Relevant bibliographies by topics / Steroid receptors

Academic literature on the topic 'Steroid receptors'

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Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Steroid receptors"

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Baker, ME. "Recent insights into the origins of adrenal and sex steroid receptors." Journal of Molecular Endocrinology 28, no. 3 (June 1, 2002): 149–52. http://dx.doi.org/10.1677/jme.0.0280149.

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The recent cloning by Thornton (2001) of estrogen, progesterone and corticoid receptors from lamprey provides important insights into the early evolution of adrenal and sex steroid receptors and an opportunity to elucidate the ancient steroids that regulated gene transcription. Inclusion of lamprey sequences in a steroid receptor phylogeny indicates that the estrogen receptor is the most ancient of these receptors, followed by the progesterone receptor and the corticoid receptor. Thornton proposed that estradiol was the earliest of the steroids to activate a steroid receptor. An alternative hypothesis is that a steroid in the Delta(5) pathway activated the ancestral estrogen receptor.
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Baker, ME. "Adrenal and sex steroid receptor evolution: environmental implications." Journal of Molecular Endocrinology 26, no. 2 (April 1, 2001): 119–25. http://dx.doi.org/10.1677/jme.0.0260119.

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The nuclear receptor family responds to a diverse group of ligands, including steroids, retinoids, thyroid hormone, prostaglandins and fatty acids. Previous sequence analyses of adrenal and sex steroid receptors indicate that they form a clade separate from other nuclear receptors. However, the relationships of adrenal and sex steroid receptors to each other and to their ancestors are not fully understood. We have used new information from androgen, estrogen, mineralocorticoid and progesterone receptors in fish to better resolve the phylogeny of adrenal and sex steroid receptors. Sequence divergence between fish and mammalian steroid receptors correlates with differences in steroid specificity, suggesting that phylogeny needs to be considered in evaluating the endocrine effects of xenobiotics. Among the vertebrate steroid receptors, the most ancient is the estrogen receptor. The phylogeny indicates that adrenal and sex steroid receptors arose in a jawless fish or a protochordate and that changes in the sequence of the hormone-binding domain have slowed considerably in land vertebrates. The retinoid X receptor clade is closest to the adrenal and sex steroid receptor clade. Retinoid X receptor is noteworthy for its ability to form dimers with other nuclear receptors, an important mechanism for regulating the action of retinoid X receptor and its dimerization partners. In contrast, the adrenal and sex steroid receptors bind to DNA as homodimers. Moreover, unliganded adrenal and sex steroid receptors form complexes with heat shock protein 90. Thus, the evolution of adrenal and sex steroid receptors involved changes in protein-protein interactions as well as ligand recognition.
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Marcinkowska, Ewa, and Antoni Wiedłocha. "Steroid signal transduction activated at the cell membrane: from plants to animals." Acta Biochimica Polonica 49, no. 3 (September 30, 2002): 735–45. http://dx.doi.org/10.18388/abp.2002_3782.

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Steroid hormones in plants and in animals are very important for physiological and developmental regulation. In animals steroid hormones are recognized by nuclear receptors, which transcriptionally regulate specific target genes following binding of the ligand. In addition, numerous rapid effects generated by steroids appear to be mediated by a mechanism not depending on the activation of nuclear receptors. Although the existence of separate membrane receptors was postulated many years ago and hundreds of reports supporting this hypothesis have been published, no animal membrane steroid receptor has been cloned to date. Meanwhile, a plant steroid receptor from Arabidopsis thaliana has been identified and cloned. It is a transmembrane protein which specifically recognizes plant steroids (brassinosteroids) at the cell surface and has a serine/threonine protein kinase activity. It seems that plants have no intracellular steroid receptors, since there are no genes homologous to the family of animal nuclear steroid receptors in the genome of A. thaliana. Since the reason of the rapid responses to steroid hormones in animal cells still remains obscure we show in this article two possible explanations of this phenomenon. Using 1,25-dihydroxyvitamin D(3) as an example of animal steroid hormone, we review results of our and of other groups concordant with the hypothesis of membrane steroid receptors. We also review the results of experiments performed with ovarian hormones, that led their authors to the hypothesis explaining rapid steroid actions without distinct membrane steroid receptors. Finally, examples of polypeptide growth factor that similarly to steroids exhibit a dual mode of action, activating not only cell surface receptors, but also intracellular targets, are discussed.
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Wiseman, Helen, and Rosanna Duffy. "Steroids, steroid receptors and disease." Trends in Molecular Medicine 7, no. 4 (April 2001): 146–47. http://dx.doi.org/10.1016/s1471-4914(01)01978-5.

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Hammes, Stephen R., and Ellis R. Levin. "Extranuclear Steroid Receptors: Nature and Actions." Endocrine Reviews 28, no. 7 (October 4, 2007): 726–41. http://dx.doi.org/10.1210/er.2007-0022.

