ライフサイエンスコーパス: diethylstilbestrol

1 ammospheres exposed to a synthetic estrogen, diethylstilbestrol.

2 , miR-9-3, in epithelial cells preexposed to diethylstilbestrol.

3 atment with a pharmacological ERR inhibitor, diethylstilbestrol.

4 related gene expression induced by postnatal diethylstilbestrol.

5 es and metabolites of the synthetic estrogen diethylstilbestrol.

6 d to PC-SPES and estrogenic agents including diethylstilbestrol.

7 ne adenocarcinoma after neonatal exposure to diethylstilbestrol.

8 al CK2) prior to treatment with etoposide or diethylstilbestrol.

9 ence of 10 nM 17beta-estradiol (E2), but not diethylstilbestrol.

10 ted s.c. on postpartum days 1 through 5 with diethylstilbestrol (2 microg/pup/d) or tamoxifen (10 mic

11 the presence of 17beta-estradiol, genistein, diethylstilbestrol, 4-tert-octylphenol, 2',3',4', 5'-tet

12 he urogenital tumors induced by arsenic plus diethylstilbestrol, 80% were malignant, and 55% were mul

13 Based on its structural similarity to diethylstilbestrol, a synthetic estrogen, we examined wh

14 stilbestrol alone (21%) groups, arsenic plus diethylstilbestrol acted synergistically, inducing a 48%

15 025 participants in the National Cooperative Diethylstilbestrol Adenosis (DESAD) Project, a US study

16 n ongoing cohort study (National Cooperative Diethylstilbestrol Adenosis Study and Dieckmann cohorts)

17 in the control (0%), arsenic alone (9%), and diethylstilbestrol alone (21%) groups, arsenic plus diet

18 Diethylstilbestrol alone induced some tumors (primarily

19 Diethylstilbestrol and 17-beta-stradiol had no effects o

20 and protein expression were induced by both diethylstilbestrol and 17beta-estradiol in estrogen rece

21 significant interactions between ever use of diethylstilbestrol and any of the other potential risk f

22 tivities distinct from those attributable to diethylstilbestrol and suggests that alterations in spec

23 Additionally, diethylstilbestrol and tamoxifen demonstrated prototypic

24 Both the nonsteroidal estrogen diethylstilbestrol and the "pure" antiestrogen ICI 164,3

25 nhibitory action of estrogens (estradiol and diethylstilbestrol) and antiestrogens (4-hydroxy-tamoxif

26 roquinoline N-oxide, ethyl methanesulfonate, diethylstilbestrol, and 2-aminoanthracene did not induce

27 Three estrogen types were used: estradiol, diethylstilbestrol, and a triphenylethylene (TPE) deriva

28 tamoxifen, calmodulin antagonists, estrogen, diethylstilbestrol, and the anti-estrogen ICI 182780 on

29 Consistent chromosomal gains, common to both diethylstilbestrol- and estradiol-induced renal neoplasm

30 ake, was unaffected by 17-beta-estradiol and diethylstilbestrol at concentrations up to 10 microM, wh

31 Like beta-estradiol, the synthetic estrogen diethylstilbestrol attenuated directed smooth muscle cel

32 sociation was not observed in women who used diethylstilbestrol before age 25 years but was seen at a

33 hen evaluating chemicals as EDCs, and we use diethylstilbestrol, bisphenol A and perchlorate as examp

34 ity, age at first birth, infertility, use of diethylstilbestrol by participant's mother, age at hyste

35 A flat estrogen such as estradiol or diethylstilbestrol can induce TGF-alpha through a correc

36 Diethylstilbestrol, coumestrol, genistein, naringenin, a

37 direct fetal injection (FI) of TP (20 mg) or diethylstilbestrol (DES) (20 mg) at d62 and d82 gestatio

38 nding domain (LBD) bound to both the agonist diethylstilbestrol (DES) and a peptide derived from the

39 The association between in utero exposure to diethylstilbestrol (DES) and clear cell adenocarcinoma (

40 included in this study belong to a series of diethylstilbestrol (DES) and indenestrol analogues whose

41 Prenatal exposure to the synthetic estrogen diethylstilbestrol (DES) causes morphogenetic alteration

42 diol and the nonsteroidal synthetic estrogen diethylstilbestrol (DES) disturbs the endocrine balance,

43 tle is known about the influence of prenatal diethylstilbestrol (DES) exposure on time to pregnancy o

44 heir own prenatal characteristics, including diethylstilbestrol (DES) exposure, maternal cigarette sm

45 o man-made estrogens, pregnant mice were fed diethylstilbestrol (DES) from gestation days 11 to 17.

