Disease relevance of diethylstilbestrol

• Rates and risks of diethylstilbestrol-related clear-cell adenocarcinoma of the vagina and cervix. An update [1].
• Prenatal exposure to diethylstilbestrol causes infertility in male mice and has been associated with malformations of the genital tract in men [2].
• Angiosarcoma of the liver occurred in a 76-year-old man who had been treated for a well-differentiated adenocarcinoma of the liver with diethylstilbestrol for 13 years [3].
• This study was designed to determine whether a cohort of males exposed in utero to diethylstilbestrol had a higher frequency of urogenital abnormalities than an unexposed cohort [4].
• An increased frequency of various genitourinary anomalies, infertility, and testicular cancer among males has been reported to follow intrauterine exposure to diethylstilbestrol, but not all studies have confirmed an association [4].

Psychiatry related information on diethylstilbestrol

• Finally, diethylstilbestrol-exposed men had no impairment of sexual function, as indicated, for example, by the frequency of intercourse or reported episodes of decreased libido [2].
• Previous research has suggested increased psychopathology in prenatally diethylstilbestrol (DES)-exposed persons [5].
• Self-concept in the diethylstilbestrol daughter [6].
• Over a 5-year period we have managed 63 diethylstilbestrol-exposed pregnant patients with a standardized protocol requiring weekly cervical examination and decreased physical activity of the patient [7].
• Both estradiol-17beta and diethylstilbestrol markedly increased the tissue content of CRBP2 mRNA in the vagina and uterus during the neonatal "critical period" but not after 15 days of age [8].

High impact information on diethylstilbestrol

• High-performance liquid chromatography, gas chromatography, and mass spectrometry showed that PC-SPES contains estrogenic organic compounds that are distinct from diethylstilbestrol, estrone, and estradiol [9].
• Within the exposed group, malformations were reported twice as often among those exposed to diethylstilbestrol before the 11th week of gestation as among those exposed later (P = 0.05) [2].
• Congenital malformations of the genitalia were reported three times as often by the diethylstilbestrol-exposed men as by the sons of the women in the placebo group [2].
• Administration of diethylstilbestrol for five days, which normally enhances prolactin responses to thyrotropin-releasing hormone, had no effect on prolactin secretion in these patients [10].
• Although isotopically labeled THC bound to macromolecules in uterine cytosol from the rhesus monkey, the binding was not displaced by unlabeled THC, diethylstilbestrol, estradiol, progesterone, cortisol, or 5 alpha-dihydrostestosterone [11].

Chemical compound and disease context of diethylstilbestrol

• Before the introduction of tamoxifen, diethylstilbestrol (DES) was widely considered to be the hormonal treatment of choice in postmenopausal women with advanced breast cancer [12].
• Effects of 17 beta-estradiol and diethylstilbestrol on concurrent development of hepatic, mammary, and pituitary tumors in WF rats: evidence for differential effect on liver [13].
• The synthesis of total proteins, growth hormone, and prolactin and the incorporation of radioactive precursors into RNA was studied in Pituitaries from normal F344 rats and rats given implants of 15 mg diethylstilbestrol (DES).Prolonged DES treatment (greater than 50 days) induced pituitary tumors in male and female rats [14].
• Of the synthetic estrogens studied, ethynylestradiol (CAS: 57-63-6) was a more potent inducer of these hepatic carcinomas than either diethylstilbestrol (CAS: 56-53-1) or hexestrol (CAS: 84-16-2) [15].
• BACKGROUND: Previous studies have shown that binding of [3H]cyclic adenosine 3',5'-monophosphate (cAMP) is increased in cytosol of diethylstilbestrol (DES)-induced pituitary tumors [16].

Biological context of diethylstilbestrol

• No pregnancies occurred, although diethylstilbestrol was not routinely used [17].
• Induction of apoptosis by diethylstilbestrol in hormone-insensitive prostate cancer cells [18].
• Massive increases in numbers and length of endometrial cell microvilli were observed at estrus, after injection of estradiol-17beta, diethylstilbestrol, estrogen plus progesterone. or the inhibitor C1628 to immature and ovariectomized rats [19].
• Primary granulosa cells were prepared from diethylstilbestrol-treated immature female rats and transfected with simian virus 40 (SV40) DNA or with SV40 plus activated human Ha-RAS oncogene [20].
• In utero diethylstilbestrol (DES) exposure alters Hox gene expression in the developing müllerian system [21].