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Rapid effects of steroid hormones result from the actions of specific receptors localized most often to the plasma membrane. Fast-acting membrane-initiated steroid signaling (MISS) 1leads to the modification of existing proteins and cell behaviors. Rapid steroid-triggered signaling through calcium, amine release, and kinase activation also impacts the regulation of gene expression by steroids, sometimes requiring integration with nuclear steroid receptor function. In this and other ways, the integration of all steroid actions in the cell coordinates outcomes such as cell fate, proliferation, differentiation, and migration. The nature of the receptors is of intense interest, and significant data suggest that extranuclear and nuclear steroid receptor pools are the same proteins. Insights regarding the structural determinants for membrane localization and function, as well as the nature of interactions with G proteins and other signaling molecules in confined areas of the membrane, have led to a fuller understanding of how steroid receptors effect rapid actions. Increasingly, the relevance of rapid signaling for the in vivo functions of steroid hormones has been established. Examples include steroid effects on reproductive organ development and function, cardiovascular responsiveness, and cancer biology. However, although great strides have been made, much remains to be understood concerning the integration of extranuclear and nuclear receptor functions to organ biology. In this review, we highlight the significant progress that has been made in these areas.
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Adcock, I. M., S. J. Lane, C. R. Brown, M. J. Peters, T. H. Lee, and P. J. Barnes. "Differences in binding of glucocorticoid receptor to DNA in steroid-resistant asthma." Journal of Immunology 154, no. 7 (April 1, 1995): 3500–3505. http://dx.doi.org/10.4049/jimmunol.154.7.3500.

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Abstract Although glucocorticosteroids are a very effective treatment for asthma and other chronic inflammatory diseases, a small proportion of patients are resistant to their therapeutic effects. The molecular mechanism for this steroid resistance is unclear. Steroid resistance cannot be explained by pharmacokinetic mechanisms, by a defect in the binding of steroids to glucocorticoid receptors, nor by defective nuclear translocation of this receptor, thereby suggesting that the molecular abnormality lies distal to nuclear translocation. We examined the ability of nuclear translocated glucocorticoid receptors to bind to their DNA binding sites (GRE) using electrophoretic mobility shift assays in PBMC from patients with steroid-sensitive and steroid-resistant asthma. The binding of the glucocorticoid receptor to DNA in these patients was also studied using Scatchard analysis. Dexamethasone induced a significant rapid and sustained twofold increase in GRE binding in PBMCs from steroid-sensitive asthmatic patients and nonasthmatic individuals, but this was markedly reduced in steroid-resistant asthmatic patients. Scatchard analysis of glucocorticoid receptor-GRE binding showed no change in binding affinity but did show a reduced number of receptors available for DNA binding in the steroid-resistant patients. These results suggest that the ability of the glucocorticoid receptor to bind to GRE is impaired in steroid-resistant patients because of a reduced number of receptors available for binding to DNA.
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Godowski, Paul J., and Didier Picard. "Steroid receptors." Biochemical Pharmacology 38, no. 19 (October 1989): 3135–43. http://dx.doi.org/10.1016/0006-2952(89)90605-9.

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Levin, Ellis R. "Extranuclear estrogen receptor's roles in physiology: lessons from mouse models." American Journal of Physiology-Endocrinology and Metabolism 307, no. 2 (July 15, 2014): E133—E140. http://dx.doi.org/10.1152/ajpendo.00626.2013.

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Steroid receptors exist and function in multiple compartments of cells in most organs. Although the functions and nature of some of these receptors is being defined, important aspects of receptor localization and signaling to physiology and pathophysiology have been identified. In particular, extranuclear sex steroid receptors have been found in many normal cells and in epithelial tumors, where they enact signal transduction that impacts both nongenomic and genomic functions. Here, I focus on the progress made in understanding the roles of extranuclear estrogen receptors (ER) in physiology and pathophysiology. Extranuclear ER serve as a model to selectively intervene with novel receptor reagents to prevent or limit disease progression. Recent novel mouse models and membrane ER-selective agonists also provide a better understanding of receptor pool cross-talk that results in the overall integrative actions of sex steroids.
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Mukudai, Shigeyuki, Ken Ichi Matsuda, Takeshi Nishio, Yoichiro Sugiyama, Hideki Bando, Ryuichi Hirota, Hirofumi Sakaguchi, Yasuo Hisa, and Mitsuhiro Kawata. "Differential Responses to Steroid Hormones in Fibroblasts From the Vocal Fold, Trachea, and Esophagus." Endocrinology 156, no. 3 (March 1, 2015): 1000–1009. http://dx.doi.org/10.1210/en.2014-1605.

