Relevant bibliographies by topics / Androgens

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Androgens'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "Androgens"

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Calado, Rodrigo T., William T. Yewdell, Keisha L. Wilkerson, Joshua A. Regal, Sachiko Kajigaya, Constantine A. Stratakis, and Neal S. Young. "Sex hormones, acting on the TERT gene, increase telomerase activity in human primary hematopoietic cells." Blood 114, no. 11 (September 10, 2009): 2236–43. http://dx.doi.org/10.1182/blood-2008-09-178871.

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Abstract Androgens have been used in the treatment of bone marrow failure syndromes without a clear understanding of their mechanism of action. Blood counts of patients with dyskeratosis congenita or aplastic anemia with mutations in telomerase genes can improve with androgen therapy. Here we observed that exposure in vitro of normal peripheral blood lymphocytes and human bone marrow–derived CD34+ cells to androgens increased telomerase activity, coincident with higher TERT mRNA levels. Cells from patients who were heterozygous for telomerase mutations had low baseline telomerase activity, which was restored to normal levels by exposure to androgens. Estradiol had an effect similar to androgens on TERT gene expression and telomerase enzymatic activity. Tamoxifen abolished the effects of both estradiol and androgens on telomerase function, and letrozole, an aromatase inhibitor, blocked androgen effects on telomerase activity. Conversely, flutamide, an androgen receptor antagonist, did not affect androgen stimulation of telomerase. Down-regulation by siRNA of estrogen receptor-α (ERα), but not ERβ, inhibited estrogen-stimulated telomerase function. Our results provide a mechanism for androgen therapy in bone marrow failure: androgens appear to regulate telomerase expression and activity mainly by aromatization and through ERα. These findings have potential implications for the choice of current androgenic compounds and the development of future agents for clinical use.
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Oosterhoff, Josien K., J. Anton Grootegoed, and Leen J. Blok. "Expression profiling of androgen-dependent and -independent LNCaP cells: EGF versus androgen signalling." Endocrine-Related Cancer 12, no. 1 (March 2005): 135–48. http://dx.doi.org/10.1677/erc.1.00897.

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Prostate cancer development often includes a shift from androgen-dependent to androgen-independent growth. It is hypothesized that, during this transition, growth factors like the epidermal growth factor (EGF) gain importance as activators of tumour cell proliferation. To study this, androgen- and EGF-regulation of growth and gene-expression was analysed in the androgen-dependent human prostate cancer cell line LNCaP-FGC (FGC) and its androgen-independent derivative line LNCaP-LNO (LNO). It was observed that androgen-dependent FGC cells require exposure to either androgens or EGF to proliferate. This is in contrast to androgen-independent LNO cells that showed significant proliferation in medium depleted of androgens and growth factors. Gene expression data were obtained for the androgen-dependent FGC and androgen-independent LNO cells cultured in the presence or absence of androgens (synthetic R1881) or EGF for different time periods. Expression profiling showed that many cell cycle genes, including a number of androgen- and EGF-regulated genes, are constitutively activated in androgen-independent LNO cells. Furthermore, the overlap between changes in gene expression activated by androgen and EGF receptor signalling pathways was found to be very high (75%). These results partly explain why androgen-independent LNO cells can proliferate in the absence of androgenic stimulation. However, possibly other, so far unknown, signal transduction pathways that induce and maintain proliferation, have also been activated.
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HERAS, MARCELO A. DE LAS, and RICARDO S. CALANDRA. "S‐Adenosyl‐L‐Methionine Decarboxylase Activity in the Rat Epididymis: Ontogeny and Androgenic Control." Journal of Andrology 12, no. 3 (May 6, 1991): 209–13. http://dx.doi.org/10.1002/j.1939-4640.1991.tb00252.x.

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ABSTRACT: The authors describe the occurrence of high levels of S‐adenosyl‐L‐methionine decarboxylase (SAMDC) activity in the rat epididymis, and its ontogeny and androgenic control. As early as 15 days of age, SAMDC activity exists, although a peak of activity is observed at 25 days. Bilateral orchidectomy resulted in a decline of epididymal SAMDC activity. However, an androgen‐independent fraction, accounting for 34% of total activity, appears to exist in the epididymis. In 45‐day‐old orchidectomized rats, SAMDC activity was stimulated by testosterone treatment in a dose‐dependent manner. However, treatment of 45‐day‐old intact animals with a high dose of the androgen failed to modify SAMDC activity, indicating that, at this age, the enzyme is maximally stimulated by endogenous androgens. The observed effect of testosterone on castrated rats was completely abolished by concomitant treatment with the antiandrogen flutamide. This compound was ineffective on the androgen‐insensitive fraction. To assess the contribution of circulating and luminal androgens to the maintenance of epididymal SAMDC, rats were unilaterally orchidectomized and activity was determined in both epididymides after 7 days. The SAMDC activity was identical in epididymides from both sides, suggesting that circulating androgens suffice to maintain normal levels of activity. It was concluded that androgens regulate epididymal SAMDC activity, although an androgen‐independent fraction appears to exist.
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Cunha, Gerald R., Annemarie A. Donjacour, and Yoshiki Sugimura. "Stromal–epithelial interactions and heterogeneity of proliferative activity within the prostate." Biochemistry and Cell Biology 64, no. 6 (June 1, 1986): 608–14. http://dx.doi.org/10.1139/o86-084.

