ライフサイエンスコーパス: oestrogen

1 sex differences in cell-cycle regulation by oestrogen.

2 boembolic complications associated with oral oestrogen.

3 mbinatorial regulation of AXIN1 by RUNX1 and oestrogen.

4 ve breast cancer cells and synergy with anti-oestrogens.

5 nd centre, to receive oral conjugated equine oestrogen (0.625 mg per day; n=5310) or matched placebo

6 rds two plausible and distinct mechanisms of oestrogen action enhancing torsadogenic effects: oestrad

7 sk of which depends on the dose and route of oestrogen administration.

8 trial who were randomly allocated to receive oestrogen alone had a lower incidence of invasive breast

9 ated by other factors including age and also oestrogen, although how pro-inflammatory cytokines withi

10 ession of EST and compromise the activity of oestrogen, an anti-inflammatory hormone.

11 The role of oestrogen, an endogenous anti-oxidant on recovery from i

12 Some of the desired physical changes from oestrogen and anti-androgen therapy include decreased bo

13 Molecular models suggest that oestrogen and dofetilide blockade can concur simultaneou

14 Here, the effects of oestrogen and progesterone are investigated to elucidate

15 Oestrogen and progesterone exposure are also associated

16 To better isolate the effects of oestrogen and progesterone on the cardiovascular and wat

17 cteristics, including tumour size and grade; oestrogen and progesterone receptor and human epidural g

18 B3 expression was positively correlated with oestrogen and progesterone receptor expression whereas B

19 were stratified by age, axillary nodes, and oestrogen and progesterone receptor status and randomly

20 ; at least one measureable lesion; and known oestrogen and progesterone receptor status.

21 itive or both] vs hormone receptor-negative [oestrogen and progesterone receptor-negative]), nodal st

22 hed in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expressio

23 y a lack of expression of hormone receptors, oestrogen and progesterone, as well as human epidermal f

24 Oestrogen and progestogen have the potential to influenc

25 nced, and inflammatory breast cancer, and by oestrogen and/or progesterone receptor positivity.

26 Evidence that oestrogens and ERalpha stimulate glucose uptake has impo

27 Oestrogens and oestrogen receptor ligands are promising

28 likely environmental concentrations of free oestrogens and the limit of detection is below the envir

29 four classes of endocrine disruptors (EDs), oestrogens, androgens, progestagens and glucocorticoids.

30 that changes in protein expression following oestrogen application led to functional changes in Kir4.

31 tmenopausal women may suggest that decreased oestrogen at menopause is partially responsible for the

32 in women is caused by a withdrawal effect of oestrogen at menopause.

33 ffects on SNA are differentially enhanced by oestrogen, at least in part via an increase in alpha-MSH

34 implify purification of the protein, and the oestrogen binding characteristics of the protein.

35 tively detect vertebrate oestrogens using an oestrogen binding protein (EBP1) present in wild type Sa

36 tion of aromatase, a rate-limiting enzyme in oestrogen biosynthesis.

37 nimal studies and clinical observations (eg, oestrogen, calcitonin, and teriparatide) or opportunisti

38 It is known that oestrogen can attenuate sympathetic responsiveness, howe

39 abdominal pain side effect of the synthetic oestrogen chlorotrianisene was mediated through its newl

40 In adults, oral oestrogen--combined with recombinant human IGF-1 in one

41 Endogenous oestrogen concentrations decline by 60% during the menop

42 Use of parenteral oestrogen could avoid the long-term complications associ

43 Parenteral oestrogen could be a potential alternative to LHRHa in m

44 ation by Fuller Albright that treatment with oestrogen could reverse the negative calcium balance tha

45 t, transgenic overexpression of EST promotes oestrogen deactivation and sensitizes mice to CLP-induce

46 ed inflammatory responses due to compromised oestrogen deactivation, leading to increased sepsis leth

47 sure to over nutrition, high-energy diet and oestrogen deficiency, are considered as significant obes

48 ds promise for treatment of inflammatory and oestrogen deficiency-mediated pathologic bone resorption

49 therefore constitute a frontline therapy for oestrogen-dependent breast cancer.

50 al role for p72 in ERalpha co-activation and oestrogen-dependent cell growth and provide evidence in

51 chromatin and oestrogen receptor to activate oestrogen-dependent genes associated with cellular proli

52 n of endogenous ERalpha-responsive genes and oestrogen-dependent growth of MCF-7 and ZR75-1 breast ca

53 ulated stromal oestrogen production enhances oestrogen-dependent transcription in oestrogen receptor-

54 p68, results in a significant inhibition of oestrogen-dependent transcription of endogenous ERalpha-

55 Herein, we demonstrate that long-term oestrogen deprivation dramatically increases sensitivity

56 atment with 250 mg fulvestrant combined with oestrogen deprivation is no better than either fulvestra

57 diol replacement at the end of the long-term oestrogen deprivation period could not prevent CA3 hyper

58 ectomy and maintained throughout the 10-week oestrogen deprivation period, it completely prevented th

59 mutations are associated with resistance to oestrogen deprivation therapy.

