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Journal articles on the topic 'Stilbestrol'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Blyth, B., C. U. McRae, and J. G. Turner. "Resolution of hepatic metastases fromcarcinoma of prostate with stilbestrol." Urology 37, no. 6 (June 1991): 574–75. http://dx.doi.org/10.1016/0090-4295(91)80328-5.

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2

Pitkin, Roy M. "Vaginal and Cervical Abnormalities After Exposure to Stilbestrol In Utero." Obstetrics & Gynecology 102, no. 2 (August 2003): 222. http://dx.doi.org/10.1097/00006250-200308000-00004.

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3

Citrin, D. L. "3 High dose estrogens (diethyL stilbestrol diphosphate, DES-P) in prostate cancer." Journal of Steroid Biochemistry 28 (January 1987): 205. http://dx.doi.org/10.1016/0022-4731(87)91657-8.

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4

Lund, F., and F. Rasmussen. "Flutamide Versus Stilbestrol in the Management of Advanced Prostatic Cancer: A Controlled Prospective Study." Journal of Urology 140, no. 1 (July 1988): 209–10. http://dx.doi.org/10.1016/s0022-5347(17)41538-2.

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5

Ferro, Michael Arthur. "Use of Intravenous Stilbestrol Diphosphate in Patients with Prostatic Carcinoma Refractory to Conventional Hormonal Manipulation." Urologic Clinics of North America 18, no. 1 (February 1991): 139–43. http://dx.doi.org/10.1016/s0094-0143(21)01401-4.

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6

Herbst, Arthur L., Howard Ulfelder, and David C. Poskanzer. "Adenocarcinoma of the vagina. Association of maternal stilbestrol therapy with tumor appearance in young women." American Journal of Obstetrics and Gynecology 181, no. 6 (December 1999): 1574–75. http://dx.doi.org/10.1016/s0002-9378(99)70411-4.

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7

Parker, C. E., L. A. Levy, R. W. Smith, K. Yamaguchi, S. J. Gaskell, and K. S. Korach. "Separation and detection of enantiomers of stilbestrol analogues by combined high-performance liquid chromatography—thermospray mass spectrometry." Journal of Chromatography B: Biomedical Sciences and Applications 344 (January 1985): 378–84. http://dx.doi.org/10.1016/s0378-4347(00)82044-7.

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8

Mastai, R., S. Laganiere, I. R. Wanless, L. Giroux, B. Rocheleau, and P. Huet. "Hepatic sinusoidal fibrosis induced by cholesterol and stilbestrol in the rabbit: 2. Hemodynamic and drug disposition studies." Hepatology 24, no. 4 (October 1996): 865–70. http://dx.doi.org/10.1002/hep.510240418.

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9

Kwack, H. S., K. S. Ryu, G. T. Han, and E. Y. Ji. "A Case of Radical Trachelectomy for Clear Cell Adenocarcinoma Who Was Not Related to DES (Diethyl Stilbestrol) Exposure." Journal of Minimally Invasive Gynecology 15, no. 6 (November 2008): 132S. http://dx.doi.org/10.1016/j.jmig.2008.09.480.

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10

Szubartowska, E., K. Gromysz-Kalkowska, and M. Stȩpień. "Stilbestrol as a factor modifying the toxicity of ekatin for the pharaoh quail (Coturnix coturnix pharaoh). I. Young birds." Comparative Biochemistry and Physiology Part C: Comparative Pharmacology 100, no. 3 (January 1991): 597–602. http://dx.doi.org/10.1016/0742-8413(91)90046-v.

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11

Gromysz-Kałkowska, K., and E. Szubartowska. "Stilbestrol as a factor modifying the toxicity of ekatin for the pharaoh quail (Coturnix coturnix pharaoh)—ii. mature birds." Comparative Biochemistry and Physiology Part C: Comparative Pharmacology 103, no. 1 (September 1992): 237–41. http://dx.doi.org/10.1016/0742-8413(92)90258-9.

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12

Wanless, I. R., J. Belgiorno, and P. Huet. "Hepatic sinusoidal fibrosis induced by cholesterol and stilbestrol in the rabbit: 1. Morphology and inhibition of fibrogenesis by dipyridamole." Hepatology 24, no. 4 (October 1996): 855–64. http://dx.doi.org/10.1002/hep.510240417.

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13

Pitkin, R. "Herbst AL, Kurman RJ, Scully RE. Vaginal and cervical abnormalities after exposure to stilbestrol in utero. Obstet Gynecol 1972;40:287–98." Obstetrics & Gynecology 102, no. 2 (August 2003): 222. http://dx.doi.org/10.1016/s0029-7844(02)03065-x.

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14

Kohno, H., W. P. Bocchinfuso, O. Gandini, S. W. Curtis, and K. S. Korach. "Mutational analysis of the estrogen receptor ligand-binding domain: influence of ligand structure and stereochemistry on transactivation." Journal of Molecular Endocrinology 16, no. 3 (June 1996): 277–85. http://dx.doi.org/10.1677/jme.0.0160277.