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Growth and functional activity within the prostate gland is known to be regulated by androgens whose effects are thought to be mediated via androgen receptors. This concept has been derived in large part through analysis of whole organ homogenates, an approach which ignores potential heterogeneity of biological activity within the gland and the importance of cell–cell interactions. In this review recent findings are summarized which demonstrate that growth of the prostatic ductal network during prepubertal periods, as well as during prostatic regeneration in androgen-treated adult castrates, is nonuniform, with ductal growth being highest at the ductal tips and much lower in proximal ducts closer to the urethra. Androgen dependency for maintenance of ductal architecture following castration follows a similar pattern in that castration results in total destruction of distal ductal architecture, while proximal ducts are maintained albeit in an atrophic state. Thus, striking differences in biological properties are found in distal versus proximal prostatic ducts. Morphogenesis, growth, and secretory cytodifferentiation within the developing prostate is eleicited by androgens which act via mesenchymal–epithelial interactions. Through analysis of chimeric prostates constructed with androgen-receptor-positive wild-type mesenchyme and androgen-receptor-negative Tfm (testicular feminization) bladder epithelium, it is now evident that androgenic effects can be elicited in androgen-receptor-deficient (androgen-insensitive) Tfm prostatic epithelium, provided that the connective tissue component of the chimeric prostate is wild type. This observation has been made for both the developing and adult prostate. From this data it is evident that certain androgenic effects (ductal morphogenesis, epithelial growth, and secretory cytodifferentiation) do not require the presence of intraepithelial androgen receptors. In fact, recent evidence indicates that the epithelial androgen receptor is neither necessary or sufficient for induction of androgenic effects. Instead, many lines of evidence support the view that epithelial response to androgens is mediated via inductive trophic influences from mesenchymal (stromal) cells which are exceedingly important androgen targets.
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Hoon Lee, Jung, Haibiao Gong, Shaheen Khadem, Yi Lu, Xiang Gao, Song Li, Jian Zhang, and Wen Xie. "Androgen Deprivation by Activating the Liver X Receptor." Endocrinology 149, no. 8 (May 1, 2008): 3778–88. http://dx.doi.org/10.1210/en.2007-1605.

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Prostate cancer is the most commonly diagnosed and the second leading cause of cancer death in men. The androgens-androgen receptor signaling plays an important role in normal prostate development, as well as in prostatic diseases, such as benign hyperplasia and prostate cancer. Accordingly, androgen ablation has been the most effective endocrine therapy for hormone-dependent prostate cancer. Here, we report a novel nuclear receptor-mediated mechanism of androgen deprivation. Genetic or pharmacological activation of the liver X receptor (LXR) in vivo lowered androgenic activity by inducing the hydroxysteroid sulfotransferase 2A1, an enzyme essential for the metabolic deactivation of androgens. Activation of LXR also inhibited the expression of steroid sulfatase in the prostate, which may have helped to prevent the local conversion of sulfonated androgens back to active metabolites. Interestingly, LXR also induced the expression of selected testicular androgen synthesizing enzymes. At the physiological level, activation of LXR in mice inhibited androgen-dependent prostate regeneration in castrated mice. Treatment with LXR agonists inhibited androgen-dependent proliferation of prostate cancer cells in a LXR- and sulfotransferase 2A1-dependent manner. In summary, we have revealed a novel function of LXR in androgen homeostasis, an endocrine role distinct to the previously known sterol sensor function of this receptor. LXR may represent a novel therapeutic target for androgen deprivation, and may aid in the treatment and prevention of hormone-dependent prostate cancer.
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Chen, Jia-Feng, Pei-Wen Lin, Yi-Ru Tsai, Yi-Chien Yang, and Hong-Yo Kang. "Androgens and Androgen Receptor Actions on Bone Health and Disease: From Androgen Deficiency to Androgen Therapy." Cells 8, no. 11 (October 25, 2019): 1318. http://dx.doi.org/10.3390/cells8111318.

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Androgens are not only essential for bone development but for the maintenance of bone mass. Therefore, conditions with androgen deficiency, such as male hypogonadism, androgen-insensitive syndromes, and prostate cancer with androgen deprivation therapy are strongly associated with bone loss and increased fracture risk. Here we summarize the skeletal effects of androgens—androgen receptors (AR) actions based on in vitro and in vivo studies from animals and humans, and discuss bone loss due to androgens/AR deficiency to clarify the molecular basis for the anabolic action of androgens and AR in bone homeostasis and unravel the functions of androgen/AR signaling in healthy and disease states. Moreover, we provide evidence for the skeletal benefits of androgen therapy and elucidate why androgens are more beneficial than male sexual hormones, highlighting their therapeutic potential as osteoanabolic steroids in improving bone fracture repair. Finally, the application of selective androgen receptor modulators may provide new approaches for the treatment of osteoporosis and fractures as well as building stronger bones in diseases dependent on androgens/AR status.
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Culig, Zoran. "Response to Androgens and Androgen Receptor Antagonists in the Presence of Cytokines in Prostate Cancer." Cancers 13, no. 12 (June 12, 2021): 2944. http://dx.doi.org/10.3390/cancers13122944.

