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

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

35 Diethylstilbestrol, coumestrol, genistein, naringenin, a

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

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

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

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

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

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

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

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

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

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

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

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

48 Diethylstilbestrol (DES) is a synthetic estrogen and wel

49 Diethylstilbestrol (DES) is a synthetic estrogen that ha

50 Diethylstilbestrol (DES) is an estrogenic endocrine disr

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

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

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

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

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

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

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

58 4 was found to be abnormally demethylated by diethylstilbestrol (DES) treatment in the mature uteri.

59 Diethylstilbestrol (DES) was widely used to treat pregna

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

61 .1 microg/kg per day) of the estrogenic drug diethylstilbestrol (DES), a known human developmental te

62 Diethylstilbestrol (DES), a nonsteroidal estrogen widely

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 Diethylstilbestrol exposure was significantly associated

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

94 75 to examine the health effects of prenatal diethylstilbestrol exposure.

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

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

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

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

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

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

101 Arsenic plus diethylstilbestrol increased ovarian, uterine, and vagin

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

103 182,780 could not inhibit 1 nM estradiol- or diethylstilbestrol-induced proliferation.

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

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

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

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

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

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

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

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

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

113 Systematic administration of diethylstilbestrol severely diminished growth and angiog

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

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

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

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