx are important enzymatic antioxidants which can react with ROS and neutralize them before these inflict damage in the brain. Hcy can increase oxidative stress by inhibiting expression and function of these antioxidants. However, it has been shown that the antioxidant abilities of both estrogen and progesterone can up-regulate the activities of SOD and GPx. These results provide further evidence that estrogen and progesterone act as antioxidants and are free radical scavengers. The discovery of neuroprotective agents is becoming important as accumulating evidence indicates the protective role of both estrogen and progesterone in Hcy-induced neurodegeneration. Thus further work in clinical trials is needed to examine whether reducing Hcy levels with HRT can become the treatment of neurodegenerative disorders, such as Alzheimer’s disease.
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Kampen, Diane L. "The relationship between estrogen and memory in healthy postmenopausal women and women in the early stages of Alzheimer's disease." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41108.
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The effects of exogenous estrogen administration on aspects of memory and cognition in women were examined in two studies. In Study 1, women receiving estrogen replacement therapy were compared to untreated women on four measures of verbal memory. Those receiving estrogen had significantly better scores on a measure of delayed memory for propositional material. In Study 2, women in the early stages of Alzheimer's Disease (AD) were administered either estrogen or placebo on a double-blind basis for six months. Women given estrogen showed improvement on a measure of verbal memory and spatial attention compared to the placebo controls. The combined results of these studies provide evidence that estrogen enhances aspects of verbal memory in both healthy postmenopausal women and in postmenopausal women in the early stages of AD as measured by neuropsychological tests. These effects might be mediated by actions of estrogen on neuronal morphology and physiology in brain areas important for memory and cognition.
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Phillips, Susana M. (Susana Maria). "The relationship between sex steroid levels and memory functions in women." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28513.
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Memory function was examined in association with sex hormone levels in women. The results of the first study suggest that self-reports of memory problems were especially prevalent among women attending a menopause clinic compared to a nonpatient sample. In the following investigation, women given placebo after undergoing a bilateral oophorectomy showed decreases in memory performance, specifically on a paired-associate learning task, coincident with declines in estrogen levels. Significant improvements were found in estrogen-treated women pre- to postoperatively in the immediate recall of paragraphs, in association with supraphysiological estrogen levels. A final study on naturally-cycling women found a decline in visual memory performance during the menstrual compared to the luteal phase of the cycle. Visual memory scores were positively correlated with progesterone levels whereas paired-associate recall scores were positively associated with estradiol levels during the luteal phase. These results suggest that certain aspects of memory covary with changes in sex steroid levels in some women.
Livros sobre o assunto "Estrogen Therapeutic use"
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The estrogen decision: A self-help program. Los Altos, Calif: Westchester Pub. Co., 1994.
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R, Bartos James, ed. Estrogens: Production, functions and applications. Hauppauge, NY: Nova Science, 2009.
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Farley, Dixie. How to take your medicine: Estrogens. [Rockville, Md: Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, Office of Public Affairs, 1993.
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Farley, Dixie. Cómo tomar las medicinas: Los estrógenos. [Rockville, Md. (5600 Fishers Lane, Rockville 20857): Departamento de Salud y Servicios Sociales, Servicio de Salud Pública, Administración de Drogas y Alimentos, Oficina de Asuntos Públicos, 1991.
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Farley, Dixie. Cómo tomar las medicinas: Los estrógenos. [Rockville, Md. (5600 Fishers Lane, Rockville 20857): Departamento de Salud y Servicios Sociales, Servicio de Salud Pública, Administración de Drogas y Alimentos, Oficina de Asuntos Públicos, 1991.
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Nachtigall, Lila. Estrogen: Revised and Expanded. New York: HarperPerennial, 1991.
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Henkel, Gretchen. Making the estrogen decision. New York: Fawcett Columbine, 1993.
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Henkel, Gretchen. Making the estrogen decision. Los Angeles: Lowell House, 1992.
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Making the estrogen decision. New York: Fawcett Columbine, 1992.
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Nachtigall, Lila. Estrogen. 2nd ed. New York: HarperPerennial, 1995.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Estrogen Therapeutic use"
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Oettel, M. "Therapeutic Use of Estrogens in Veterinary Medicine." In Handbook of Experimental Pharmacology, 603–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60107-1_27.
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Espino y Sosa, Salvador, Myriam Cortés Fuentes, Jacobo Alejandro Gómez Rico, and Manuel Cortés Bonilla. "Non-polymeric Microspheres for the Therapeutic Use of Estrogens: An Innovative Technology." In Estrogen. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.82553.