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Non-steroidal anti-androgens have a major role in the treatment of non-localized prostate cancer. Interleukins are involved in the regulation of many cellular functions in prostate cancer and also modify cellular response to anti-androgens. A specific role of selected IL is presented in this review. IL-8 is a cytokine expressed in prostate cancer tissue and microenvironment and promotes proliferation and androgen receptor-mediated transcription. In contrast, IL-1 displays negative effects on expression of androgen receptor and its target genes. A subgroup of prostate cancers show neuroendocrine differentiation, which may be in part stimulated by androgen ablation. A similar effect was observed after treatment of cells with IL-10. Another cytokine which is implicated in regulation of androgenic response is IL-23, secreted by myeloid cells. Most studies on androgens and IL were carried out with IL-6, which acts through the signal transducer and activator of the transcription (STAT) factor pathway. IL-6 is implicated in resistance to enzalutamide. Activation of the STAT-3 pathway is associated with increased cellular stemness. IL-6 activation of the androgen receptor in some prostate cancers is associated with increased growth in vitro and in vivo. Molecules such as galiellalactone or niclosamide have an inhibitory effect on both androgen receptor and STAT-3 pathways.
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Smyth, Kendra N., Lydia K. Greene, Tim Clutton-Brock, and Christine M. Drea. "Androgens predict parasitism in female meerkats: a new perspective on a classic trade-off." Biology Letters 12, no. 10 (October 2016): 20160660. http://dx.doi.org/10.1098/rsbl.2016.0660.

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The immunocompetence handicap hypothesis posits that androgens in males can be a ‘double-edged sword’, actively promoting reproductive success, while also negatively impacting health. Because there can be both substantial androgen concentrations in females and significant androgenic variation among them, particularly in species portraying female social dominance over males or intense female–female competition, androgens might also play a role in mediating female health and fitness. We examined this hypothesis in the meerkat ( Suricata suricatta ), a cooperatively breeding, social carnivoran characterized by aggressively mediated female social dominance and extreme rank-related reproductive skew. Dominant females also have greater androgen concentrations and harbour greater parasite loads than their subordinate counterparts, but the relationship between concurrent androgen concentrations and parasite burdens is unknown. We found that a female's faecal androgen concentrations reliably predicted her concurrent state of endoparasitism irrespective of her social status: parasite species richness and infection by Spirurida nematodes, Oxynema suricattae , Pseudandrya suricattae and coccidia were greater with greater androgen concentrations. Based on gastrointestinal parasite burdens, females appear to experience the same trade-off in the costs and benefits of raised androgens as do the males of many species. This trade-off presumably represents a health cost of sexual selection operating in females.
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Chen, Yue, Jeffrey D. Zajac, and Helen E. MacLean. "Androgen regulation of satellite cell function." Journal of Endocrinology 186, no. 1 (July 2005): 21–31. http://dx.doi.org/10.1677/joe.1.05976.

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Androgen treatment can enhance the size and strength of muscle. However, the mechanisms of androgen action in skeletal muscle are poorly understood. This review discusses potential mechanisms by which androgens regulate satellite cell activation and function. Studies have demonstrated that androgen administration increases satellite cell numbers in animals and humans in a dose–dependent manner. Moreover, androgens increase androgen receptor levels in satellite cells. In vitro, the results are contradictory as to whether androgens regulate satellite cell proliferation or differentiation. IGF-I is one major target of androgen action in satellite cells. In addition, the possibility of non-genomic actions of androgens on satellite cells is discussed. In summary, this review focuses on exploring potential mechanisms through which androgens regulate satellite cells, by analyzing developments from research in this area.
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Vanderschueren, Dirk, Liesbeth Vandenput, Steven Boonen, Marie K. Lindberg, Roger Bouillon, and Claes Ohlsson. "Androgens and Bone." Endocrine Reviews 25, no. 3 (June 1, 2004): 389–425. http://dx.doi.org/10.1210/er.2003-0003.

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Loss of estrogens or androgens increases the rate of bone remodeling by removing restraining effects on osteoblastogenesis and osteoclastogenesis, and also causes a focal imbalance between resorption and formation by prolonging the lifespan of osteoclasts and shortening the lifespan of osteoblasts. Conversely, androgens, as well as estrogens, maintain cancellous bone mass and integrity, regardless of age or sex. Although androgens, via the androgen receptor (AR), and estrogens, via the estrogen receptors (ERs), can exert these effects, their relative contribution remains uncertain. Recent studies suggest that androgen action on cancellous bone depends on (local) aromatization of androgens into estrogens. However, at least in rodents, androgen action on cancellous bone can be directly mediated via AR activation, even in the absence of ERs. Androgens also increase cortical bone size via stimulation of both longitudinal and radial growth. First, androgens, like estrogens, have a biphasic effect on endochondral bone formation: at the start of puberty, sex steroids stimulate endochondral bone formation, whereas they induce epiphyseal closure at the end of puberty. Androgen action on the growth plate is, however, clearly mediated via aromatization in estrogens and interaction with ERα. Androgens increase radial growth, whereas estrogens decrease periosteal bone formation. This effect of androgens may be important because bone strength in males seems to be determined by relatively higher periosteal bone formation and, therefore, greater bone dimensions, relative to muscle mass at older age. Experiments in mice again suggest that both the AR and ERα pathways are involved in androgen action on radial bone growth. ERβ may mediate growth-limiting effects of estrogens in the female but does not seem to be involved in the regulation of bone size in males. In conclusion, androgens may protect men against osteoporosis via maintenance of cancellous bone mass and expansion of cortical bone. Such androgen action on bone is mediated by the AR and ERα.
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Dissertations / Theses on the topic "Androgens"

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Van, Oeveren Margaret Ann. "Interpersonal functional flexibility : an antecedent of authoritative parenting?" Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28305.