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Abstract There is accumulating evidence that fibroblasts are target cells for steroids such as sex hormones and corticoids. The characteristics of fibroblasts vary among tissues and organs. Our aim in this study is to examine differences in responses to steroid hormones among fibroblasts from different cervicothoracic regions. We compared the actions of steroid hormones on cultured fibroblasts from the vocal folds, which are considered to be the primary target of steroid hormones, and the trachea and esophagus in adult male rats. Expression of steroid hormone receptors (androgen receptor, estrogen receptor α, and glucocorticoid receptor) was identified by immunofluorescence histochemistry. Androgen receptor was much more frequently expressed in fibroblasts from the vocal fold than in those from the trachea and esophagus. Cell proliferation analysis showed that administration of testosterone, estradiol, or corticosterone suppressed growth of all 3 types of fibroblasts. However, mRNA expression for extracellular matrix–associated genes, including procollagen I and III and elastin, and hyaluronic acid synthase I was elevated only by addition of testosterone to fibroblasts from the vocal fold. These results indicate that each steroid hormone exerts region-specific effects on cervicothoracic fibroblasts with different properties through binding to specific receptors.
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Plese, J. P. P., V. R. Martins, M. T. P. Lopes, and M. M. Brentani. "Steroid receptors in meningiomas." Arquivos de Neuro-Psiquiatria 43, no. 4 (December 1985): 365–71. http://dx.doi.org/10.1590/s0004-282x1985000400005.

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Cytosolic estrogen (ER), progesterone (PR), androgen (AR) and glucocorticoid receptors (GR) were evaluated in 10 meningiomas using a dextran charcoal coated method. We consider as positive specific receptor values >10fMol/mg protein. In this study 20% of the meningiomas contained very low titers of specific ER. PR was detectable in 90% of the tumors, at high levels. The mean PR content of PR+ tumors was 60±38fMol/mg prot. GR and AR were present in moderate levels, in 70% of the tumors. Competition studies demonstrated steroid specificity for these hormone-binding proteins. Female patients have a higher receptor incidence and titer. In conclusion, it can be hypothesized that the meningioma are a target tissue for steroids and that endocrine therapy may be relevant to unoperable and/or reccurent tumors.
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Dissertations / Theses on the topic "Steroid receptors"

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Malouitre, Sylvanie Désirée Marie. "Glucocorticoid receptor function, interactions with oestrogen receptors and a steroid inhibitor." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413737.

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Brady, P. "A thermodynamic approach to steroid-based receptors." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596861.

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Chapter 1 begins with a brief overview of molecular recognition and then presents a review of recently developed methods for lead generation and the synthesis of self-defining host molecules. Chapter 2 describes a strategy for the synthesis of functionally active molecules which combines advantageous features of some of the methods described in Chapter 1. Relevant literature and precedents are then introduced followed by a discussion of theoretical considerations. In Chapter 3, after an introduction to the use of cholate building blocks in supramolecular chemistry, the synthesis of the new steroidal molecules studied is described, together with a discussion of their structural properties. Chapter 4 outlines the development of an effective method for the reversible macrocyclisation of steroidal building blocks by transesterification. The application of this method to the thermodynamically-controlled, and metal ion-templated, cyclisation of the steroid derivatives is then discussed in Chapter 5. An investigation into the metal ion building properties of the steroid derivatives using electrospray mass spectrometry is described in Chapter 6. The chapter begins with initial experiments to explore the circumstances in which the technique can generate meaningful information and then summarises the metal ion binding characteristics of the steroids investigated. Chapter 7 explores transorthoesterification as a milder reversible reaction for the synthesis of macrocycles and then describes initial studies towards a host capable of binding a porphyrin guest. In Chapter 8, the results of the cyclisation experiments and the binding study are compared with each other and put into the wider context of the long term goals of the project. That is followed by some ideas for future directions of this work.
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Hazell, Georgina Grace Joan. "Deorphanising G protein-coupled receptors : the search for fast steroid receptors." Thesis, University of Bristol, 2011. http://hdl.handle.net/1983/12fbf473-f360-4831-8123-42698aff4950.