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Trombetta, Giulia, Monica Della Martina, Martina Venier, and Angelo Cagnacci. "Hormonal Replacement Therapy After Neoplasia Treatment." In NEOPLASIA and FERTILITY, 175–86. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050141122010012.
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Post-menopausal hormonal therapy (HT) may help to improve quality of life and prevent long-term consequences of estrogen deficiency. The use of HT in postmenopausal cancer survivors is controversial, particularly for those women having survived hormone-dependent tumors, like breast or gynecological cancers. Endometrial cancer is the most frequent gynecological cancer. The limited data of the literature on women having suffered from endometrial cancer do not show an increased recurrence or death with HT use, but guidelines do not yet indicate the generalized use of HT in these women. HT should be avoided in uterine sarcomas. Breast cancer survivors suffer from climacteric symptoms after menopause or as a consequence of adjuvant hormonal anti-estrogen treatment. The risk of cancer recurrence with HT is uncertain: the two randomized prospective controlled trials were prematurely stopped. Actually, clinical guidelines contraindicate HT use in breast cancer survivors. New therapeutic approach for selected symptoms such as ospemifene (a SERM molecule) can be promising. There is no strong evidence for denying HT to patients treated for ovarian cancer, independently of disease stage. Even for women with an endometrioid carcinoma of the ovary, an estrogen-sensitive tumor, evidence indicates no harm from HT. More controversial is the use of HT after granulosa cell tumors. HT can be administered in women treated for squamous cancers of the cervix and the vulva or vaginal neoplasm. The approach to cervical adenocarcinoma should follow that of endometrial cancer. In conclusion, HT is not contraindicated in all women with a history of gynecological cancer, but its use is dependent on the type of cancer the woman has suffered from.
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Fidalgo, Javier, Ana Novo Barros, and Ana Casas. "Resveratrol: Apromising Antiaging Agent for Cosmetic Skin Treatments." In Resveratrol - Recent Advances, Application, and Therapeutic Potential [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107860.
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Nowadays, resveratrol, a polyphenolic phytoalexin is increasingly included in the formulas of cosmetic products and dermatology as an active ingredient, as a consequence of the well-known health beneficial properties, namely antioxidant, anti-inflammatory, anti-viral and anti-bacterial effects. This important compound can be biosynthesized naturally by plants or by industrial synthetic processes. Apart from its anti-inflammatory and antioxidant effects, a broad spectrum of effects has been attributed to the use of this compound such as anti-aging, skin-whitening, anti-angiogenic, collagen I and III stimulation (in fibroblasts) and estrogen-like effects, as well as the ability to protect cells against hydrogen peroxide-induced oxidative stress and UV-irradiation-mediated cell death. In cosmetology and dermatology has been popular because of its ability to penetrate the skin barrier and its anti-aging activity. In fact, resveratrol as an important impact on the regulation of inflammation and, as consequence, repair-related processes in skin. Furthermore, when administered either topically or orally has been proven to be safe and also to overcome the skin barrier. This review will focus in its potential application on melasma treatment and in photo-aging. Resveratrol chemistry, pharmacology, mechanism of action and evidence of its efficacy as photo skin aging protector and its potential use in melasma is discussed.
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Ramasamy, Kumaraguruparan, Cathy Samayoa, Naveen Krishnegowda, and Rajeshwar R. Tekmal. "Therapeutic Use of Estrogen Receptor β Agonists in Prevention and Treatment of Endocrine Therapy Resistant Breast Cancers: Observations From Preclinical Models." In Progress in Molecular Biology and Translational Science, 177–94. Elsevier, 2017. http://dx.doi.org/10.1016/bs.pmbts.2017.08.002.
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Yousuf, Hanna. "Role of Estrogens in Addiction-Related Learning." In Estrogens and Memory, 456–74. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190645908.003.0027.
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Females exhibit more vulnerability to cocaine abuse compared to males. Sexually dimorphic patterns of cocaine seeking have been observed in both humans and rodents during the different stages of the addiction cycle. While cocaine pharmacokinetics play a minimal role in driving sex differences in addictive behaviors, hormonal influences may be responsible for the reinforcing properties of cocaine in females. In particular, 17β-estradiol (E2), enhances performance in a variety of learning paradigms and may act to enhance the formation of drug-related learning. Paradoxically, preclinical work demonstrates that the memory-enhancing effects of E2 may also aid to suppress cocaine seeking via extinction training. In addition to discussing how E2 mediates cocaine use in females, this chapter provides neurobiological mechanisms underlying E2’s influence on cocaine addiction. Finally, this chapter discusses potential strategies for novel therapeutic interventions for female cocaine addicts.