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It has been asserted that androgynous individuals are both competent and flexible and that, as such, they should be most likely to be authoritative parents (highly demanding/highly responsive) (Spence & Helmreich, 1978). However, studies examining the association between psychological androgyny and this optimal parenting strategy (Baumrind, 1982; Spence & Helmreich, 1978) have reached conflicting conclusions. The position taken in this study is that there is a logical association between androgyny and authoritative parenting at the construct level, but that the component of androgyny critical to this link is functional flexibility (the ability to appropriately deploy both masculine and feminine attributes across multi-interpersonal domains) rather than the simple possession of both masculine and feminine traits per se. In view of this argument, earlier studies share a significant limitation. Their operational definitions of androgyny fail to reflect the functional flexibility aspect of the construct definition, thus allowing individuals who possess both masculine and feminine traits but who are not functionally flexible to be classified as androgynous. This study had two objectives. The first was to retest Spence and Helmreich's (1978) hypothesis that androgyny is positively related to authoritative parenting using a measure which would assess functional flexibility. The second objective was to demonstrate that authoritative parenting requires flexibility with respect to a whole range of interpersonal abilities rather than simply masculine and feminine attributes. A sample of 96 mothers with children between the ages of 7 and 12 were asked to complete a battery of questionnaires which included Bern's (1974) Sex Role Inventory (BSRI), Paulhus and Martin's (1987) Battery of Interpersonal Capabilities (BIC), and the Block (1965) Childrearing Practices Report: Q-Sort (CRPR). Contrary to what was expected, neither androgyny nor flexibility with respect to the whole range of interpersonal attributes was positively associated with authoritative parenting. Certain problems with the content of the parenting measure may have contributed to the lack of association. To minimize some of the problems with its content the method of using the parenting Q-sort was revised. The new analyses involved categorizing mothers according to warmth and demandingness--a method similar to that used in earlier studies. In these further analyses few significant differences in parenting style were found between androgynous mothers and other mothers. The most notable difference arose when the sex of the child was considered. Although, overall, androgynous mothers were not more likely to be bad parents, they were more likely than other mothers to be permissive with their sons.
Arts, Faculty of
Social Work, School of
Graduate
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Sharp, Danae Maree. "Androgens induce gender- & dose- specific effects on atherogenesis." Connect to full text, 2008. http://hdl.handle.net/2123/4158.

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Thesis (M. Sc. Med.)--University of Sydney, 2009.
Submitted in fulfilment of the requirements for the degree of Master of Science in Medicine to the Discipline of Medicine, Faculty of Medicine. Degree awarded 2009; thesis submitted 2008. Title from title screen (viewed Apr. 14, 2008) Includes bibliography. Also available in print form.
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Suri, Narinder K. "Androgens and the endometrium." Thesis, University of Nottingham, 1988. http://eprints.nottingham.ac.uk/13915/.

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The role of C19 steroids in the human endometrium is at present unclear. In order to gain an insight into their action, radioimmunoassay procedures were developed which had sufficient specificity and accuracy to measure testosterone, 5α-DHT, oestradiol, progesterone and androstenedione in endometrial samples. Amounts of androstenedione were greater (range 1.2-20.8 ng/mg tissue) than other steroids. Samples were obtained from patients presenting with a variety of conditions: subfertility, postmenopausal bleeding, dysfunctional uterine bleeding and abdominal pain. Patients admitted for sterilisation were used as normal controls. A significant positive correlation (r = 0.80) was found between the levels of testosterone and 5α-DHT measured in the same tissue which suggests the presence of a 5α reductase enzyme. No relationship was observed in tissue steroid concentration and age of the patients. Steroid concentrations were found to be high in tissues obtained from patients with endometrial carcinomas whereas progesterone concentration being low in subfertiles. The oestrogen, progesterone and androgen receptor levels of endometrial tissues from subfertile women were also determined using the DCC technique and not the procedure based on protamine sulphate precipitation since endometrial tissue available was very small. No correlation was found between receptor binding sites and day of cycle for any of the three steroids analysed; nor was there any correlation between age and receptor binding sites. A cyclic variation followed by normal women was seen in the oestrogen and progesterone receptor concentrations in the menstrual cycle. Such a variation was also observed in subfertile women on clomiphene citrate therapy. It is concluded that normal endometrium contains measurable quantities of androgens and that a receptor for 5α-DHT is present. The difference in steroid concentrations between normal and pathological states suggest that C19 steroids may be induced in the development of abnormalities.
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Tyndall, Victoria. "Androgens and the ovary." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5591.