60 hat most of the side-effects associated with oestrogen deprivation were not attributable to treatment

61 en fulvestrant in combination with continued oestrogen deprivation.

62 Resistance to oestrogen-deprivation therapy is common in oestrogen-rec

63 Other therapies, such as anti-oestrogen drugs for breast cancer prevention, should be

64 In women in the low oestrogen (E(2)) phase of the menstrual cycle, PE evoked

65 Incubation with oestrogen (E2, 0.1-1.0 nm) increased I(Ca,L) ( approxima

66 For all SERMs, incidence of invasive oestrogen (ER)-positive breast cancer was reduced both d

67 Oestrogen/ERalpha signalling promotes haematopoietic ste

68 particular the principle female sex steroid oestrogen, exerts potent effects upon the immune respons

69 eves hot flush symptoms without the need for oestrogen exposure.

70 -up of 11.8 years (IQR 9.1-12.9), the use of oestrogen for a median of 5.9 years (2.5-7.3) was associ

71 However, our data do not support use of oestrogen for breast cancer risk reduction because any n

72 es known to catalyse the biosynthesis of all oestrogens from androgens.

73 e targeting approach with the steroidal anti-oestrogen fulvestrant in combination with continued oest

74 tor dysfunction have shown improvements with oestrogen, gabapentin, paroxetine, and clonidine, but li

75 Fewer women in the oestrogen group died from any cause after a breast cance

76 Nine (50%) of 18 events in the oestrogen group occurred after crossover to LHRHa.

77 In the oestrogen group, fewer women died from breast cancer (si

78 ceiving LHRHa and 111 (92%) of 121 receiving oestrogen had achieved castrate testosterone concentrati

79 ltigram scale, the enantiomer of a selective oestrogen has been synthesized, and a novel ent-steroid

80 17alpha-ethinylestradiol (EE2), a synthetic oestrogen in oral contraceptives, is one of many pharmac

81 tromal cells are the primary source of local oestrogens in adipose tissue, aberrant production of whi

82 In this environment, theca cells form, oestrogen is produced and germ cells appear feminized.

83 mortality from endotoxemia, demonstrate that oestrogen is responsible for an increased susceptibility

84 Oestrogen levels increased during pregnancy, increasing

85 AXIN1's second intron, and RUNX1 antagonizes oestrogen-mediated AXIN1 suppression.

86 Progesterone inhibited oestrogen-mediated growth of ERalpha(+) cell line xenogr

87 these results identify a novel mechanism of oestrogen-mediated neuroprotection in CuZn superoxide di

88 ogen receptor alpha (ERalpha) is involved in oestrogen-mediated regulation of glucose metabolism and

89 Oestrogen, often via oestrogen receptor alpha (ERalpha)

90 significant association between PPI use and oestrogen-only and combined HRT treatment.

91 tatistically significant association between oestrogen-only hormone and GORD and PPI use.

92 ation remained statistically significant for oestrogen-only treatment (OR 1.49; 1.18-1.89).

93 When adjusted for covariates, oestrogen-only treatment was significant (OR 1.34; 95% C

94 adjusted analysis, all forms of hormone use (oestrogen-only, tibolone, combined HRT and progestogen)

95 We have discovered that oestrogen or androgen treatment can positively regulate

96 icantly increased with the administration of oestrogen or progesterone (P<0.001) and is reduced in re

97 receptor status (hormone receptor-positive [oestrogen or progesterone receptor-positive or both] vs

98 Endocrine changes, such as oestrogen or vitamin D deficiency, contribute to a ferti

99 tractility are two opposing determinants for oestrogen output of adipose stromal cells.

100 14.9) and 18 events in 17 (10.1%) men in the oestrogen-patch group (6.0-15.6).

101 LHRHa group and -0.16 mmol/L (-2.4%) in the oestrogen-patch group (p=0.004), and for fasting cholest

102 n the LHRHa group vs 104 [75%] of 138 in the oestrogen-patch group), hot flushes (44 [56%] vs 35 [25%

103 n, in a 2:1 ratio, to four self-administered oestrogen patches (100 mug per 24 h) changed twice weekl

104 hed (1.7 nmol/L or lower) men received three oestrogen patches changed twice weekly.

105 l 85 patients started LHRHa, and 168 started oestrogen patches.

106 assigned to receive LHRHa and 169 to receive oestrogen patches.