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ABSTRACT The mouse estrogen receptor (mER) exhibits ligand stereochemical specificity for indenestrol A (IA), a stilbestrol estrogen. IA has a chiral C3 methyl group, and the mER preferentially binds the S-enantiomer (IA-S), resulting in elevated biological activity when compared with the IA-R enantiomer. To elucidate the mechanisms for this stereochemical recognition, we have constructed a series of mERs with individual amino acid substitutions at Met521, His528, Met532, and Val537. The abilities of yeast-expressed wild-type and mutant mERs to transactivate an estrogenresponsive reporter gene construct were measured in the presence of diethylstilbestrol (DES) and IA enantiomers. The concentration of IA-S required to induce half-maximal transactivation by wild-type mER was 10-fold lower than IA-R, which is attributed to the 15-fold greater binding affinity for IA-S. Wild-type mER displayed similar dose—response curves for IA-R and demethyl IA, which lacks a C3 methyl group, demonstrating that the presence and correct orientation of the C3 methyl group on the IA compound is required for high-affinity ligand binding and transcriptional activity. Each mutant exhibited a reduced preference for IA-S enantiomer with respect to transactivation, suggesting that this region of the mER functions in ligand stereochemical recognition and activation. A mutation at Met532 diminished DES-and IA-S-induced transactivation by 7·5-fold and 40-fold respectively, with minimal change on their binding affinity. These data suggest that Met532 is required for transactivation induced by the potent agonist, IA-S, and the M532G mutation effectively uncouples IA-S ligand binding from transactivation. Use of these stereochemically different ligands in combination with mutagenesis of the mER demonstrates that ligand structure could influence transactivation by specifically altering the conformation of the mER AF-2 region.

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15

Shapiro, Eugene D. "Analytic Strategies in Hospital Epidemiology: Case-Control Studies." Infection Control & Hospital Epidemiology 10, no. 4 (April 1989): 167–69. http://dx.doi.org/10.1086/645993.

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Case-control studies (sometimes referred to as case-referent studies) have long been important in epidemiologic research. This technique has been instrumental in allowing researchers to discover the associations between cigarettes and lung cancer, thromboembolism and oral contraceptives, and stilbesterol and vaginal cancer, just to cite a few examples. The case-control method is also a very useful technique for studies in hospital epidemiology. This article will briefly review this technique, its advantages, and some of its potential pitfalls.

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16

Kluess, Brigitte, Wolfgang Kreiser, Tony Sukri, Wolfgang Poll, and Hartmut Wunderlich. "(R)-5-[(1R,2R)-1-Ethyl-2- (4-oxocyclohexyl)butyl]oxepan-2-one, an Enantiopure ‘Pseudosteroid′." Zeitschrift für Naturforschung B 61, no. 1 (January 1, 2006): 111–12. http://dx.doi.org/10.1515/znb-2006-0122.

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The title compound C18H30O3 represents an optically pure member of a class of ‘pseudosteroids’, i. e. perhydrostilbene derivatives which mimic steroidal androgens (in the way like hexestrols or stilbestrols serve to substitute natural estrogens). The molecule 2 is characterized by three consecutive chiral centers leading to eight possible stereoisomers including four diastereomers. All enantiomers have been separated and their biological profile has been determined. As the result of the crystal structure presented here the two symmetry independent molecules display the configuration R,R,R at the centers of chirality.

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17

Curtis, S. W., H. Shi, C. Teng, and K. S. Korach. "Promoter and species specific differential estrogen-mediated gene transcription in the uterus and cultured cells using structurally altered agonists." Journal of Molecular Endocrinology 18, no. 3 (June 1997): 203–11. http://dx.doi.org/10.1677/jme.0.0180203.