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Between 10-15% of women suffer from polycystic ovary syndrome (PCOS), making it the most common cause of female infertility. Clinical features of PCOS include high circulating levels of ovarian androgens (T and A4), anovulation and obesity. The aetiology of this reproductive endocrinopathy is likely to be multifactorial, through the interplay of genetics, epigenetics and environmental factors. Primate research into sexual behaviour development noted that fetally androgenised monkeys developed symptoms like those of PCOS. There are now multiple animal models of PCOS using primates, sheep, rats and transgenic mice. The investigations described in this thesis use rodent models to examine the role of androgens in the pathogenesis of female infertility. An attempt to generate a granulosa cell specific androgen receptor knockout mouse model will first be described, followed by several studies into the developmental programming of female Wistar rat infertility and metabolism by steroid hormones. Initial investigations showed that testosterone proprionate (TP) administered to female rats during different windows of fetal and neonatal life alters the reproductive and metabolic axes of the adult animals. Fetal plus neonatal TP exposure led to complete ovarian dysgenesis, while postnatal exposure produced a PCOS-like phenotype. Animals which received TP postnatally were heavier and had an increased proportion of primordial follicles in their ovaries by postnatal day (pnd) 90 of life. Evaluation of this PCOS model showed that neonatally androgenised rats had ovarian follicles with larger antra and a greater ovarian stromal compartment. In addition, these animals were heavier when compared to controls. However, unlike human studies, neonatally androgenised rats showed no differences in circulating gonadotrophin or ovarian androgen levels. Nor did they show any programming effect of neonatal TP upon the theca interna by pnd 90. Further investigations to narrow the windows and dose of TP required to produce a PCOS phenotype showed that TP administered in an early window of neonatal life, between postnatal days (pnd) 1-6 not only led to anovulation, but potentially reprogrammed the hypothalamic-pituitary axis, as there was minimal gonadotrophin response to reduced ovarian negative feedback (inhibin B and estradiol) in these rats. Neonatal TP also affected the rat metabolic axis with adult animals becoming heavier after weaning without any change in food intake. Animals developed mesenteric and retroperitoneal obesity along with insulin resistance (IR). Increased hepatic glucocorticoid turnover and altered adipokine expression were also noted in neonatally androgenised females, possibly contributing to the pathogenesis of obesity. No effect of TP dose upon the severity of infertility or metabolic abnormalities in adult animals was observed. To delineate which features of the rat PCOS model resulted from androgenic, estrogenic or corticosteroid action, a final study used administration of different steroids during the early window of postnatal life: TP, estradiol valerate (EV), dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA) and dexamethasone (DEX). The anovulatory PCO-like phenotype observed with TP was also seen in animals which received EV, but not those which received DHT, DHEA or DEX. TP and EV treatment also resulted in a reduction of ovarian follicle numbers and activated follicle proportions, with an increase in primordial follicle proportions. Although glucose tolerant, animals treated with TP and EV were highly IR. Unlike dexamethasone, DHT and DHEA also produced IR in adult animals, to a lesser extent than TP and EV. Taken collectively, the results described in this thesis demonstrate that the PCOS-like phenotype observed in the neonatally androgenised female rat is likely to be due to the estrogenic actions of testosterone, potentially through as yet unknown epigenetic mechanisms. The programming of the metabolic components described may additionally be due to the actions of androgens. Furthermore, these studies demonstrate a novel estrogenic effect of neonatal steroids upon primordial follicle populations and show that the neonatally androgenised rat may be a rational PCOS model in a poly-ovulatory species.
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Cloke, Brianna. "The role of Androgens and the Androgen receptor in human endometrial stromal cell decidualization." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510758.

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Zahaf, Amina. "Rôle inattendu de la signalisation des androgènes dans le système nerveux central démyélinisé de la souris femelle : Identification de spécificités liées au sexe de l'animal." Thesis, université Paris-Saclay, 2022. http://www.theses.fr/2022UPASL046.

