Relevant bibliographies by topics / Type 5 17β-hydroxysteroid dehydrogenase

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Academic literature on the topic 'Type 5 17β-hydroxysteroid dehydrogenase'

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Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Type 5 17β-hydroxysteroid dehydrogenase"

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Krazeisen, A., R. Breitling, G. Möller, and J. Adamski. "Phytoestrogens inhibit human 17β-hydroxysteroid dehydrogenase type 5." Molecular and Cellular Endocrinology 171, no. 1-2 (January 2001): 151–62. http://dx.doi.org/10.1016/s0303-7207(00)00422-6.

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Poirier, Donald, Patrick Bydal, Martin R. Tremblay, Kay-Mane Sam, and Van Luu-The. "Inhibitors of type II 17β-hydroxysteroid dehydrogenase." Molecular and Cellular Endocrinology 171, no. 1-2 (January 2001): 119–28. http://dx.doi.org/10.1016/s0303-7207(00)00427-5.

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Brožič, Petra, Barbara Golob, Nataša Gomboc, Tea Lanišnik Rižner, and Stanislav Gobec. "Cinnamic acids as new inhibitors of 17β-hydroxysteroid dehydrogenase type 5 (AKR1C3)." Molecular and Cellular Endocrinology 248, no. 1-2 (March 2006): 233–35. http://dx.doi.org/10.1016/j.mce.2005.10.020.

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Rheault, Patrick, Annie Charbonneau, and Van Luu-The. "Structure and activity of the murine type 5 17β-hydroxysteroid dehydrogenase gene." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1447, no. 1 (October 1999): 17–24. http://dx.doi.org/10.1016/s0167-4781(99)00106-2.

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Byrns, Michael C., Yi Jin, and Trevor M. Penning. "Inhibitors of type 5 17β-hydroxysteroid dehydrogenase (AKR1C3): Overview and structural insights." Journal of Steroid Biochemistry and Molecular Biology 125, no. 1-2 (May 2011): 95–104. http://dx.doi.org/10.1016/j.jsbmb.2010.11.004.

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Boutin, Sophie, and Donald Poirier. "Structure Confirmation and Evaluation of a Nonsteroidal Inhibitor of 17β-Hydroxysteroid Dehydrogenase Type 10." Magnetochemistry 4, no. 3 (July 23, 2018): 32. http://dx.doi.org/10.3390/magnetochemistry4030032.

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17β-Hydroxysteroid dehydrogenase type 10 (17β-HSD10) is a steroidogenesis enzyme known for its potential role in Alzheimer’s disease. For comparison purposes between steroidal and nonsteroidal 17β-HSD10 inhibitors 1 and 2, respectively, we attempted the chemical synthesis of benzothiazole phosphonate derivative 2. Instead of a one-pot synthesis, we report a two-step synthesis with characterization of both imine intermediate 5 and final compound 2. Furthermore, complete assignation of 1H and 13C nuclear magnetic resonance (NMR) signals of 2 is provided, as we observed a divergence of NMR data with those published previously. Finally, biological assays showed that 1 and 2 inhibited the oxidation of estradiol (E2) into estrone (E1) by the 17β-HSD10 recombinant protein. However, in human embryonic kidney (HEK)-293 intact cells transfected with 17β-HSD10, only the steroidal inhibitor 1 induced a dose-dependent inhibition of E2 to E1 transformation.
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Chai, Zhonglin, Phillip Brereton, Takashi Suzuki, Hironobu Sasano, Varuni Obeyesekere, Genevieve Escher, Richard Saffery, Peter Fuller, Carla Enriquez, and Zygmunt Krozowski. "17β-Hydroxysteroid Dehydrogenase Type XI Localizes to Human Steroidogenic Cells." Endocrinology 144, no. 5 (May 1, 2003): 2084–91. http://dx.doi.org/10.1210/en.2002-221030.

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We searched expressed sequence tag databases with conserved domains of the short-chain alcohol dehydrogenase superfamily and identified another isoform of 17β-hydroxysteroid dehydrogenase, 17βHSDXI. This enzyme converts 5α-androstane-3α, 17β-diol to androsterone. The substrate has been implicated in supporting gestation and modulating γ-aminobutyric acid receptor activity. 17βHSDXI is colinear with human retinal short-chain dehydrogenase/reductase retSDR2, a protein with no known biological activity (accession no. AAF06939). Of the proteins with known function, 17βHSDXI is most closely related to the retinol-metabolizing enzyme retSDR1, with which it has 30% identity. There is a polymorphic stretch of 15 adenosines in the 5′ untranslated region of the cDNA sequence and a silent polymorphism at C719T. A 17βHSDXI construct with a stretch of 20 adenosines was found to produce significantly more enzyme activity than constructs containing 15 or less adenosines (43% vs. 26%, P < 0.005). The C719T polymorphism is present in 15% of genomic DNA samples. Northern blot analysis showed high levels of 17βHSDXI expression in the pancreas, kidney, liver, lung, adrenal, ovary, and heart. Immunohistochemical staining for 17βHSDXI is strong in steroidogenic cells such as syncytiotrophoblasts, sebaceous gland, Leydig cells, and granulosa cells of the dominant follicle and corpus luteum. In the adrenal 17βHSDXI, staining colocalized with the distribution of 17α-hydroxylase but was stronger in the mid to outer cortex. 17βHSDXI was also found in the fetus and increased after birth. Liver parenchymal cells and epithelium of the endometrium and small intestine also stained. Regulation studies in mouse Y1 cells showed that cAMP down-regulates 17βHSDXI enzymatic activity (40% vs. 32%, P < 0.05) and reduces gene expression to undetectable levels. All-trans-retinoic acid did not affect 17βHSDXI expression or activity, but addition of the retinoid together with cAMP significantly decreased activity over cAMP alone (32% vs. 23%, P < 0.05). Cloning and sequencing of the 17βHSDXI promoter identified the potential nuclear receptor steroidogenic factor-1 half-site TCCAAGGCCGG, and a cluster of three other potential steroidogenic factor-1 half-sites were found in the distal part of intron 1. Collectively, these results suggest a role for 17βHSDXI in androgen metabolism during steroidogenesis and a possible role in nonsteroidogenic tissues including paracrine modulation of 5α-androstane-3α, 17β-diol levels. 17βHSDXI could act by metabolizing compounds that stimulate steroid synthesis and/or by generating metabolites that inhibit it.
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Qin, K. "Expression of 17β-hydroxysteroid dehydrogenase type 5 in human ovary: a pilot study." Journal of the Society for Gynecologic Investigation 7, no. 1 (February 2000): 61–64. http://dx.doi.org/10.1016/s1071-5576(99)00067-2.