46 veral million women were exposed in utero to diethylstilbestrol (DES) given to their mothers to preve

47 Women exposed to diethylstilbestrol (DES) in utero develop abnormalities,

48 Women exposed to diethylstilbestrol (DES) in utero frequently develop vag

49 tions in pregnancy, exposure to the estrogen diethylstilbestrol (DES) in utero induces developmental

50 Diethylstilbestrol (DES) is a synthetic estrogen and wel

51 Diethylstilbestrol (DES) is a synthetic estrogen that ha

52 Diethylstilbestrol (DES) is an estrogenic endocrine disr

53 Prenatal exposure to diethylstilbestrol (DES) is known to cause an increased

54 carcinogenic effect of prenatal exposure to diethylstilbestrol (DES) is the classic example.

55 perinatal exposure to the synthetic estrogen diethylstilbestrol (DES) leads to feminization of the se

56 ERKO -/- mice were injected with 2 microg of diethylstilbestrol (DES) or oil (controls) on days 1, 3,

57 ere conducted in the CWR22 model with either diethylstilbestrol (DES) or surgical castration.

58 tal administration of the synthetic estrogen diethylstilbestrol (DES) to mice and humans produces ute

59 Ten weeks of diethylstilbestrol (DES) treatment caused female F344 ra

60 4 was found to be abnormally demethylated by diethylstilbestrol (DES) treatment in the mature uteri.

61 Diethylstilbestrol (DES) was widely used to treat pregna

62 hat reduce fetal ITT in rats (dexamethasone, diethylstilbestrol (DES)) also maintain/induce LC nuclea

63 .1 microg/kg per day) of the estrogenic drug diethylstilbestrol (DES), a known human developmental te

64 Diethylstilbestrol (DES), a nonsteroidal estrogen widely

65 ting the association of prenatal exposure to diethylstilbestrol (DES), a potent endocrine disruptor,

66 We have recently found that diethylstilbestrol (DES), a synthetic estrogen agonist,

67 PC-SPES are different from those found when diethylstilbestrol (DES), a synthetic estrogen, is used,

68 evelopmental exposure to 17beta-estradiol or diethylstilbestrol (DES), a synthetic estrogen.

69 The estrogenic compounds, E2, diethylstilbestrol (DES), and estrone (EST), activated e

70 As proof of principle, cyclophosphamide and diethylstilbestrol (DES), for which both human and anima

71 Therapy with diethylstilbestrol (DES), leuprolide, or bilateral orchi

72 tive MCF-7 breast cancer cells using G-1 and diethylstilbestrol (DES), ligands that selectively activ

73 eks of treatment with the synthetic estrogen diethylstilbestrol (DES), pituitary mass, an accurate su

74 try (SOCE) was blocked by the SOCE inhibitor diethylstilbestrol (DES), STIM1 silencing using RNA inte

75 nsor assay, we have identified the stilbenes diethylstilbestrol (DES), tamoxifen (TAM), and 4-hydroxy

76 opmental exposure to an estrogenic chemical, diethylstilbestrol (DES), to determine causative factors

77 t monthly intervals (1.0 to 6.0 months) from diethylstilbestrol (DES)-treated castrated male hamsters

78 emicals (EDCs) such as bisphenol-A (BPA) and diethylstilbestrol (DES).

79 s 4-hydroxytamoxifen (4-OHT), tamoxifen, and diethylstilbestrol (DES).

80 , bisphenol A (BPhA), nonylphenol (NPh), and diethylstilbestrol (DES).