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G protein coupled receptors (GPCRs) are the largest family of transmembrane receptors in the genome and are activated by a multitude of ligands including neuropeptides, hormones and sensory signals. The paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus are important mediators in homeostatic control. Many modulators of PVN/SON activity, including neurotransmitters and hormones act via GPCRs - in fact over 100 non-chemosensory GPCRs have been detected in either the PVN or SON. The introduction to this thesis begins with a comprehensive summary of GPCR expression within the PVN/SON, with a critique of the detection techniques used within the literature. Also discussed are some aspects of the regulation and known roles of GPCRs in the PVN/SON, as well the possible functional significance of orphan GPCRs. Particular interest is paid to the recently 'deorphanised' G protein-coupled oestrogen (E2) receptor, GPER, which is the first receptor to be acknowledged as a steroid binding GPCR (although there are conflicting studies regarding its affinity for E2) and is expressed in the PVN and SON. Steroids are known to have fast non-genomic effects that are thought to be mediated in-part by membrane-associated forms of the traditional steroid receptors (members of a family of transcription factors). However, the possible discovery of a fast E2 GPCR has raised speculation regarding the existence of other steroid binding GPCRs. Thus the experimental Chapters were undertaken to explore the concept of fast steroid receptors, with particular emphasis on their possible roles in neuroendocrine systems. Firstly, the distribution of the putative E2 receptor was investigated to give further insight into its possible in vivo roles. In the rodent, high levels of GPER gene and protein expression were detected in the oxytocin and vasopressin neurones in the PVN and SON, the anterior and intermediate lobe of the pituitary, adrenal medulla and renal medulla and pelvis, suggesting roles for GPER in multiple functions including hormone release. To clarify the controversy surrounding GPER as an E2 receptor, we investigated GPER function in vitro using a series of cell signalling assays. However, E2 did not stimulate GPER-mediated signalling, suggesting that either GPER remains an orphan GPCR, or the cell lines used in this study lacked a vital component for E2 activation of GPER. As the rapid effects of glucocorticoid have been reported in numerous brain regions (including the PVN and SON), endocrine, and other tissues, the second part of this thesis focussed on the search for a possible fast glucocorticoid receptor. We compared the tissue distribution gene expression profiles of approximately 125 orphan GPCRs common to human and rodent with tissues that are known to exhibit fast effects of steroids (e.g., hippocampus, PVN, SON, thymus, kidney, etc.). Of the 125 orphans,3 GPCRs (GPR108, GPR146, and TMEM87B) had distribution profiles that closely matched the regions/tissues of interest. These orphans were tested for glucocorticoid activation using a universal deorphanisation assay. However, the identity of the fast glucocorticoid receptor remains unknown, as none of the candidate orphan GPCRs responded to glucocorticoids.
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Fischer, Katharina. "The mineralocorticoid receptor amino terminal transactivation domain investigation of structural plasticity and protein-protein interactions /." Thesis, Available from the University of Aberdeen Library & Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24694.

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Thesis (Ph.D.)--Aberdeen University, 2008.
Title from web page (viewed on Feb. 23, 2009). With: Natural disordered sequences in the amino terminal domain of nuclear receptors : lessons from the androgen and glucocorticoid receptors / Iain J. McEwan ... et al. Nuclear Receptor Signalling. 2007: 5. Includes bibliographical references.
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Nawaz, Zafar. "Molecular Mechanism of Action of Steroid Hormone Receptors." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc798398/.

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A novel bacterial expression system that is capable of producing high levels of soluble, stable, biologically active human vitamin D3 and estrogen receptors has been developed. The method utilizes ubiquitin fusion technology and a low temperature nalidixic acid induction of the lambda PL promoter. This system can produce large quantities of receptor antigen, but only a small fraction displays wild-type DNA and hormone binding properties. Therefore, the use of this system to overproduce receptors for crystallization studies is not practical. To overcome these problems, a 2 um based ubiquitin fusion system which allows regulated expression of the estrogen receptor in yeast (Saccharomyces cerevisiae) was developed. This system produces the estrogen receptor to a level of 0.2% of the total soluble protein. Moreover, this protein is undegradable, soluble, and biologically active. To test the transcriptional activity of the estrogen receptor produced in yeast, a cis-trans transcription assay was developed. This assay revealed that the transcriptional activity of the human estrogen receptor expressed in yeast was similar to that observed in transfected mammalian cells. This reconstituted estrogen transcription unit in Saccharomyces cerevisiae was utilized to examine the regulation of estrogen receptor functions by antiestrogens, to develop a random and rapid approach for identifying novel estrogen response elements, to characterize estrogen receptor variants cloned from human breast tumors, and to examine the effect of estrogen receptor on the regulation of osteocalcin gene.
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Smith, Robert A. "The Role of the Steroid Nuclear Receptor Genes in Breast Cancer." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365401.