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La sclérose en plaques (SEP) est la plus commune des maladies démyélinisantes du système nerveux central (SNC). Elle se caractérise par une succession d'épisodes inflammatoires en partie liés à une dérégulation du système immunitaire et ciblant les cellules synthétisant la myéline, les oligodendrocytes. Ces épisodes sont d'abord suivis de phases de rémission correspondant à la régénération spontanée de la myéline détruite, encore appelée remyélinisation. Cependant, au fur et à mesure de la progression de la pathologie, la remyélinisation échoue notamment en raison d'une modification de l'environnement lésionnel qui devient inadapté au processus de réparation. Cette pathologie chronique et neurodégénérative est à l'heure actuelle considérée comme la première cause de handicaps lourds d'origine non traumatique chez l'adulte jeune. Elle concerne 3 femmes pour 1 homme. Au cours des dernières décennies, de nombreuses molécules visant le système immunitaire ont été identifiées afin de réduire la fréquence des attaques et leur sévérité. Ces molécules sont donc efficaces dans les formes récurrentes-rémittentes, mais deviennent inefficaces quand la maladie progresse. Le défi thérapeutique actuel est par conséquent l'identification de molécules qui permettraient également de favoriser la régénération de la myéline. Le rôle des hormones sexuelles mâles ou androgènes dans les modèles animaux de démyélinisation du SNC a fait l'objet de nombreuses études montrant leurs propriétés immunomodulatrices, neuroprotectrices et remyélinisantes chez le mâle. Puisque les souris femelles et les femmes produisent aussi des androgènes - bien qu'à un niveau beaucoup plus faible que les animaux mâles ou les hommes - l'objectif de mon projet de thèse était de déterminer la contribution des androgènes aux processus de protection et de régénération impliqués dans un contexte de démyélinisation chez les animaux femelles. Dans des modèles immuns (EAE) et non-immuns (LPC) de démyélinisation du SNC, les effets des androgènes ont été analysés par des immunomarquages et la visualisation de l'ultrastructure des axones et de la myéline, par des approches de tri des cellules immunitaires périphériques présentes dans les organes lymphoïdes et infiltrées dans le SNC. Les données indiquent des activités remyélinisantes, anti-inflammatoires et neuroprotectrices majeures des androgènes chez la femelle comme précédemment observé chez le mâle avec néanmoins plusieurs spécificités. Par ailleurs, une analyse transcriptomique de la moelle épinière des animaux EAE nous a conduit à identifier des gènes dont l'expression est dérégulée de façon cohérente avec les données histologiques et fonctionnelles. Ce projet suggère que le maintien d'un taux physiologique d'androgènes doit être pris en considération chez les patientes atteintes de SEP
Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS). The pathology is characterized by successive inflammatory insults, which are related to the dysregulation of the immune system and target the cells synthesizing myelin in the CNS, the oligodendrocytes. These insults are followed by steps of remission corresponding to the spontaneous regeneration of myelin, also called remyelination. However, when the disease progress, remyelination fails namely due to a lesion environment becoming inappropriate. The pathology characterized as chronic and neurodegenerative concerns 3 women for 1 men and is currently considered as the first cause of non traumatic disabilities in the young adults. During the last decades, a substantial number of molecules targeting the immune system has been identified in order to reduce the frequency and severity of the insults. These molecules are efficient on the relapsing-remitting form of the disease, but they become inefficient with disease progression. The current therapeutic challenge is the identification of molecules also able to boost the regeneration of myelin. The role of the male sexual hormones or androgens in models of CNS demyelination has been thoroughly investigated in males, which led to show their immunomodulatory, pro-myelinating and neuroprotective properties. Since females also produce androgens - though at a much lower level than males - the objective of my PhD project was to delineate the contribution of androgens to the protective and regenerative processes involved in the context of CNS demyelination in female mice. In immune (EAE) and non-immune (LPC) models of CNS demyelination, the effects of androgens have been analyzed via immunostaining experiments, visualization of myelin and axon ultrastructure, fluorescence-activated sorting of peripheral immune cells present in the lymphoid organs or infiltrated in the CNS. The data indicate major remyelinating, anti-inflammatory and neuroprotective activities of androgens in females as previously observed in males with however some specificities. Moreover, transcriptomic analysis of the spinal cord from EAE animals led us to identify profiles of deregulated genes tightly correlated with the histological and functional data. Altogether these results suggest that the administration of appropriate doses of androgens would deserve to be further considered in female patients presenting with multiple sclerosis
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Shiwlochan, Amrita G. "Prenatal androgens and visceral fat." Honors in the Major Thesis, University of Central Florida, 2009. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/1327.

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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.
Bachelors
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Anthropology
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Pettiford, Jasmine. "Effect of garlic-deriveds-allylmercaptocysteine on androgen receptor expression in androgen-independent prostate cancer." Thesis, Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41005545.

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Santana, Luís Carlos Leal. "Impacto de andrógenos sobre a proliferação e atividade de fibroblastos e células epiteliais em cultura celular /." Araraquara, 2016. http://hdl.handle.net/11449/138766.

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Orientador: Luis Carlos Spolidório
Resumo: Hormônios esteroides sexuais participam de diversos eventos celulares e moleculares, e exercem influência sobre o epitélio e tecido conjuntivo do periodonto. A testosterona (T), principal hormônio androgênico, pode ser convertida em estradiol (E2) pela ação da enzima aromatase, ou em di-hidrotestosterona (DHT) pela ação da enzima 5α-redutase. Para elucidar o impacto de andrógenos sobre as células que compõem os tecidos conjuntivo e epitelial, fibroblastos e queratinócitos foram avaliados em relação aos efeitos de diferentes concentrações de T e DHT, além da exposição ao anastrozol (ANA), flutamida (FLU), fulvestranto (FUL), e às associações farmacológicas T+ANA, T+FLU e T+FUL. Os resultados do presente estudo indicaram que, de modo geral, hormônios esteroides androgênicos exercem efeitos opostos sobre eventos celulares de fibroblastos gengivais humano e células epiteliais HaCaT em cultura celular. Enquanto a T e a DHT agem promovendo o aumento da proliferação e atividade de fibroblastos, a exposição de células HaCaT a estes mesmos andrógenos resulta em inibição ou exiguidade do crescimento celular, atividade metabólica ou a capacidade de repovoamento da área de arranhão in vitro. Além disso, o tratamento farmacológico com ANA, FLU, FUL, e suas respectivas associações à T, parece influenciar eventos celulares de fibroblastos gengivais humano e células epiteliais HaCaT in vitro.
Abstract: Sex steroid hormones take part in different cellular and molecular process and exert their functions on the epithelium and connective tissue of the periodontium. Testosterone (T), the main androgenic hormone can be converted to estradiol (E2) through the aromatase enzyme action, or into dihydrotestosterone (DHT) by 5α-reductase activity. To elucidate the impact of androgens on the cells that constitute the connective and epithelial tissues, fibroblasts and keratinocytes were evaluated under the effects of different concentrations of T and DHT, besides to be both exposed to anastrozole (ANA), flutamide (FLU), fulvestrant (FUL), and the pharmacological associations T+ANA, T+FLU and T+FUL. The results of this study indicated that, in general, androgenic steroid hormones exert opposite effects on cellular events of human gingival fibroblasts and epithelial cells. While androgens act stimulating gingival fibroblasts, in HaCaT cells androgens promotes a shortage or inhibition of cell growth and activity. Furthermore, pharmacological treatment with ANA, FLU, FUL, and their associations to T, appears to influence cellular events of human gingival fibroblasts and HaCaT cells in vitro.
Mestre
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Xu, Huiping. "Electrophilic androgen receptor ligands as chemotherapeutic agents for prostate cancer." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1089126757.