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Hubbard, W. J., and I. H. Chaudry. "The Use of Estrogen for the Treatment of Traumatic Brain Injury." In New Therapeutics for Traumatic Brain Injury, 161–77. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-802686-1.00010-9.
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Goswami, Nandini, Shalini Jain, and Sreemoyee Chatterjee. "Nutritive Importance and Medicinal Properties of Foeniculum vulgare Mill. (Fennel) and Trachyspermum ammi L. (Ajwain)." In Therapeutic Implications of Natural Bioactive Compounds, 135–54. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815080025122030010.
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In tropical and sub-tropical countries, spices have a long history in traditional food preparations. Several spices are described to have medicinal effects. Among them are Foeniculum vulgare Mill. and Trachyspermum ammi L. belonging to the Apiaceae family are the most common spices known for their highly aromatic nature and flavor with culinary and traditional uses. F. vulgare seeds increase urine flow, improve the digestive system, promote menstruation and improve milk flow. Various pharmacological activities of F. vulgare such as antioxidant, hepatoprotective, antimicrobial, estrogenic, acaricidal, antihirutism, antidiabetic, anti-inflammatory, and antithrombotic, have been reported in the literature. T. ammi seeds are used for relieving flatulence, dyspepsia, spasmodic disorders, common cold, acute pharyngitis, sore and congested throat, dipsomania, and hysteria. T. ammi seeds are reported to possess antimicrobial, antioxidant, hepatoprotective, nematicidal, antihelmintic, and gastroprotective activities. The review presents an overview of the traditional uses, phytochemical constituents, and pharmacological properties of F. vulgare and T. ammi seeds.
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Hussain, Syed Faisal Jahir, Mohammed Adil A., Durga Munireddy, and Ashok Kumar Kumar Pandurangan. "Effects of Nigella sativa and Its Active Ingredient Thymoquinone on Breast Cancer." In Handbook of Research on Natural Products and Their Bioactive Compounds as Cancer Therapeutics, 249–63. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-9258-8.ch012.
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Breast cancer (BC) is the most prevalent malignancy in women. The main treatment for BC is surgery and chemotherapy. Generally, the chemotherapeutic drugs used for treatment cause numerous side effects. Substances derived from natural products have proven to exhibit anti-cancer effects without causing side effects. For instance, biochannin A found in cabbage and cauliflower reduced the growth of estrogen dependent MCF 7 cells. Another example is curcumin present in turmeric exhibits anti-proliferative and inhibitory effect against BC. The active compound of Nigella sativa is thymoquinone. The oil extracted from Nigella sativa reduced blood pressure. Nigella sativa exerts anti-pyritic, anti-inflammatory, and anti-microbial activity. Thymoquinone is found in seeds of Nigella sativa. Thymoquinone is a promising anti-neoplastic, anti-carcinogenic, anti-proliferative agent. In this chapter, the authors emphasize the anticancer potential of Nigella sativa and its derivatives and the mechanism of action against BC.
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Sadik, Saabira Banu Sahubar, Prathibha Sivaprakasam, Nishanthi Ramasami, and Ashok Kumar Pandurangan. "The Molecular Mechanisms Involved in Suppressing Triple Negative Breast Cancer Using Natural Agents." In Handbook of Research on Natural Products and Their Bioactive Compounds as Cancer Therapeutics, 45–71. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-9258-8.ch003.
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Breast cancer is an aggressive and primary cause of death among women globally. Triple negative breast cancer (TNBC) is one of the sub types of breast cancer. TNBC lacks the expression of progesterone receptor (PR), estrogen receptor (ER), and human epidermal factor 2 (HER2), which leads to poor diagnosis resulting in lack of targeted therapies. On the other hand, natural products are also cost efficient, non-toxic, and abundantly available in nature. Natural products have also been reported to exert various pharmacological activities including cardioprotective, anti-diabetic, antimicrobial, anti-inflammatory, etc. In this chapter, summarization of 12 well known natural products such as chebulinic acid, maslinic acid, apigenin, piperlongumine, Liquiritigenin, berberine, icariin, bufalin, which are targeted against TNBC through regulation of different pathways, and their mechanism are briefly explained. These natural products are already used to treat various diseases at the preclinical level and also have shown to have effective anti-tumor effect and can act as potent anti-TNBC agents.