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Penning, Trevor M., Michael E. Burczynski, Joseph M. Jez, Hseuh-Kung Lin, Haiching Ma, Margaret Moore, Kapila Ratnam, and Nisha Palackal. "Structure-function aspects and inhibitor design of type 5 17β-hydroxysteroid dehydrogenase (AKR1C3)." Molecular and Cellular Endocrinology 171, no. 1-2 (January 2001): 137–49. http://dx.doi.org/10.1016/s0303-7207(00)00426-3.

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Steckelbroeck, Stephan, Matthias Watzka, Birgit Stoffel-Wagner, Volkmar H. J. Hans, Lioba Redel, Hans Clusmann, Christian E. Elger, Frank Bidlingmaier, and Dietrich Klingmüller. "Expression of the 17β-hydroxysteroid dehydrogenase type 5 mRNA in the human brain." Molecular and Cellular Endocrinology 171, no. 1-2 (January 2001): 165–68. http://dx.doi.org/10.1016/s0303-7207(00)00432-9.

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Dissertations / Theses on the topic "Type 5 17β-hydroxysteroid dehydrogenase"

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Xu, Dan (Ph D). "Role of 17β-hydroxysteroid dehydrogenase type 5 in breast cancer studied by intracrinology." Doctoral thesis, Université Laval, 2015. http://hdl.handle.net/20.500.11794/27239.

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Dans cette thèse, je présente une étude (1) du rôle de la 17β-HSD5 dans la modulation des taux d'hormones et dans la prolifération, et l'impact de l'expression de la 17β-HSD5 sur d’autres protéines de BC cellules; (2) une étude comparative sur trois enzymes (17β-HSD1, 17β-HSD7 et 3α-HSD3) avec la provision de DHEA et ses substrats directes soit l’E1 ou la DHT. Les principaux résultats obtenus dans cette étude sont les suivants: (1) en utilisant l'ARN d’interférence de la 17β-HSD5, des immunodosages enzymatiques et des tests de prolifération de cellules démontrent que l'expression de la 17β-HSD5 est positivement corrélée à un niveau de T et de DHT dans les BCC, mais négativement corrélée pour l’E2 et la prolifération des cellules de BC (2) les analyses quantitatives de PCR en temps réel et de Western blot ont démontré que l’inhibition de l’expression de la 17β-HSD5 régule à la hausse l'expression de l'aromatase dans les cellules MCF-7. (3) L’analyse d’ELISA de la prostaglandine E2 a vérifié que l'expression accrue de l'aromatase a été modulée par des niveaux élevés de PGE2 après l’inactivation de l’expression du gène de la 17β-HSD5. (4) Le test de cicatrisation a montré que l’inactivation de l’expression du gène de la 17β-HSD5 favorise l’augmentation de la migration cellulaire. (5) L'expression du gène 17β-HSD5 dans des échantillons cliniques, à partir de l'analyse de base de données ONCOMINE, a montré que sa plus faible expression a été corrélée avec le statut de l’HER-2 et de la métastase de la tumeur. (6) Les données protéomiques révèlent également que des protéines impliquées dans les voies métaboliques sont fortement exprimées dans les cellules MCF-7 après l’inactivation de l’expression du gène de la 17β-HSD5. (7) L’étude n'a démontré aucune différence dans la fonction biologique de la 17β-HSD1 et de la 17β-HSD7 lorsqu'elles sont cultivées avec différentes stéroïdes: tel que les niveaux de stéroides, la prolifération cellulaire et les protéines régulées. (8) Toutefois, la supplémentation du milieu de culture se révèle avoir un impact marqué sur l'étude de la 3α-HSD3. (9). Nous avons proposé que l'utilisation de la DHEA comme source d'hormone puisse entraîner une meilleure imitation des conditions physiologiques post-ménopausales en culture cellulaire selon l’intracrinologie.
Human 17β-hydroxysteroid dehydrogenase type 5 (17β-HSD5) mainly synthesizes the activate androgen testosterone (T) from △4-androstenedione (4-dione), then 4-dione and T aromatazion to estrone (E1) and estradiol (E2) by the action of aromatase. 17β-HSD1 and 7 catalyze the formation of E2 from E1 and inactivate androgen dihydrotestosterone (DHT). In this thesis, I present the study of (1) the roles of 17β-HSD5 in the modulation of hormone levels and in the proliferation. and the proteomic study of the impact of the 17β-HSD5 knock down in BCC; (2) a comparative study of three enzymes (17β-HSD1，7 and 3α-HSD3) with the provision of DHEA and the direct substrates, E1 or DHT. The main results obtained in this study are as follow: (1) Using RNA interference of 17β-HSD5, enzyme immunoassays, and cell proliferation assays demonstrate that 17β-HSD5 expression is positively correlated with T and DHT levels in BCC, but negatively correlated with E2 levels, and BCC proliferation. (2) Quantitative real-time PCR analyzes and western blot showed that 17β-HSD5 knockdown up-regulates aromatase expression in MCF-7 cells. (3) Prostaglandin E2 ELISA assay verified that aromatase expression increase was modulated by elevated PGE2 levels after 17β-HSD5 knockdown. (4) Wound healing assay showed that with the knockdown of 17β-HSD5 expression, cell migration increased. (5)17β-HSD5 gene expression in clinical samples from ONCOMINE analysis showed its lower expression was correlated with HER-2 status and tumor metastasis. (6) The proteomic data also reveal that proteins involved in metabolic pathways are highly expressed in 17β-HSD5 knockdown MCF-7 cells. (7) Cell biology study showed no difference in biological function for 17β-HSD1 and 17β-HSD7 when cultured with different steroids cell proliferation and estradiol levels decreased, whereas DHT accumulated; cyclin D1, PCNA, and pS2 were down-regulated after knocking down these two enzymes. (8) The culture medium supplementation was found to have a marked impact on the study of 3α-HSD3. (9) We first proposed that using DHEA as hormone source may result in better mimicking of the physiological conditions of post-menopausal in cell culture according intracrinology.
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Wang, Ruixuan. "Expression and role of 17BETA-hydroxysteroid dehydrogenase type 1, 5 and 7 in epithelial ovarian cancer." Master's thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/29632.