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Breast cancer is a great source of morbidity and mortality in the developed world, being the most common cause of cancer death in Australian women and affecting roughly 1 in 10 women. The development and progression of cancers is a multi-stage process, involving numerous perturbations to normal cellular functions, especially to those genes which control cellular growth, cellular differentiation and DNA repair. Over time, these alterations combine to change normal cells into cancerous ones that typically no longer respond to normal control stimuli and grow with great rapidity. The nuclear receptors are a family of proteins which accept incoming signals from various molecules, and then alter gene expression or affect cell behavior directly. The steroid nuclear receptors receive transducer signals from hormones such as estrogen and testosterone and are intimately involved in affecting cellular growth and differentiation. Stimulation of the steroid receptors have been used as successful treatment avenues, so how these genes behave in cancer is of great interest. Accordingly, this study has examined the expression of various nuclear receptors and some related genes in a number of tissue samples derived from breast tumours and from surrounding areas, and examined how various pathological parameters affect their expression. Tissue samples were first microdissected to separate tumour tissue from the surrounding stroma and then subjected to RNA extraction procedures to allow gene expression to be quantitated. RNA was then converted into cDNA by reverse transcription and the genes of interest amplified and quantitated using semiquantitative polymerase chain reaction. Expression data was then normalized by expressing it as a ratio of the gene of interest to the 18S ribosomal gene and differences in expression analysed by analysis of variance (ANOVA) testing. The first portion of the study dealt with the progesterone and glucocorticoid receptors in tumour tissue. Progesterone is an anti-mitogenic signal for breast tissue and the stimulation of the receptor is a useful part of combined hormonal therapy for breast cancer. The glucocorticoid receptor plays a similar role to the progesterone receptor, slowing breast tissue growth and promoting apoptosis. The complete tissue population of 25 samples from control, grade 1, grade 2 and grade 3 tumours underwent PCR for the glucocorticoid and progesterone receptor genes and was normalized using 18S. Analysis of the expression data by ANOVA showed that the progesterone and glucocorticoid receptors were more highly expressed in grade 3 tumour tissue (p=0.023 and p=O.00033, for the progesterone and glucocorticoid receptors, respectively). Most advanced tumours cease being responsive to growth repressing hormones, so these results indicated that the control of the expression of these receptors in tumour tissue was more complicated than might have been expected. The increase in expression observed may be the result of intact growth preventing feedback mechanisms which have malfunctioned in some manner. There are several mechanisms the tumours may be using to escape an increase in progesterone or glucocorticoid sensitivity. The mRNA detected may simply not be being translated into completed proteins or be being spliced into isoforms of the receptors that favour tissue growth. The second portion of the study dealt with the estrogen receptors alpha and beta in tumour tissue. The estrogen receptors control estrogen signaling and are highly important in breast cancer, since estrogen is the primary growth inducing hormone for breast tissue. For the estrogen receptors alpha and beta, the complete tissue population of 25 samples from control, grade 1, grade 2 and grade 3 tumours underwent PCR and were normalized using 18S. ANOVA analysis found that the expression of the estrogen receptors did not change significantly in any grade of cancer (p= 0.057 and p=O.7'38, for ESRα and ESRβ, respectively) nor in tissues that are negative for the estrogen receptor alpha protein, a poor prognostic factor in breast cancer (p= 0.794 and p=O.7l6, for ESRα and ESRβ, respectively). These results indicated that the loss of estrogen receptor in advanced cancers is not controlled at the level of mRNA. The mRNA observed in this study may be being spliced into alternate and possibly inactive isoforms, or may be being degraded post transcriptionally, preventing estrogen stimulation in these tumours. This could prove an excellent area for further study, since if the mechanism that prevents or distorts ESR mRNA translation can be discovered, it would allow manipulation of one of the most important treatment avenues for breast cancer. The third portion of the study dealt with the expression of the androgen receptor in tumour tissue. Androgens are a strong anti-growth signal in breast tissue and despite the side effects that androgens have on women, they have been used to treat breast cancer with some success. The complete tissue population of 25 samples from control, grade 1, grade 2 and grade 3 tumours underwent PCR for the androgen receptor gene and normalized using 18S. The results obtained for androgen receptor expression in tumour tissue showed that androgen receptor expression was significantly elevated in grade 2 and grade 3 tumour tissue, as well as in ESRα negative tumours (p= 0.014 and p=O.O25, respectively). An increase in expression in late stage tumours would seem to be unusual for an anti-mitogenic receptor, however many advanced breast tumours have been found to be receptive to androgen stimulation, even when they no longer respond to other hormones. The increased expression of AR may be a normal response to cellular over-growth, or it may be a mechanism by which the tumour prevents stimulation by other growth retarding hormones, by sequestering all available receptor co-enzymes with a receptor that is unlikely to be stimulated. The fourth portion of the study examined the expression of the estrogen alpha, estrogen beta, progesterone, glucocorticoid and androgen nuclear receptors in stromal tissue derived from the tumours studied in previous chapters. Tumours have been observed in other studies to manipulate the activities of the cells that surround them through the release of cofactors and vice versa. These cofactors include the steroid hormones, among others, and hence the study of how the tumour and stroma interacts is a valuable extension to the results obtained in the previous sections. PCR was performed for all nuclear receptors, except for the estrogen receptor alpha, in the complete tissue population of 25 samples of tissue derived from the stroma of the grade 1, grade 2 and grade 3 tumours used in the previous studies as well as the control tissues. Due to difficulties in PCR optimization for estrogen receptor alpha, only three stromal samples from each grade and four controls were able to produce results, for a total population of 13 samples. Of all the receptors tested, only the progesterone and glucocorticoid receptors displayed significant changes in expression in stromal tissue, with PgR having significantly lower expression in all stromal samples compared to control, while GR was more highly expressed in stroma derived from high grade tumours (p= 5.908x107 and p=2.761x105, for PgR and GR, respectively). UR expression was also increased in stroma derived from ESRα negative tumours (p=5.85x105). These alterations reflect the kind of stimulation a tumour is likely to apply to the surrounding stroma, using progesterone to stimulate the cells into differentiating to provide a more suitable environment, hence the loss in PgR expression. The increase in GR expression may be the result of the high level of growth stimulating factors that tumours produce, priming the local cells to be more sensitive to growth suppressors, a situation that is also mirrored in results previously obtained for the tumour tissue. The fifth part of the study concerned the expression of the nuclear receptor coactivator 1 and nuclear receptor co-activator 3 genes. These proteins are required for the activation and function of the nuclear receptors and both have been implicated in cancer development, being found to be over-expressed in several tissues and cell lines. As integral parts of the nuclear receptor pathway, their level of expression is important for determining how effective any nuclear receptors present will be when stimulated. The complete tissue population of 25 samples from control, grade 1, grade 2 and grade 3 tumours underwent PCR for both nuclear receptor co-activator genes and normalized using 18S. The result of ANOVA analysis on the NCoA data showed that NCoA3 expression remained unaltered in all grades of cancer and stroma and in both ESRα positive and negative tissue. NCoA1 however, was significantly upregulated in grade 3 tumours as compared to grade 1 tumours and also in ESRα negative tumours. This increase in expression would seem to indicate that these tissues would be more capable of acting on any received hormonal stimulation. That this increase in expression occurs in more advanced cancers could be evidence that the nuclear receptor expression observed in prior sections is resulting in NR splice variants that favour, rather than repress, growth, as advanced cancers usually do not respond normally to hormonal stimulation. The final part of the study investigated the possibility of correlations between the expression of the nuclear receptors, between the nuclear receptor co-activators and between all of the tested genes and other pathological parameters, including tumour size, metastasis, site of tumour, carcinoma in situ invasiveness, age of patient and the presence of calcification. The data generated in the prior studies was analyzed using ANOVA for categorical data and correlation analysis for numerical data. The ANOVA and correlation analysis revealed a number of interactions between these factors, which provide additional information on the relationships between the tested genes. Expression of the progesterone receptor was found to be correlated with the expression of GR, AR and NCoA1 (p= 0.022, p=O.OO3, and p=O.0i9, respectively). Likewise the expression of GR and AR were found to be correlated (p=O.O29). Additionally, AR was found to be associated with tumour size (p=O.O36) while GR was found to be associated with both tumour size and metastasis (p= 0.006 and p=7.6x106, respectively). ESRα and ESRβ expression were found to be negatively correlated (p=O.O44M), as were patient age and the amount of ductal carcinoma in situ invasion. Given the results of previous analyses, it is not surprising that PgR, GR, AR and NCoA1 expression are related, and the negative correlations between ESRα and ESRβ expression, as well as between age and ductal carcinoma in situ invasion have been documented in other studies. Hence, these results provide reinforcement for previous observations, as well as providing new information, particularly on AR and GR.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
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Judd, Luke William. "Cholapods and cholaphanes : steroid based receptors for anion transport." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544424.