Trabalhos de conferências sobre o assunto "Estrogen Therapeutic use"
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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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Ramasamy, Kumaraguruparan, Cathy Samayoa, Naveen K. Krishnegowda, Ratna K. Vadlamudi та Rajeshwar R. Tekmal. "Abstract 3616: Potential therapeutic use of Estrogen Receptor β agonist in the prevention and progression of breast cancer using HER-2/neu mouse model". У Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3616.
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Ferreri, Suzanne, and Yi-Xian Qin. "Alteration of Bone’s Nonlinear Elastic and Viscoelastic Nanomechanical Properties Is Triggered by Low Intensity Pulsed Ultrasound." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206711.
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Dynamic mechanotransduction, particularly under high frequency, low amplitude signals, has been proven effective in mediating bone loss and improving mechanical strength for tissues affected by estrogen deficient osteopenia. Ultrasound, which behaves as an alternating pressure wave in bone, may offer an effective, non-invasive technology for delivery of anabolic signals. In vitro, dynamic mechanical signals delivered using ultrasound have been shown to increase osteoblast proliferation [1], and in vivo studies have established ultrasound as an effective treatment for delayed and non-union fractures [2]. Previously, we showed that ultrasound signals similar to those currently used in a clinical setting for fracture healing were effective in mediating decreases in bone volume and mechanical strength at the millimeter length-scale in response to estrogen deficient osteopenia [3]. Due to bone’s inherent viscoelasticity and the dynamic nature of the applied ultrasound signals, it is particularly important to consider both elastic and viscous components of bone’s adaptive response to applied loads. In light of these findings, the goal of this study was to determine the role of therapeutic ultrasound signal intensity in modulating changes in bone’s nanoscale elastic and viscoelastic material properties associated with estrogen deficient osteopenia. We hypothesize that bone is sensitive to dynamic mechanical signals delivered via ultrasound and that bone’s tissue level nano-scale material properties, particularly nonlinear viscoelastic properties, are sensitive to ultrasound signal intensity.
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Lima, Beatriz Alves, Andressa da Silva Pereira, Bruna Alves Lima, Diana Gonçalves Lima, Leonardo Ferreira Pucci, Renato Moraes Ferreira, Tiago Castro Ferreira, and Henrique Ferreira Pucci. "PREDICTORS OF BREAST CANCER PROGNOSIS BASED ON TUMOR BIOMARKERS." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2022.
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Objective: To analyze the tumor biological markers of breast cancer associated with the prognostic of the disease. Methodology: A systematic review was carried out on the Scielo, PubMed, and the National Cancer Institute databases on the topic. Descriptors used were: tumor biomarkers, breast cancer, and prognosis. Thus, 15 articles published between 2001 and 2020 were selected. Results: Breast cancer, characterized by the disordered multiplication of breast cells, is the most incident in women in the world, representing 24.2% of the total cases in 2018, and the most frequent cause of death in this gender. Accordingly, tumor markers are complementary tests for early diagnosis, since they are macromolecules derived from the tumor and biological fluids. The evaluation of tumor markers is of paramount importance due to the great diversity in clinical progression of breast cancer, for example, those hormone receptors (estrogen and progesterone), MIB-1, Ki-67, PCNA, p53, and c-erbB-2. Hence, about two-thirds of breast cancers are positive for hormone receptors and are related to a more favorable prognosis. PCNA (36 kDa protein perceptible in the cell nucleus from the late G1 to the S phase of the cell cycle) and MIB-1 (direct antibody against parts of the Ki-67 antigen) have a high proportion of tumor cells associated with a high-degree tumor differentiation, indicating a worse prognosis. Furthermore, mutations in the p53 and c-erbB-2 genes report low levels of estrogen and progesterone receptors, leading to a worse prognosis. Conclusion: In brief, the recognition of the main markers helps in the identification of patients with potentially aggressive tumors and in the mortality reduction of breast cancer, through treatments that can alter the course of the disease. On account of this, it is known that the tumor markers must be used in combination with the other methods such as diagnostic, prognostic, and therapeutic modifications.
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Nunes, Mirella Laranjeira, Carlos Eduardo Caiado Anunciação, Vidianna Barbosa Sampaio, Rossano Robério Fernandes Araújo, Cinthya Roberta Santos de Jesus, Ana Leide Guerra dos Santos, Bruno Pacheco Pereira, and João Esberard de Vasconcelos Beltrão Neto. "OCCULT PRIMARY BREAST CARCINOMA: A CASE REPORT." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2049.