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Le cancer de l’ovaire est l’une des cinq causes les plus fréquentes de décès par cancer chez les femmes dans le monde développé. Environ 90% des cancers de l’ovaire proviennent de l’épithélium que l’on nomme cancer de l’ovaire épithélial (EOC). Le EOC est un cancer hormono-dépendant et les stéroïdes sexuels jouent un rôle crucial en favoriant la prolifération et de la survie des cellules. Les 17β-hydroxystéroïdes déshydrogénases (17β-HSDs) jouent un rôle important pour le contrôle de la concentration intracellulaire de tous les stéroïdes sexuels actifs. Le mécanisme qui reculent le fonctionnent et l’expression des 17β-HSDs dans le EOC sont très peu compris. L’inhibition de certains 17β-HSDs pourrait être un traitement de l’EOC et ette approche thérapeutique doit être étudiée. Les résultats de notre étude ont démontré que les 17β- HSD types 1, 5 et 7 sont tous exprimés dans les cellules OOC-3, mais que la type 1 est la plus abondante. L’expression des 17β-HSD types 1 et 7 dans les tumeurs ovariennes épithéliales que dans les ovaires normaux (type 1, 2.2 fois; type 7, 1.9 fois). Mais l’expression de la 17β-HSD 5 est significativement plus faible dans les tumeurs, suite au développement de l’EOC (-5.217 fois). De plus, la prolifération cellulaire a diminué à la suite du knockdown la 17β-HSD type 1 ou type 7 par des siRNAs spécifiques dans les cellules OVCAR-3, mais, le knockdown de la type 5 a un effet contraire. Nous suggérons que la 17β-HSD 5 peut être impliquée dans une signalisation d’hormones stéroïdiennes pour le développement du cancer de l’ovaire épithélial. Les 17β-HSD 1 et 7 pourraient être des biomarqueurs importants pour l’EOC diagnostiqué tôt et ils peuvent également être de nouvelles cibles pour le traitement de l’EOC.
Ovarian cancer is one of the top five commonest causes of female cancer death in the developed world. About 90% of ovarian cancer have epithelial origins. Epithelial ovarian cancer (EOC) is a hormone-dependent cancer, in which the sex steroids play a crucial role in maintaining the cell proliferation and survival. The 17β-hydroxysteroid dehydrogenases (17β-HSDs) are important in the control of intracellular concentration of all active sex steroids. The function and expression of 17β-HSDs in EOC is not fully understood. Whether or not 17β-HSDs could be a therapeutic approach for the EOC treatment needs to be studied. Our results showed that 17β-HSD types 1, 5 and 7 are all expressed in EOC cells OVCAR-3 and type 1 is the highest one. The expression of 17β-HSD types 1 and 7 is higher in epithelial ovarian tumor tissues than in normal ovaries (type1, 2.2-fold; type7, 1.9-fold), but the expression of 17β-HSD type 5 is significantly lower in the tumor, following the EOC development (-5.2-fold). We found that cell proliferation was decreased after 17β-HSD type 1 or 7 knockdown by specific siRNAs in OVCAR-3 cells. While knocking down type 5 has the opposite effect. We suggest that 17β- HSD type 5 may be involved in steroid hormone signaling in EOC development. Moreover, 17β-HSD types 1 and 7 could be important biomarkers for early diagnosed EOC and novel targets for EOC treatment.
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Santos, Betânia Rodrigues dos. "Estudo da associação entre polimorfismos do gene do receptor de vitamina D (VDR) e do SNP-71 A/G do gene 17 beta- hidroxiesteróide desidrogenase tipo 5 (HSD17B5) e variáveis clínicas, hormonais e metabólicas em pacientes com pubarca precoce e controles." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/31696.