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Cziko, Paul. "Molecular Physiological Evolution: Steroid Hormone Receptors and Antifreeze Proteins." Thesis, University of Oregon, 2015. http://hdl.handle.net/1794/18733.

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For my dissertation research I explored the diversity and functional evolution of steroid hormone receptors (SRs) in animals and the physiological implications of the evolution of antifreeze proteins in Antarctic notothenioid fishes. For the former, I discovered multiple new SRs from the vast and under-sampled swath of animal diversity known as invertebrates. I used the sequences of these and other newly discovered related receptors in combination with genomic data and molecular phylogenetic techniques to revise the understanding of the evolutionary history of this important gene family. While previous studies have suggested that vertebrate SR diversity arose from a gene duplication in an ancestor of all bilaterian animals, my work presents strong evidence that this duplication occurred much later, at the base of the chordates. Furthermore, to determine the implications of added diversity and a revised phylogeny on inferences of the functional evolution of SRs, I functionally characterized heretofore-unknown SRs from hemichordates, an acoelomate flatworm, and a chaetognath and statistically reconstructed and functionally characterized ancestral SRs. My results expand the known sequence and functional repertoire of SRs in animals while reinforcing the previous inference that all SRs evolved from an estrogen-sensitive ancestral receptor. I also explored the consequences of the evolution of antifreeze proteins in Antarctic notothenioid fishes, a crucial adaptation to their icy, polar environment. These special proteins adsorb to ice crystals that enter a fish's body and prevent further growth, thereby averting death. I discovered that, in addition to their lifesaving growth-inhibiting ability, AFPs also prevent the melting of internal ice crystals at temperatures above the expected equilibrium melting point. Together with a decade-long temperature record of one of the coldest fish habitats on earth, my experimental results show that the evolution and expression of antifreeze proteins is accompanied by a potentially detrimental consequence: the lifelong accumulation of ice inside these fishes' bodies. This dissertation includes previously published co-authored material as well as unpublished co-authored material.
2017-01-14
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Shatnawi, Aymen Ahmad. "New Mechanisms of Transcriptional Regulation of the Folate Receptor and other genes by steroid Receptors." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1201810595.