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ABSTRACT Certain types of estrogenic compounds have been shown to have tissue-specific actions. In addition, some tissues may exhibit differential gene regulation by agonists and antagonists. Our previous studies using structurally modified estrogenic molecules had indicated differential effects on specific estrogen responses, indicating that the activity of the estrogen receptor protein can be altered depending not only upon the structure of the bound ligand but also the regulated gene itself. The mechanism of differential induction, however, was not determined, and might involve altered binding to the estrogen response element (ERE), altered transcription, or post-transcriptional modification of gene products. Our previous studies indicated that differential induction by modified diethylstilbestrol (DES) agonists could not be accounted for by differences in ligand affinity for the estrogen receptor (ER) or differential binding of the ER to a consensus vitellogenin A2 (vit A2) ERE. To determine if this differential hormonal responsiveness was reflected at the level of transcription, we analyzed mouse uterine mRNA of several estrogen-responsive genes, including glucose-6-phosphate dehydrogenase (G6PD), ornithine decarboxylase (ODC) and lactoferrin, by Northern blot following injection with the modified agonists DES, indenestrol A (IA), indenestrol B (IB) and Z-pseudo DES (ZPD). All compounds induced the G6PD message, although IB and ZPD induced expression only transiently, while DES and IA maintained the message for 24 h. No difference in induction was seen for ODC message, which was induced equally by all the compounds. In contrast, lactoferrin, a highly estrogen-responsive gene, was induced only by DES and IA and not by the other agonists IB or ZPD, showing that the lactoferrin gene was differentially regulated by these compounds. To determine whether this difference was due to altered transcriptional activity, the mouse lactoferrin estrogen-responsive module (mERM) linked to a chloramphenicol acetyl transferase (CAT) reporter gene was tested in transfected cells. Using the mouse estrogen receptor in RL95 cells, DES and IA induced expression of CAT, but IB did not, confirming the differential response seen in vivo. To show whether this difference in transcription occurred because of altered binding to the lactoferrin ERE, which is not a perfect consensus ERE, a gel shift assay was used to examine DNA binding of ER bound to the agonists. All ligands produced equivalent binding to the lactoferrin ERE suggesting that differential regulation was not a result of altered DNA binding. Taken together, these observations indicate that the differential induction of lactoferrin by these compounds occurs via altered activation of the transcriptional components unique to lactoferrin and is likely to involve altered interaction with co-activators. Surprisingly, unlike the mouse ER, the human estrogen receptor activated and induced expression of lactoferrin estrogen-responsive module-CAT with all the compounds. Mouse ER is also known to vary from the human ER in its activity with the triphenylethylene estrogen tamoxifen, which has agonist activity with the mouse ER but mixed antagonist/agonist activity with the human ER. The data show that human and mouse estrogen receptors are activated differently by this group of stilbestrol estrogen ligands when assayed on the lactoferrin response element, which is the first description of this type of gene and species specific difference. Lactoferrin gene regulation by estrogen receptor can be used as a model to study the mechanism of differential gene activation by different estrogen agonists and antagonists using a more physiological situation than commonly used with in vitro gene reporter systems.

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18

Idris, Ibrahim M., Arthur L. Burnett, and Michael R. DeBaun. "Epidemiology and treatment of priapism in sickle cell disease." Hematology 2022, no. 1 (December 9, 2022): 450–58. http://dx.doi.org/10.1182/hematology.2022000380.

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Abstract Ischemic priapism is a common but underrecognized morbidity affecting about 33% of adult men with sickle cell disease (SCD). The onset of priapism occurs in the prepubertal period and tends to be recurrent with increasing age. Significantly, priapism is associated with an unrecognized high burden of mental duress and sexual dysfunctions. The diagnosis of priapism is clinical. Many episodes of priapism will resolve spontaneously, but when an episode lasts longer than 4 hours, the episode is considered a urologic emergency requiring quick intervention with either corporal aspiration or shunt surgery. Only 3 randomized clinical trials (stilbesterol, ephedrine or etilefrine, and sildenafil) have been conducted for secondary priapism prevention in SCD. All 3 trials were limited with small sample sizes, selection biases, and inconclusive results after completion. The current molecular understanding of the pathobiology of priapism suggests a relative nitric oxide (NO) deficiency secondary to chronic hemolysis in SCD and associated phosphodiesterase type 5 dysregulation. We posit an increase in NO levels will restore the normal homeostatic relationship between voluntary erection and detumescence. Currently, 2 randomized phase 2 trials (1 double-blind, placebo-controlled trial and 1 open-label, single-arm intervention) are being conducted for secondary priapism prevention in men at high risk for recurrent priapism (NCT03938454 and NCT05142254). We review the epidemiology and pathobiology of priapism, along with mechanistic therapeutic approaches for secondary prevention of priapism in SCD.

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19

ELKIK, E., and C. FRANCESCH. "ChemInform Abstract: Synthesis of Fluoro Derivatives Related to Diethyl Stilbestrol." Chemischer Informationsdienst 17, no. 15 (April 15, 1986). http://dx.doi.org/10.1002/chin.198615175.

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20

Japanese Journal of Urology 88, no. 2 (1997): 202. http://dx.doi.org/10.5980/jpnjurol.88.202_3.

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21

Sandabe, U. K., and W. Y. Timothy. "The effects of progesterone, stilbesterol and its combination on the haematological parameters in female albino rats." Nigerian Veterinary Journal 28, no. 2 (May 9, 2008). http://dx.doi.org/10.4314/nvj.v28i2.3550.

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22

Soloway, Albert H. "Potential Carcinogens from Steroid Hormones and Diethyl Stilbesterol (DES): Chemical Relationships between Breast, Ovarian and Prostate Cancers." Journal of Drug Metabolism & Toxicology 05, no. 02 (2014). http://dx.doi.org/10.4172/2157-7609.1000170.

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