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A pubarca precoce (PP) é definida como o desenvolvimento de pêlos pubianos antes dos 8 anos de idade em meninas e 9 anos de idade em meninos. Embora a PP não interfira diretamente com os eventos da puberdade, algumas evidências sugerem que estas meninas tenham maior risco para desenvolver, mais tarde, a Síndrome dos Ovários Policísticos (PCOS). A 17ß-hidroxiesteróide desidrogenase tipo 5 (17ßHSD5) é a principal responsável pela conversão de androstenediona em testosterona. Variações no gene que codifica para essa enzima, em especial os polimorfismos de nucleotídeo único (SNPs), podem estar relacionados com hiperandrogenismo e PCOS. A vitamina D, além dos efeitos sobre metabolismo ósseo, parece modular outras ações extra-esqueléticas, incluindo secreção e sensibilidade tecidual à insulina. A Vitamina D vem sendo associada com resistência insulínica e variantes do gene do receptor da vitamina D (VDR), vem sendo estudadas em populações de risco como no diabetes. No entanto, pouco se sabe sobre o envolvimento destes polimorfismos na PP. Os objetivos do presente trabalho foram: Avaliar os níveis de 25-hidroxivitamina D; determinar a frequência dos polimorfismos FokI, BsmI, ApaI e TaqI do gene do VDR e do SNP-71AG do gene da 17ßHSD5; verificar se existe associação entre esses polimorfismos com variáveis antropométricas, metabólicas e hormonais em uma amostra de pacientes com PP e controles do sul do Brasil. Foram arroladas 36 meninas com PP e 197 controles saudáveis. As genotipagens foram realizadas por PCR em tempo real para os SNPs -71AG, BsmI e FokI e por PCR-RFLP para os SNPs ApaI e TaqI. O SNP -71 AG do gene da 17ßHSD5 apresentou distribuição genotípica de 52,4% AA, 39,1% AG e 8,6% GG, sendo a frequência dos alelos A:G de 0,72:0,28. Analisando os dois grupos, verificamos uma maior freqüência do alelo variante (G) no grupo de meninas com PP quando comparadas aos controles (0,37 e 0,26, respectivamente), no entanto sem diferença estatística (p=0,054); não foram verificadas associações do polimorfismo com os dados clínicos e hormonais. As meninas com PP apresentaram níveis séricos de 25(OH)D inferiores aos das meninas controles (18,08±8,32 versus 21,27±7,03; p=0,032). Na análise dos polimorfismos, observou-se que o genótipo polimórfico GG do SNP ApaI TG, apresentou uma frequência maior em PP (30,6%) do que nas controles (16,2%) (Odds Ratio: 2,269; 95% Intervalo de Confiança: 1,015 – 5,076; p=0,042). Este genótipo foi também associado com níveis mais baixos de estradiol (35,30 (14,80 – 50,48) versus 12,22 (6,49 – 23,69); p=0,030) e testosterona total (0,52 (0,39 – 0,84) versus 0,20 (0,11 – 0,47); p=0,009) nas meninas com PP, mas não foi associado com os níveis de 25(OH)D. Por outro lado, verificou-se associação entre a presença dos polimorfismos TaqI TC (genótipo TC+CC) e BsmI GA (genótipo GA+AA) e níveis séricos de 25(OH)D mais elevados no grupo de meninas saudáveis (19,86±7,16 versus 22,55±6,69, p=0,007; 19,53±6,94 versus 22,88±6,76, p=0,001, respectivamente). Em conclusão, os dados deste estudo indicam que: 1) houve maior freqüência do alelo variante G SNP -71 AG do gene da 17βHSD5, com uma associação limítrofe desse alelo com o diagnóstico clínico de PP; 2) o polimorfismo ApaI TG associou-se com PP e parece estar modulando os processos esteroidogênicos nas meninas com PP; 3) houve uma interação entre os polimorfismos TaqI TC e BsmI GA e concentrações circulantes de vitamina D em meninas do sul do Brasil.
Precocious pubarche (PP) is usually defined as the development of pubic hair before the age of 8 in girls and age of 9 in boys. Although the PP does not interfere directly in puberty events, some evidence suggests that these girls have higher risk for the development of Polycystic Ovary Syndrome (PCOS) at later ages. The Type 5 17β-Hydroxysteroid Dehydrogenase (17ßHSD5) is the principal responsible for the conversion of androstenedione to testosterone. Variations in the gene encoding for this enzyme, especially Single Nucleotide polymorphisms (SNPs), may be related with hyperandrogenism, and PCOS. Besides the effects on bone metabolism, vitamin D appears to modulate other extra-skeletal actions, including secretions and tissue sensitivity to insulin. Vitamin D has been associated with insulin resistance and variants in the vitamin D receptor (VDR) gene, have been studied in populations at risk of Diabetes. However, little is known about these polymorphisms in the PP. The aims of this work were: to evaluate the levels of the 25-hydroxyvitamin D; to determine the polymorphisms FokI, BsmI, ApaI and TaqI in VDR gene and SNP -71AG in 17ßHSD5 gene frequencies; to asses if exist association between this SNPs and anthropometric, metabolic and hormonal characteristics in patients with PP and controls of the southern Brazil. Were enrolled 36 girls with PP and 197 healthy controls. Genotypic analyzes were evaluated by Real Time for the SNPs -71AG, BsmI and FokI and by PCR-RFLP for the ApaI e TaqI polymorphisms. Genotype frequency for SNP -71 AG of the 17ßHSD5 gene was 52.4% AA, 39.1% AG and 8.6% GG, A:G allelic frequency was 0.72:0.28. Analyzing both groups, higher frequency of the variant allele (G) in patient PP than controls (0.37 e 0.26, respectively) was found but without statistical difference (p=0.054); there were no associations between this polymorphism and clinical and hormonal features. PP girls have serum levels of 25(OH)D lower than those from control group (18.08±8.32 versus 21.27±7.03; p=0.032). The polymorphism analyze was observed that genotype GG of the SNP ApaI TG showed a higher frequency in PP (30.6%) than controls (16.2%) (Odds Ratio: 2.269; 95% confidence interval: 1.015 – 5.076; p=0.042). The same genotype was associated with lower estradiol (35.30 (14.80 – 50.48) versus 12.22 (6.49 – 23.69); p=0.030) and total testosterone levels (0.52 (0.39 – 0.84) versus 0.20 (0.11 – 0.47); p=0.009), in girls with PP. There were no association between this polymorphism and serum 25(OH)D. On the other hand, there was association between the presence of the polymorphisms TaqI TC (TC + CC genotype) and BsmI GA (GA + AA genotype) and higher serum 25(OH)D in the group of healthy girls (19.86 ± 7.16 versus 6.69 ± 22:55 , p = 0.007; 19:53 ± 6.94 versus 22.88 ± 6.76, p = 0.001, respectively). In conclusion, data from this study indicate that: 1) there was a higher frequency of the variant allele G of the SNP -71 AG of the 17ßHSD5 gene, with a borderline association of this allele with the clinical diagnosis of PP; 2) ApaI TG polymorphism is associated with PP and seems to modulate the processes steroidogenesis in girls with PP; 3) there was an interaction between the polymorphisms TaqI TC and BsmI GA and vitamin D concentrations in girls from southern Brazil.
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Bailey, Helen Victoria. "Drug design and novel anti-cancer therapeutics : inhibitors of 17β hydroxysteroid dehydrogenase type 3." Thesis, University of Bath, 2007. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512267.