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Ayling, Alan J. "Steroidal electroneutral receptors for anions : synthesis and evaluation." Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367663.

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Books on the topic "Steroid receptors"

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Castoria, Gabriella, and Ferdinando Auricchio, eds. Steroid Receptors. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1346-6.

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C, Spelsberg T., and Kumar Rajiv 1949-, eds. Steroid and sterol hormone action. Boston: Nijhoff, 1987.

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Pertschuk, Louis P. Immunocytochemistry for steroid receptors. Boca Raton: CRC Press, 1990.

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1948-, Henderson David, ed. Steroid receptors and antihormones. New York, N.Y: New York Academy of Sciences, 1995.

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A, Lieberman Benjamin, ed. Steroid receptor methods: Protocols and assays. Totowa: Humana Press, 2001.

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Castoria, Gabriella, and Ferdinando Auricchio. Steroid receptors: Methods and protocols. New York: Humana Press, 2014.

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1925-, Pertschuk Louis P., and Lee Sin Hang 1932-, eds. Localization of putative steroid receptors. Boca Raton. Fla: CRC Press, 1985.

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1950-, Watson Cheryl S., ed. The identities of membrane steroid receptors: ... and other proteins mediating nongenomic steroid action. Boston: Kluwer Academic Publishers, 2003.

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Meadow Brook Conference on Steroid Receptors in Health and Disease (1st 1987 Rochester, Mich.). Steroid receptors in health and disease. New York: Plenum Press, 1988.

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Watson, Cheryl S., ed. The Identities of Membrane Steroid Receptors. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0339-2.

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Book chapters on the topic "Steroid receptors"

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Greiner, E. F., T. Wintermantel, and G. Schütz. "Steroid Receptors." In Transgenic Models in Pharmacology, 575–606. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18934-0_19.

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Barber, Hugh R. K. "Sex Steroid Receptors." In Ovarian Carcinoma, 273–87. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9232-3_26.

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Jensen, E. V. "Steroid Hormone Receptors." In Current Topics in Pathology, 365–431. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75515-6_11.

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Müller, Judith M., and Roland Schüle. "Sex Steroid Receptors: Androgen Receptor, Estrogen Receptors, Progesterone Receptor." In Encyclopedia of Molecular Pharmacology, 1415–21. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_163.

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Müller, Judith M., and Roland Schüle. "Sex Steroid Receptors: Androgen Receptor, Estrogen Receptors, Progesterone Receptor." In Encyclopedia of Molecular Pharmacology, 1–7. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_163-1.

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Migliaccio, Antimo, Gabriella Castoria, and Ferdinando Auricchio. "Non-Genomic Action of Sex Steroid Hormones." In Nuclear Receptors, 365–79. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3303-1_15.

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Bergqvist, A. "Steroid receptors in endometriosis." In Modern Approaches to Endometriosis, 33–55. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3864-2_3.

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Gorski, Jack. "Steroid Receptors: A Historical Perspective." In Steroid Receptors in Health and Disease, 25–31. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5541-0_2.

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Schlanger, Simon, and Hannelore V. Heemers. "Functional Studies on Steroid Receptors." In Methods in Molecular Biology, 117–30. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7845-8_7.

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Lambert, J. J., J. A. Peters, S. C. Harney, and D. Belelli. "Steroid Modulation of GABAA Receptors." In Pharmacology of GABA and Glycine Neurotransmission, 117–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56833-6_4.

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Conference papers on the topic "Steroid receptors"

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Noriega, Yamilet, Miguel Rivas, and Elizabeth Langley. "Abstract C56: Characterization of PinX1 as a coregulator of steroid hormone receptors." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-c56.

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Massah, Shabnam, Na Li, Sarah Truong, Jane Foo, Gail Prins, and Ralph Buttyan. "Abstract 4397: Gli Activation by Steroid Receptors in Prostate and Breast Cancer Cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4397.