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Introduction: Occult breast carcinoma (OBC) is the histologically proven axillary lymph node (LN) metastasis, consistent with primary breast cancer, with no identifiable primary site. It is most commonly found in women above 60 years. Owing to the absence of protocols, management is challenging. According to the National Comprehensive Cancer Network (NCCN), the therapeutic options are mastectomy plus lymphadenectomy with or without radiotherapy, or lymphadenectomy with breast irradiation with or without axillary irradiation. Mastectomy is often used, but advances in neoadjuvant chemotherapy have made the survival between mastectomy and conservative breast management same. The prognosis is controversial, with lymph node (LN) involvement being the main factor. Case Report: A 45-year-old female presents with suspicious palpable right axillary lesion at level 1 topography of 2.5 cm size on the physical examination. No breast mass was palpable. Mammography was BIRADS classification 1. Breast and axillar ultrasound done 2 months before showed benign findings on the left side and axillary LN of 2.3 cm and breast nodule of 1.1 cm × 0.9 cm on the right side. Core-needle biopsy showed fibroadenoma in the right-sided breast nodule and metastatic carcinoma in the axillary LN. Immunohistochemistry expression of the markers was consistent with breast origin and was progesterone and estrogen receptors positive and HER-2 negative. Magnetic resonance imaging (MRI) showed this atypical LN with 1.5 cm. Clinical staging is T0N1M0. Neoadjuvant chemotherapy was performed with Adriamycin, cyclophosphamide, and paclitaxel. There was tumor remission with another MRI and ultrasonography showing the node metastasis with 1 cm. Right radical mastectomy was performed. Anatomopathology showed cytoarchitectural changes due to chemotherapy, complete pathological response in the LN, and immunohistochemistry unchanged. In addition, tumorectomy were performed in the left-sided nodule, with anatomopathology showing ductal ectasia and histiocitary abscess. Radiotherapy at the supraclavicular area and tangents was performed, and tamoxifen was prescribed. The patient remained cancer free for 2 years after surgery.
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Santos, Catharine Coelho, Camila Santos Farabotti, Pedro Santos Gomes, Luiz Henrique Gebrim, and André Santos Mattar. "IMMUNOHISTOCHEMICAL PROFILE STRATIFIED IN AGE RANGE IN11,326 PATIENTS FROM THE BRAZILIAN UNIFIED HEALTH SYSTEM (SUS) IN SÃO PAULO." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1047.
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Introduction: The development of breast cancer is heterogeneous and there are variations in its morphologic and biological characteristics. Several risk factors for breast cancer have already been identified, including the age group. It is wellestablished that the incidence of breast cancer increases from the age of 65. Older patients are more likely to have tumors which are positive estrogen receptors (ER) and progesterone receptors (RP) and, HER2 negative, which are associated with better outcomes. In contrast, younger patients with triple-negative breast cancer and HER2 positive are associated with reduced survival and poor prognosis. Objectives: To evaluate immunohistochemical profiles stratified by age group in patients diagnosed with breast cancer at Pérola Byington Hospital. Methods: A retrospective cross-sectional study was carried out at the Referral Center for Women’s Health - Hospital Pérola Byington– São Paulo (SP), Brazil. The data were removed from the collection system during the period of January 2011 to December 2018. Such women were stratified through the subtype histochemical analysis and evaluated in relation to their age at diagnosis. Results: We analyzed the immunohistochemical profile of 11,326 patients treated at Hospital Pérola Byington from January 2011 to December 2018. Lumum tumors A corresponded to 2,629 cases and among these 7.3% were under 40 years old, 23.1% between 40 and 50 years old and 60.5% were over 50 years old. The rate of tumors lumen B was 3,494 cases, with 10.1% in patients under 40, 24.2% between 40 and 50 years old and 65.6% over 50 years old. Acheampong et al. carried out a study on the incidence of molecular subtypes in the USA between 2010 and 2016 and concluded that from the 32,0124 women included, 72.6% were classified as luminal A, 11.2% luminal B, 4.8% overexpression of HER2 and 11.3% tumors. Conclusions: Based on the molecular markers, we classified the subtypes into four breast carcinomas: luminal B was the most frequent, followed by luminal A. The subtypes showed no significant difference in relation to their histological type nor age. Thus, the correlation between histological diagnosis and immunohistochemistry can improve the treatment and survival of women with breast cancer and, consequently, improve the therapeutic response of patients.