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Herein, we describe the design and synthesis of novel inhibitors of 17β-hydroxysteroid dehydrogenase type 3 which convert androstenedione into testosterone, which is then converted into dihydrotestosterone (DHT). This isozyme has been implicated in the growth of prostate cancer. Using an in silico pharmacophore model initial targets were planned, based around a diphenylether hydrophobic head linked to a 4-substituted piperidine ring. Over 45 compounds were synthesised and many show significant biological activity when evaluated in a 17β-HSD type 3 biological assay. The most potent compound in this series is 1-(4-[2-(4-chloro-phenoxy[-phenylamino]-piperidin)1-yl) ethanone with an IC₅₀ of 700 nM. The amine linked compounds are significantly more active than the amide equivalents. Synthesis of the amine-linked compounds was problematic and led to the development of a novel and general microwave assisted procedure for the reductive amination of anilines, enabling aromatic amine-linked compounds to be synthesised in excellent yields. A series of benzylamine linked inhibitors was also prepared. Over 30 analogues were synthesised and several show very promising biological activity. The most active compound is N-(2-([2-(4-Chloro-phenoxy)-phenylamino]-methyl)-phenyl)-acetamide, which exhibits an IC₅₀ of 900 nM. The synthesis of compounds with a benzophenone linked hydrophobic head group led to an unexpected product. X-ray crystallography was used to determine the structure, as a quinoline derivative. This led to optimisation of a novel modification of the Friedländer synthesis of quinolines. The potent inhibitors synthesised are selective over 17β-HASD Types 1 and 2. One inhibitor also shows potentially interesting activity against the leukaemia cell line CCRF-CEM, in the NCI screening, with a GI₅₀ of 10 nM.
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Moreira, Ricardo Paranhos Pires. "Análise de fatores genéticos associados ao desenvolvimento da síndrome metabólica durante a terapia com glicocorticoide em pacientes portadores da deficiência da 21-hidroxilase." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5166/tde-01042016-161323/.