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Thesis (Ph. D.)--Ohio State University, 2004.
Document formatted into pages; contains xxviii, 261 p. Includes bibliographical references (p. 141-149). Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2005 July 6.
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Books on the topic "Androgens"

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Chang, Chawnshang, ed. Androgens and Androgen Receptor. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8.

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1955-, Chang Chawnshang, ed. Androgens and androgen receptor: Mechanisms, functions, and clinical applications. Boston: Kluwer Academic Publishers, 2002.

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T, Tulandi, and Gelfand Morrie M, eds. Androgens and reproductive aging. London: New York, 2006.

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Bagatell, Carrie, and William J. Bremner. Androgens in Health and Disease. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593887.

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name, No. Androgens in health and disease. Totowa, NJ: Humana Press, Inc., 2003.

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Bagatell, Carrie J., and William J. Bremner, eds. Androgens in Health and Disease. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-388-0.

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1953-, Bhasin Shalender, ed. The therapeutic role of androgens. London: Baillière Tindall, 1998.

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J, Bagatell Carrie, and Bremner William J, eds. Androgens in health and disease. Totowa, N.J: Humana Press, 2003.

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J, Bagatell Carrie, and Bremner William J, eds. Androgens in health and disease. Totowa, N.J: Humana Press, 2003.

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Fischer, Leslie Michele. Androgen-directed development of the Xenopus laevis larynx: Androgen receptor expression and its relation to tissue differentiation. [New York]: [Columbia University], 1993.

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Book chapters on the topic "Androgens"

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Bon-chu, Chung, and Hu Meng-Chun. "Androgen Biosynthesis And Degradation." In Androgens and Androgen Receptor, 1–15. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_1.

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Kobayashi, Yasushi, and Gen Sobue. "Androgen Receptor with Expanded Poly-Q Length in SBMA (Kennedy Disease)." In Androgens and Androgen Receptor, 265–70. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_10.

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Nawata, Hajime, Kiminobu Goto, Taijiro Okabe, Masatoshi Nomura, and Toshihiko Yanase. "Androgen Insensitivity Syndrome (Testicular Feminization)." In Androgens and Androgen Receptor, 271–77. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_11.

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Olsen, Nancy J., and William J. Kovacs. "Androgens in Immunology and Autoimmune Diseases." In Androgens and Androgen Receptor, 279–88. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_12.

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Chang, Johnny A., Hiep T. Nguyen, and Tom F. Lue. "Androgens in Penile Development, Penile Erection, and Erectile Dysfunction." In Androgens and Androgen Receptor, 289–98. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_13.

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Collins, Loretta L., and Chawnshang Chang. "Androgens and the Androgen Receptor in Male Sex Development and Fertility." In Androgens and Androgen Receptor, 299–323. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_14.

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Handa, Robert J., and Robert F. McGivern. "Androgens and Brain Function: Behavioral Perspectives." In Androgens and Androgen Receptor, 325–44. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_15.

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Vanderschueren, D., L. Vandenput, A. Verstuyf, JV Swinnen, R. Bouillon, and S. Boonen. "Androgens, Skeletal Homeostasis, and Osteoporosis." In Androgens and Androgen Receptor, 345–59. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_16.

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von Eckardstein, Arnold, and Fredrick C. W. Wu. "Androgens and Coronary Artery Disease." In Androgens and Androgen Receptor, 361–86. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_17.

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Spratt, Daniel. "Androgen Therapy in Nonendocrine Illnesses." In Androgens and Androgen Receptor, 387–409. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1161-8_18.

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Conference papers on the topic "Androgens"

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Kasra, Mehran, Carla Vanin, Robert Casper, and Marc Grynpas. "The Effects of Androgens and Estrogen on the Mechanical Properties of Bone in the Aged Ovariectomized Rat." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1153.

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Abstract Sex steroids regulate normal bone metabolism. Deficiency of gonadal hormones in both males and females leads to osteopenia and osteoporosis (1,2). Estrogen is necessary for maintaining bone density in pre- and post-menopausal women, but the role of androgen is still unclear. The effects of testosterone and anabolic steroids on bone in women appear to be positive (3). There is also data supporting a positive effect of androgens on bone maintenance in ovariectomized rats. Testosterone can be converted to estrogen in vivo, unlike its metabolite 5 alpha dihydrotestosterone (DHT), which also binds to androgen receptors with high affinity. The objective of this study was to determine the effects of a non-aromatizable androgen (DHT) alone, or in combination with estrogen, on mechanical properties of cortical and trabeular bone in the aged ovariectomized female rat.
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Onopchenko, M. A., G. V. Vasil'ev, A. V. Osadchuk, and L. V. Osadchuk. "ETHNIC DIFFERENCES IN THE LENGTH OF CAG REPEATS IN THE ANDROGEN RECEPTOR GENE AND TESTOSTERONE LEVELS IN YOUNG MEN OF THE SIBERIAN REGION OF RUSSIA." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-99.