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Massah, Shabnam, Na Li, Sarah Truong, Jane Foo, Gail Prins, and Ralph Buttyan. "Abstract 4397: Gli Activation by Steroid Receptors in Prostate and Breast Cancer Cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4397.

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Herceg, Megan, and Amarda Shehu. "Structure- and Energy-based Analysis of Small Molecule Ligand Binding to Steroid Nuclear Receptors." In BCB '23: 14th ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3584371.3612949.

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Conzen, SD. "Abstract ES9-3: Androgen, progesterone and glucocorticoid receptors: Drivers of breast tumor progression or reprogramming of steroid receptors during breast tumor progression." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-es9-3.

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Bekić, Sofija S., Ivana Kuzminac, Srđan Bjedov, Jovana Ajduković, Marina Savić, Edward Petri, and Anđelka Ćelić. "Use of Fluorescent Yeast-Based Biosensors for Evaluation of the Binding Affinities of New Steroid Hormone and Bile Acid Derivatives for Select Steroid Receptors." In IECB 2022. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/iecb2022-12282.

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Poulard, Coralie, and Michael Stallcup. "Abstract 3622: Crosstalk between automethylation and phosphorylation tightly regulates G9a and GLP coactivator function with steroid hormone receptors." In 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.am2017-3622.

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McNamara, KM, F. Guestini, T. Sauer, JC Lindstrøm, H. Sasano, and J. Geisler. "Abstract P3-05-08: Steroid receptors and steroidogenic enzymes in human breast cancer: Associations with breast cancer subtypes and clinical outcome." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p3-05-08.

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Tomasevic, Z., S. Nikolic, M. Jevric, G. Pupic, Z. Milovanovic, M. Skender, M. Inic, et al. "Comparison between Steroid Receptors and Her2 Status in Primary Breast Carcinoma and Completely Resected Breast Carcinoma Metastases from Different Visceral Organ Sites." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4048.

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Dzichenka, Yaraslau, Michail Shapira, Sergei Usanov, Marina Savić, Ljubica Grbović, Jovana Ajduković, and Suzana Jovanović-Šanta. "NOVEL LIGANDS OF HUMAN CYP7 ENZYMES – POSSIBLE MODULATORS OF CHOLESTEROL BLOOD LEVEL: COMPUTER SIMULATION STUDIES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.435d.

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Abstract:
Our in vitro studies showed that a couple of perspective steroidal derivatives showed previously biomedical potential via enzyme inhibition, receptor binding or antiproliferative effect against the cancer cells of reproductive tissues are able to bind to human CYP7 enzymes – key enzymes taking part in hydroxylation of cholesterol, 25-, 27-hydroxycholesterol and a number of steroidal hormones. In silico screening of binding affinity of the modified steroids toward CYP7 enzymes showed that interaction energy for the new ligands is comparable with consequent values, calculated for the ‘essential’ substrates of the enzymes – cholestenone (CYP7A1) and DHEA (CYP7B1). However, no correlation between binding energy and the affinity of the ligand was found. Novel ligands interact with conserved amino acids taking part in stabilization of natural substrates of CYP7 enzymes. A couple of structural features, governing ligand binding, were identified. Among which are planar structure of A-ring for CYP7A1 ligands, absence of many polar fragments in side-chain and presence of polar group at C3 position. Analysis of the docking results showed that CYP7B1 higher selectivity in comparison with CYP7A1 is connected by the structure of the cavity formed by α-helices I and B`. The data obtained will be used for the explanation of ligand specificity of human sterol- hydroxylases.
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Reports on the topic "Steroid receptors"

1

Roth, Sharon Y. P/CAF Function in Transcriptional Activation by Steroid Hormone Receptors and Mammary Cell Proliferation. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada375129.

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Roth, Sharon Y. P/CAF Function in Transcriptional Activation by Steroid Hormone Receptors and Mammary Cell Proliferation. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada392348.

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Jeng, Meei-Huey. Roles of Steroid Receptor Coactivators in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada404705.

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Jeng, Meei-Hue Y. Roles of Steroid Receptor Coactivators in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada426309.

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Jeng, Meei-Huey. Roles of Steroid Receptor Coactivators in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada423247.

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McKenna, Neil J. The Role of Steroid Receptor Coactivator-1 in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada381169.

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Pietras, Richard J. Antiangiogenic Steroids and Growth Factor Receptors in Human Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada431966.

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Riegel, Anna T. Ribozyme Targeting of Steroid Receptor Co-Activators: A Therapeutic Approach to Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada403442.

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Cho, Jang H. The Role of Steroid Receptor Coactivators (SRCs) in the Development of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada411955.

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Riegel, Anna T. Ribozyme Targeting of Steroid Receptor Co-Activators: A Therapeutic Approach to Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada412143.

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