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Introdução: A deficiência da 21-hidroxilase (21-OHD) é um frequente erro herdado do metabolismo que resulta no comprometimento da síntese do cortisol e/ou aldosterona e aumento da produção de andrógenos. A doença é caracterizada por uma diversidade fenotípica, variando desde virilização pré-natal da genitália externa de fetos femininos e pós-natal em ambos os sexos, com ou sem perda de sal, até quadros assintomáticos. Em seu tratamento é necessária reposição com glicocorticoide para se evitar a insuficiência adrenocortical e os sinais de virilização. Um fino ajuste na dose diária do glicocorticoide é essencial para se evitar sub ou supertratamento, com o objetivo de preservar o potencial de estatura final e fertilidade. Entretanto, tem sido observada maior frequência de obesidade e outras comorbidades metabólicas nestes pacientes; porém, a prevalência destas complicações ainda não é conhecida, bem como se estariam associadas à exposição ao glicocorticoide e/ou com fatores genéticos. Objetivos: avaliar a frequência de obesidade e de síndrome metabólica (SM) em pacientes com 21OHD; caracterizar a distribuição alélica dos polimorfismos dos genes do receptor de glicocorticoide (NR3C1) e da enzima 11beta-hidroxiesteróide desidrogenase tipo I (HSD11B1), e correlacionar a distribuição destes polimorfismos com a presença das complicações metabólicas. Métodos: Foram selecionados 109 pacientes (60 PS/49 VS), sendo 41 crianças e adolescentes (idade média 11,4 ± 3,9 anos) e 68 adultos (idade média 28,4 ± 9 anos) em tratamento com glicocorticoide e com adequado controle hormonal. Pacientes com a forma PS também receberam fludrocortisona. Adequado controle foi caracterizado por concentração normal de atividade plasmática de renina e de andrógenos de acordo com o sexo e idade nos últimos 2 anos. A obesidade nos adultos foi definida pelo IMC >= 30 kg/m² e em crianças e adolescentes pelo IMC acima do percentil 95. Síndrome metabólica foi definida segundo o critério do National Cholesterol Education Program em adultos e crianças. História familiar de hipertensão arterial, diabetes, dislipidemia, obesidade e/ou doença cardiovascular também foi avaliada. Foram mensuradas glicemia, lipoproteínas, triglicérides, colesterol total e insulina. Os alelos BclI, A3669G, ER22/23EK e N363S do gene NR3C1 e o alelo 4436InsA do gene HSD11B1 foram genotipados e as análises de associação com os fenótipos foram realizadas por meio dos testes Chi-quadrado, t-studant e análise de regressão. As análises de correlação foram feitas utilizando o teste de correlação de Pearson. Resultados: Obesidade foi observada em 31,7% das crianças e 23,5% dos adultos. Síndrome metabólica foi observada em 14,6% das crianças e 7,3% dos adultos. A prevalência dos componentes da SM foi maior no grupo dos obesos quando comparada a de pacientes não obesos (crianças e adultos). Não houve correlação significante entre o IMC, sexo, forma clínica da 21-OHD, duração da terapia e dose de GC. História familiar positiva para obesidade, hipertensão, dislipidemia e doença cardiovascular foi mais frequente nos pacientes obesos quando comparada a de pacientes não obesos, em adultos e crianças. Os polimorfismos BclI, A3669G e 4436InsA foram identificados em 23,2%, 9,7% e 14,6% dos alelos das crianças, respectivamente, e nos adultos em 26,4%, 9,6% e 18,4% dos alelos, respectivamente. A variante A3669G foi associada à maiores concentrações de LDL-c em crianças quando comparada aos carreadores do alelo selvagem. Os pacientes adultos carreadores do polimorfismo BclI apresentaram maior IMC, circunferência abdominal e PAS quando comparados aos carreadores do alelo selvagem. Não observamos diferenças estatisticamente significantes no perfil metabólico entre pacientes carreadores e não carreadores do polimorfismo 4436InsA (adultos e crianças). Conclusão: observamos que pacientes 21-OHD possuem maior prevalência de obesidade, e o grupo pediátrico maior prevalência de SM em relação à população de referência, sendo ambas independentes da dose de glicocorticoide e do tempo do tratamento. A presença de perfil metabólico adverso esteve associada à obesidade e à predisposição genética, tais como história familiar e variantes genéticas do receptor de glicocorticoide
Introduction: Congenital adrenal hyperplasia due to 21-hydroxylase deficiency (21OHD) is a common autosomal recessive disorder that leads to decreased glucocorticoid secretion, with or without mineralocorticoid deficiency, and increased androgen production. The disease is characterized by phenotypic variability, including a severe form with prenatal virilization of the external genitalia in female fetuses and postnatal virilization in both sexes, with or without salt loss. Current therapy aims to provide adequate glucocorticoid (GC) replacement and to suppress the abnormal androgen secretion; mineralocorticoid replacement aims to control the renal salt balance to avoid adrenal crisis. Nevertheless, these therapeutic goals are difficult to achieve in practice due to the complexity of replicating the physiologic cortisol circadian rhythm. Increased prevalence of obesity, insulin resistance, hypertension and adverse lipid profile have been observed among CAH patients under GC therapy; however, the extent of its prevalence and also whether it is associated with the GC dose or with genetic factors are not known. Objectives: to evaluate the obesity and metabolic syndrome (SM) frequencies in 21-OHD patients; to characterize the allelic distribution of the NR3C1 and HSD11B1 polymorphisms, and to correlate with the metabolic profile. Methods: One hundred and nine patients (60SW/49SV) were selected, 41 being children and adolescents (mean age 11.4 ± 3.9 yrs) and 68 adults (mean age 28.4 ± 9 yrs) all of whom received GC treatment and had adequate hormonal control. SW patients also received fludrocortisone. Adequate hormonal control was characterized by normal plasmatic rennin activity and androgen levels according to age and sex for at least two years. Blood fasting was used to obtain glucose, lipoproteins, triglycerides, total cholesterol and insulin levels. Obesity in the adult group was defined by BMI >= 30 kg/m², and in the young group by BMI > 95th percentile. Metabolic syndrome was defined by the NCEP ATPIII criteria. Family history of the hypertension, diabetes, dyslipidemia, obesity and/or cardiovascular disease was also evaluated. The BclI, A3669G, ER22/23EK and N363S alleles of the NR3C1 gene and 4436InsA of the HSD11B1 gene were genotyped and association analyses with phenotype were carried out with Chi-square, t-test and regression analysis. Correlation analyses were performed by Pearson correlation test. Results: obesity was observed in 31.7% of children and 23.5% of adults. SM was observed in 14.6% of young and 7.3% of adult patients. SM prevalence was higher in the obese group than the nonobese group (children and adults). There was no significant correlation between GC dose and BMI, sex, clinical form or treatment duration. Prevalence of family history of obesity, hypertension, dyslipidemia and cardiovascular disease was higher in the obese than in non-obese patients (children and adults). The BclI, A3669G and 4436InsA polymorphisms were found in 23.2%, 9.7% and 14.6% of the alleles in children, respectively and in 26.4%, 9.6% and 18.4% of the alleles in adults. The A3669G variant was associated to increased LDL-c levels in comparison with noncarriers in the young group. The BclI adult carriers presented higher BMI, abdominal circumference and systolic blood pressure in comparison with noncarriers. Statistically significant differences were not observed in the metabolic profile between carriers and non-carriers of the 4436InsA polymorphism (children and adults). Conclusion: in the present study, which analyzed the clinical and metabolic profile of 21-OHD patients, high obesity prevalence, independent of GC dose and treatment duration, was observed. Adverse metabolic profile was mainly associated with obesity and genetic predisposition, such as family history and NR3C1 polymorphisms
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Sivik, Tove. "Elucidating the role of 17β hydroxysteroid dehydrogenase type 14 in normal physiology and in breast cancer." Doctoral thesis, Linköpings universitet, Onkologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-84686.