Anatomical context of diethylstilbestrol

• Diethylstilbestrol regulates trophoblast stem cell differentiation as a ligand of orphan nuclear receptor ERR beta [22].
• Long-term responses of the mouse uterus to neonatal diethylstilbestrol treatment and to later sex hormone exposure [23].
• Granulosa cells from immature hypophysectomized diethylstilbestrol-treated rats displayed pronounced intracellular and intercellular changes after 48 hr of exposure to follicle-stimulating hormone (FSH) in vitro [24].
• The effect of 17 beta-estradiol (0.00018-180 nM in gel or 0.018-180 nM on gel) and diethylstilbestrol (DES; 0.0186-186 nM in gel) on the growth of vaginal epithelial cells was examined [25].
• Diethylstilbestrol induces fish oocyte maturation [26].

Associations of diethylstilbestrol with other chemical compounds

• In a study on the long-term effects of dietary diethylstilbestrol or 17 beta-estradiol on C3H mice, estrogens induced a proliferation of osseous trabeculae and increased the incidence and hastened the development of osteofibrotic areas in the sterna [27].
• A cohort of 3,139 obstetric patients, who delivered children between 1946 and 1965, was followed retrospectively to assess the relationship between exposure to diethylstilbestrol [(DES) CAS: 56-53-1; alpha, alpha'-diethyl-4,4'-stilbenediol] or other estrogenic substances during pregnancy and subsequent cancer incidence [28].
• Young adult female rats of either the Sprague-Dawley stock or the ACI strain were each given an implant of a compressed pellet of 5 mg diethylstilbestrol (DES) and 15 mg cholestrol 2 days before irradiation with 0.4, 1.3, or 4.0 rads of 0.43-MeV neutrons [29].
• One compressed 20-mg pellet containing cholesterol only or cholesterol mixed with 0.98, 1.6, 2.6, or 3.9 mg of diethylstilbestrol (DES) was implanted into each of 203 female F344 rats [30].
• Inhibitory effect of antiestrogen on hepatic tumorigenesis in WF rats treated with diethylstilbestrol alone or in combination with N-nitrosobutylurea [31].

Gene context of diethylstilbestrol

• Wild-type (WT) mice, homozygous mutant ER (ERKO) alpha -/- mice, and betaERKO -/- mice were injected with 2 microg of diethylstilbestrol (DES) or oil (controls) on days 1, 3, and 5 of life [32].
• Mice heterozygous for a Brca1 or Brca2 mutation display distinct mammary gland and ovarian phenotypes in response to diethylstilbestrol [33].
• We show a distinct increase in Fas-FasL expression in spermatogenic cells upon exposure to diethylstilbestrol [34].
• Vasoactive intestinal polypeptide antiserum affects rat prolactin mRNA in 40-day but not 110-day diethylstilbestrol-induced prolactinoma tissue [35].
• A HOXA10 estrogen response element (ERE) is differentially regulated by 17 beta-estradiol and diethylstilbestrol (DES) [36].

Analytical, diagnostic and therapeutic context of diethylstilbestrol

• To assess the long-term effects of diethylstilbestrol we conducted a health survey among 693 mothers who had taken the drug during pregnancy and a comparable group of 668 who had not [37].
• Groups III, IV, and V received pellet implants of 5.0 mg diethylstilbestrol (DES) concurrently with castration [38].
• Mammary tumorigenesis was studied in female ACi rats after treatment with X-irradiation or neutron-irradiation, with or without diethylstilbestrol (DES) treatment [39].
• The effects of ovariectomy on the growth of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumors were investigated after rats ahd been exposed prenatally to diethylstilbestrol (DES) [40].
• BACKGROUND: An association between prenatal diethylstilbestrol (DES) exposure and cancer in men, especially testicular cancer, has been suspected, but findings from case-control studies have been inconsistent [41].

References