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The aim of the study was to identify ethnic differences in the number of CAG repeats of the androgen receptor gene (AR), anthropometric and hormonal indicators in men of three ethnic groups (Slavs, Buryats and Yakuts) living in the Russa. The androgen receptor mediates the effects of androgens on a wide range of organs and tissues in men. The AR is characterized by polymorphism of CAG repeats, which can be an ethno-dependent trait and determine functional and morphogenetic effects of testosterone. The study established the ethnic differences in the length of CAG repeats between the Slavs, Buryats and Yakuts (23, 24, 25 triplets, respectively), as well as in anthropometric and hormonal indicators. LH concentrations were higher in Buryats than in Slavs or Yakuts, but the testosterone level was the lowest in Buryats compared to Slavs or Yakuts.
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Coleman, Daniel, Katy Van Hook, Robert Lisac, Carly King, Nicholas Wang, Jacob Schwartzman, Martin Gleave, et al. "Abstract 3592: Androgens interfere with enzalutamide agonism of mutant F876L androgen receptor." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3592.

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Mizokami, Atsushi, Misako Kumaki, Takashi Shima, Kouji Izumi, Yoshifumi Kadono, Hiroyuki Konaka, and Mikio Namiki. "Abstract 360: Effect of adrenogenic androgens on androgen receptor activity in prostate cancer microenvironment." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-360.

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de Bono, Johann S. "Abstract CN08-02: Androgens, biomarkers, and abiraterone." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-cn08-02.

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Chiodo, C., F. Montalto, C. Morelli, S. Marsico, S. Aquila, D. Sisci, F. De Amicis, S. Andò, and M. Lanzino. "PO-058 Unravelling the protective role of androgens/androgen receptorin breast cancer: when BAD goes good." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.102.

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Osgood, R. S., D. I. Kasahara, H. Tashiro, Y. Cho, A. P. Cardoso, and S. A. Shore. "Androgens Alter the Pulmonary Response to Ozone in Mice." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2390.

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Creevey, L., A. Ali, R. Bleach, ADK Hill, L. Young, and M. McIlroy. "Abstract P3-04-18: The impact of circulating androgens on the androgen receptor in aromatase inhibitor resistant breast cancer." 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-p3-04-18.

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Cai, Kai, Debra H. Phillips, Chris Elliott, Edwige Van der Heiden, Marie-Louise Scippo, Marc Muller, and Lisa Connolly. "Removal of Androgens and Estrogens from Water by Reactive Materials." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5514857.

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Chun, Yae Yeon, Nagalakshmi Nadiminty, Wei Lou, Joy Yang, Christopher P. Evans, Hsing-Jien Kung, and Allen C. Gao. "Abstract 1727: Interleukin-6 and intracrine androgens in prostate cancer cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1727.

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Reports on the topic "Androgens"

1

Liu, A., K. E. Carlson, J. A. Katzenellenbogen, H. F. VanBrocklin, C. J. Mathias, and M. J. Welch. Androgen receptor-based imaging agents for the prostate: Synthesis and tissue distribution studies with tritium and fluorine-18 labeled androgens. Office of Scientific and Technical Information (OSTI), December 1990. http://dx.doi.org/10.2172/10133430.

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Chinni, Sreenivasa R. Uncarboxylated Osteocalcin and Gprc6a Axis Produce Intratumoral Androgens in Castration-Resistant Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2015. http://dx.doi.org/10.21236/ada621327.

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Katzenellenbogen, J. A. (Radiolabeled androgens and progestins as imaging agents for tumors of the prostate and breast). Office of Scientific and Technical Information (OSTI), January 1991. http://dx.doi.org/10.2172/5622070.

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Katzenellenbogen, J. A. Radiolabeled androgens and progestins as imaging agents for tumors of the prostate and breast. Office of Scientific and Technical Information (OSTI), August 1992. http://dx.doi.org/10.2172/6853675.

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Abdel-Mageed, Asim B. Adipose Stem Cell-Based Therapeutic Targeting of Residual Androgens in African Americans with Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada571627.

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Katzenellenbogen, J. A. [Radiolabeled androgens and progestins as imaging agents for tumors of the prostate and breast]. Progress report. Office of Scientific and Technical Information (OSTI), December 1991. http://dx.doi.org/10.2172/10126688.

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Hornsby, Peter. Human Adrenal Androgens: Regulation of Biosynthesis and Role in Estrogen-Responsive Breast Cancer in a Mouse Model. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada383881.

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Katzenellenbogen, J. A. Radiolabeled androgens and progestins as imaging agents for tumors of the prostate and breast. Technical progress report, February 1, 1992--January 31, 1993. Office of Scientific and Technical Information (OSTI), August 1992. http://dx.doi.org/10.2172/10110956.

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Coetzee, Gerhard A., Judd Rice, and Li Jia. Androgen Receptor-Mediated Escape Mechanism from Androgen Ablation Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada501983.

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Balk, Steven P. Androgen Metabolism in Progression to Androgen-Independent Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada502868.

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