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Oestrogens play key roles in the development of the majority of breast tumours, a fact that has been exploited successfully in treating breast cancer with tamoxifen, which is a selective oestrogen receptor modulator. In post-menopausal women, oestrogens are synthesised in peripheral hormone-target tissues from adrenally derived precursors. Important in the peripheral fine-tuning of sex hormone levels are the 17β hydroxysteroid dehydrogenases (17βHSDs). These enzymes catalyse the oxidation/reduction of carbon 17β of androgens and oestrogens. Upon receptor binding, the 17β-hydroxy conformation of androgens and oestrogens (testosterone and oestradiol) triggers a greater biological response than the corresponding keto-conformation of the steroids (androstenedione and oestrone), and the 17βHSD enzymes are therefore important mediators in pre-receptor regulation of sex hormone action. Breast tumours differ substantially with regards to molecular and/or biochemical signatures and thus clinical courses and response to treatment. Predictive factors, which aim to foretell the response of a patient to a specific therapeutic intervention, are therefore important tools for individualisation of breast cancer therapy. This thesis focuses on 17βHSD14, which is one such proposed marker, aiming to learn more of properties of the enzyme in breast cancer as well as in normal physiology. We found that high 17βHSD14 levels were correlated with clinical outcome in two separate subsets of breast tumour materials from trials evaluating adjuvant tamoxifen therapy. Striving to understand the underlying mechanisms, immunohistochemical 17βHSD14 expression patterns were analysed in a large number of human tissues using an in-house generated and validated antibody. The 17βHSD14 protein was expressed in several classical steroidogenic tissues such as breast, ovary and testis which supports idea of 17βHSD14 being an actor in sex steroid interconversion. Furthermore, using a radio-high pressure liquid chromatography method, cultured cells transiently expressing HSD17B14 were found to oxidise both oestradiol and testosterone to their less potent metabolites oestrone and androstenedione respectively. The evaluation of a mouse model lacking Hsd17b14 revealed a phenotype with impaired mammary gland branching and hepatic vacuolisation which could further suggest a role for 17βHSD14 in oestrogen regulation. Although other mechanisms of the enzyme cannot be ruled out, we suggest that 17βHSD14 relevance in tamoxifen-treated breast cancer is related to oestradiol-lowering properties of the enzyme which potentiate the anti-proliferative effects of tamoxifen. Translating into the clinical setting, patients with oestrogen receptor positive tumours expressing low levels of oestradiol-oxidising enzymes such as 17βHSD14 would likely receive more clinical benefit from alternative treatments to tamoxifen such as aromatase inhibitors or in the future possibly inhibitors of reductive 17βHSD-enzymes.
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Bertoletti, Nicole [Verfasser], and Gerhard [Akademischer Betreuer] Klebe. "Structural Characterization of 17β-Hydroxysteroid Dehydrogenase Type 14 and Inhibitor Optimization Using Crystallography and Computational Techniques / Nicole Bertoletti ; Betreuer: Gerhard Klebe." Marburg : Philipps-Universität Marburg, 2018. http://d-nb.info/1159702721/34.

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Abdelrahim, Mohamed Salah Rezk [Verfasser]. "Development of the first dual inhibitors for steroid sulfatase (STS) and 17β-hydroxysteroid dehydrogenase type 1 (17β-HSD1) : a novel treatment approach for endometriosis / Mohamed Salah Rezk Abdelrahim." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2019. http://d-nb.info/1236897048/34.

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Härkönen, P. (Päivi). "17β-Hydroxysteroid dehydrogenases/17-ketosteroid reductases (17HSD/KSRs) in prostate cancer:the role of 17HSD/KSR types 2, 5, and 7 in steroid hormone action and loss of heterozygosity at chromosome region 16q." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514279379.