81 neonatal treatment with the potent estrogen diethylstilbestrol (DES).

82 reatment with the highly estrogenic compound diethylstilbestrol (DES).

83 ated with early-onset fibroids were in utero diethylstilbestrol (DES; RR = 2.02; 95% CI: 1.28, 3.18),

84 being synthetic (17alpha-ethynyloestradiol, diethylstilbestrol, dienestrol and hexestrol) and one me

85 l exposure to the strong synthetic estrogen, diethylstilbestrol, downregulated expression of a group

86 omas, we show that an early-life exposure to diethylstilbestrol during development of the uterus incr

87 examined the association between the use of diethylstilbestrol during pregnancy and the risk of subs

88 -up study of the offspring of women who took diethylstilbestrol during pregnancy.

89 ng various ER ligands, including Raloxifene, Diethylstilbestrol, E2, and 4-hydroxytamoxifen, by emplo

90 nic organic compounds that are distinct from diethylstilbestrol, estrone, and estradiol.

91 ate cancer and other cells (by etoposide and diethylstilbestrol) evokes an enhancement in CK2 associa

92 In 1994, 1,753 diethylstilbestrol-exposed and 1,050 unexposed women fro

93 The present findings indicate that diethylstilbestrol-exposed women have a higher risk of i

94 rlier menopause was associated with in-utero diethylstilbestrol exposure (hazard ratio (HR) = 1.45, 9

95 a positive association between a history of diethylstilbestrol exposure (reported by 3.9% of all wom

96 stent with those of several other studies of diethylstilbestrol exposure and breast cancer.

97 Diethylstilbestrol exposure was significantly associated

98 e risks were computed for the association of diethylstilbestrol exposure with specific types of infer

99 75 to examine the health effects of prenatal diethylstilbestrol exposure.

100 th estrogen agonists (17beta-estradiol [E2], diethylstilbestrol, genistein), but not antagonists (tam

101 nd bladder carcinoma induced by arsenic plus diethylstilbestrol greatly overexpressed estrogen recept

102 ple, a murine model of perinatal exposure to diethylstilbestrol has proven useful in studying mechani

103 eir isobars (e.g., bisphenol A, (Z)- and (E)-diethylstilbestrol, hexestrol, estrone, alpha-estradiol,

104 strongly responsive targets to the estrogen diethylstilbestrol in the mouse hypothalamus.

105 it is well established that women exposed to diethylstilbestrol in utero have an increased risk of sp

106 Arsenic plus diethylstilbestrol increased ovarian, uterine, and vagin

107 creased PRL secretion to 1% of estradiol- or diethylstilbestrol-induced prolactin secretion suggestin

108 182,780 could not inhibit 1 nM estradiol- or diethylstilbestrol-induced proliferation.

109 he PRL response because 0.01 pM estradiol or diethylstilbestrol induces half-maximal growth induction

110 Inhibition of ORAI channels by BTP2 and diethylstilbestrol or silencing of ORAI expression impai

111 enicity, together with postnatal exposure to diethylstilbestrol or tamoxifen, was studied.

112 tition studies with excess 17beta-estradiol, diethylstilbestrol, or moxestrol, but not with R5020 or

113 ical cancer, women with in utero exposure to diethylstilbestrol, or women who are immunocompromised (

114 d in mammosphere-derived epithelial cells on diethylstilbestrol preexposure.

115 ution studies of both compounds were done on diethylstilbestrol-pretreated and DHT-blocked Sprague-Da

116 Neonatal exposure of mice to estrogen (diethylstilbestrol) results in a high incidence (90%) of

117 ort of participants predominantly exposed to diethylstilbestrol, results suggest that prenatal exposu

118 Systematic administration of diethylstilbestrol severely diminished growth and angiog

119 formations of the ER liganded with 4OHTAM or diethylstilbestrol, the TPEs optimally occupy the 4OHTAM

120 age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]).

121 y, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclamp

122 inatal factors, but birth order and maternal diethylstilbestrol use were underreported among cases an

123 ed triphenylethylene synthetic estrogens and diethylstilbestrol were used.