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Abstract Prostate cancer is the most frequently diagnosed cancer in men in industrialized countries. Despite the substantial clinical importance of the disease, the mechanisms underlying the development and progression of prostate cancer are poorly understood. In the present study, fragment analysis of chromosome arm 16q was carried out with the aim of searching for sites of consistent chromosomal deletion, possibly uncovering the location of target genes that become inactivated in prostate carcinogenesis. The highest percentage of loss of heterozygosity (LOH) was found at chromosomal region 16q24.1-q24.2, including the gene for 17β-hydroxysteroid dehydrogenase/17-ketosteroid reductase (17HSD/KSR) type 2, HSD17B2. The data further indicated an association between loss of the most commonly deleted region and clinically aggressive features of the disease. A fragment analysis performed using sequential primary and locally recurrent prostate cancer specimens suggested the location of the genes related to prostate cancer progression to be at 16q24.3 and, further, gave rise to a hypothesis of the potential role of locus HSD17B2 as a prognostic marker for prostate cancer progression. Quantitative real-time polymerase chain reaction (PCR) revealed a decreased HSD17B2 gene copy number in prostate cancer specimens compared to their normal counterparts. A diminished HSD17B2 gene copy number was significantly associated with poor differentiation of the tumor. The progression of prostate cancer during androgen deprivation is a serious clinical problem, the molecular mechanisms of which largely remain to be clarified. The present data of enzyme activity measurements performed using high-performance liquid chromatography (HPLC) provided evidence of a substantial decrease in oxidative and an increase in reductive 17HSD/KSR activity during the transition of prostate cancer LNCaP cells into an androgen-independent state. Further, the changes detected in the activities largely coincided with the changes in the relative expression levels of genes for the potential 17HSD/KSR isoenzymes; 17HSD/KSR types 2, 5, and 7, as evidenced by relative quantitative reverse transcription PCR (RT-PCR). The data on the expression analysis of mRNA for 17HSD/KSR types 5 and 7 in prostate tissue specimens performed using in situ hybridization showed a moderately low but constitutive level for 17HSD/KSR7 mRNA in tissues of cancerous as well as hyperplastic origin. The expression of mRNA for 17HSD/KSR type 5, instead, varied considerably between different specimens, the highest expressions being strongly associated with aggressive and metastatic prostate cancer. Interestingly, furthermore, the intense expression of 17HSD/KSR5 was significantly associated with the androgen deprivation achieved either surgically or medically. Since 17HSD/KSRs critically contribute to the control of the bioavailability of active sex steroid hormones locally in the prostate, the variation in intraprostatic 17HSD/KSR activity might be crucially involved in the regulation of the growth and function of the organ.
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Grgano, Emanuele Marco [Verfasser], and Rolf W. [Akademischer Betreuer] Hartmann. "Development of 17β-hydroxysteroid dehydrogenase type 2 and type 1 inhibitors for the treatment of osteoporosis and estrogen dependent diseases / Emanuele Marco Grgano ; Betreuer: Rolf W. Hartmann." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/1120985005/34.

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Book chapters on the topic "Type 5 17β-hydroxysteroid dehydrogenase"

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Krazeisen, A., R. Breitling, G. Möller, and J. Adamski. "Human 17β-Hydroxysteroid Dehydrogenase Type 5 is Inhibited by Dietary Flavonoids." In Flavonoids in Cell Function, 151–61. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-5235-9_14.

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Scott*, James S., and Jasen Chooramun. "Chapter 5. 11β-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1) Inhibitors in Development." In Drug Discovery, 109–41. Cambridge: Royal Society of Chemistry, 2012. http://dx.doi.org/10.1039/9781849735322-00109.

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Esteves, Cristina L., Ewa A. Rog-Zielinska, Val Kelly, Mark Nixon, Jonathan R. Seckl, and Karen E. Chapman. "Transcriptional Up-Regulation of 11β-Hydroxysteroid Dehydrogenase Type 1 by Pro-Inflammatory Cytokines Is Mediated by C/EBPβ Transcription Factor." In BASIC - Gene Regulation of Growth Control & Homeostasis, OR10–5—OR10–5. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.or1.or10-5.

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Felicia, Maria, and Luciano Cavallo. "17β-Hydroxysteroid Dehydrogenase Type 3 Deficiency: Diagnosis, Phenotypic Variability and Molecular Findings." In Steroids - Basic Science. InTech, 2012. http://dx.doi.org/10.5772/27190.

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Cornel, Karlijn, Bert Delvoux, Laura Visconti, Roy Kruitwagen, and Andrea Romano. "Overexpression of 17β-Hydroxysteroid Dehydrogenase Type 1 Increases the Exposure of Endometrial Cancer to 17β-Estradiol." In CLINICAL/TRANSLATIONAL - Ovarian & Endometrial Cancer, P2–217—P2–217. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p31.p2-217.

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Day, JM, PA Foster, HJ Tutill, JD Hargrave, F. Schmidlin, N. Vicker, BVL Potter, MJ Reed, and A. Purohit. "STX2171, a 17β-Hydroxysteroid Dehydrogenase Type 3 (17β-HSD3) Inhibitor, Is EfficaciousIn Vivoin a Novel Hormone-Dependent Prostate Cancer Model." In Posters I, P2–41—P2–41. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p1.p2-41.

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Ayan, Diana Paula, Rene Maltais, Jenny Roy, and Donald Poirier. "A New Potent and Non-Estrogenic Steroidal Inhibitor of 17β-Hydroxysteroid Dehydrogenase Type 1 Inhibits the Formation of Estrogen EstradiolIn VitroandIn Vivo." In BASIC/TRANSLATIONAL - Hormones & Breast Cancer, P1–68—P1–68. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.p3.p1-68.

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Conference papers on the topic "Type 5 17β-hydroxysteroid dehydrogenase"

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Hilborn, Erik, Alexander Hung, and Agneta Jansson Jansson. "Abstract 3304: 17β-hydroxysteroid dehydrogenase type 1 is under negative regulation from miR-210 and 518c in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3304.

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Hilborn, Erik, Olle Stal, and Agneta Jansson. "Abstract A52: The microRNA control of 17β-hydroxysteroid dehydrogenase type 1 and 2 in breast cancer." In Abstracts: AACR Special Conference: Advances in Breast Cancer; October 17-20, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.advbc15-a52.

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