107 e-daily tablet of 0.625 mg conjugated equine oestrogen plus 2.5 mg medroxyprogesterone acetate (n=850

108 WHI) trial, women assigned to treatment with oestrogen plus progestin had a higher risk of cancer tha

109 Although treatment with oestrogen plus progestin in postmenopausal women did not

110 HOTAIR expression is negatively regulated by oestrogen, positively regulated by FOXA1 and FOXM1, and

111 Mechanically stimulated stromal oestrogen production enhances oestrogen-dependent transc

112 Additionally, the combined oestrogen-progestagen contraceptive pill might decrease

113 o the hormone-binding domain of the modified oestrogen receptor (ER(TAM)) can be regulated by provisi

114 INCX upregulation by E2 was blunted by an oestrogen receptor (ER) antagonist (fulvestrant, 1 mum),

115 stry are more likely to have young-onset and oestrogen receptor (ER) negative breast cancer for reaso

116 ith different survival patterns according to oestrogen receptor (ER) status.

117 ession of the progesterone receptor (PR) and oestrogen receptor (ER) was associated with subtype-spec

118 tor-1 (SRC-1), a coregulatory protein of the oestrogen receptor (ER), has previously been shown to ha

119 ancer subtypes in 690 Irish women with known oestrogen receptor (ER), progesterone receptor (PR), and

120 1, was significantly associated with risk of oestrogen receptor (ER)-negative breast cancer (odds rat

121 significant associations (P<5 x 10(-8)) with oestrogen receptor (ER)-negative breast cancer and BRCA1

122 scent staining of tumour sections from human oestrogen receptor (ER)-negative breast cancer patients

123 PHGDH protein levels are elevated in 70% of oestrogen receptor (ER)-negative breast cancers.

124 nt of axillary nodes, 276 (33%) patients had oestrogen receptor (ER)-negative disease, and 191 (27%)

125 rs of breast cancer survival involving 1,804 oestrogen receptor (ER)-negative patients treated with c

126 More aggressive and therapy-resistant oestrogen receptor (ER)-positive breast cancers remain a

127 For women with oestrogen receptor (ER)-positive early breast cancer, tr

128 UNX1 expression did not influence outcome of oestrogen receptor (ER)-positive or HER2-positive diseas

129 investigate the role of the top prioritized oestrogen receptor (ER)-regulated lncRNA, DSCAM-AS1.

130 ted by a specific amino acid sequence of the oestrogen receptor (ER).

131 mines tamoxifen sensitivity by regulation of oestrogen receptor (ER)alpha.

132 5 nm) but not the beta- (DPN, 5 nm) subtype oestrogen receptor (ERalpha/ERbeta) upregulated I(Ca,L)

133 Expression of oestrogen receptor (ESR1) determines whether a breast ca

134 ntly shown to activate the G protein-coupled oestrogen receptor (GPER) in vascular cells.

135 )-inducible telomerase reverse transcriptase-oestrogen receptor (TERT-ER) under transcriptional contr

136 fied a subset of VMHvl neurons marked by the oestrogen receptor 1 (Esr1), and investigated their role

137 Oestrogen receptor 1-expressing (Esr1(+)) neurons in the

138 ut a very different pattern was observed for oestrogen receptor 2 (ER2).

139 ith hormone-receptor-positive breast cancer (oestrogen receptor [ER] positive, progesterone receptor

140 through regulation of androgen receptor and oestrogen receptor activity.

141 In addition to its activity as an oestrogen receptor agonist/antagonist, tamoxifen also mo

142 st cancer cells 17beta-oestradiol (E2)-bound oestrogen receptor alpha (ER-alpha) causes a global incr

143 liferation, decreased apoptosis and elevated oestrogen receptor alpha (ERalpha) expression.

144 functions as a coactivator of the endogenous oestrogen receptor alpha (ERalpha) in breast cancer cell

145 Oestrogen receptor alpha (ERalpha) is a nuclear receptor

146 The oestrogen receptor alpha (ERalpha) is expressed in prost

147 Previous studies suggest oestrogen receptor alpha (ERalpha) is involved in oestro

148 Oestrogen, often via oestrogen receptor alpha (ERalpha) signalling, regulates

149 crine therapies target the activation of the oestrogen receptor alpha (ERalpha) via distinct mechanis

150 r clinical studies have linked response with oestrogen receptor alpha expression and other biomarkers

151 nor FGFR2 allele associates most strongly in oestrogen receptor alpha positive (ERalpha) breast tumou

152 light the essential elements of the membrane oestrogen receptor alpha, noting where conserved aspects

153 and FOXM1, and is inversely correlated with oestrogen receptor and directly correlated with FOXM1 in

154 age, radiotherapy intent, nodal status, and oestrogen receptor and HER-2 status.

155 st-line treatment), hormone receptor status (oestrogen receptor and progesterone receptor positive vs

156 4.1 expression reduced in the presence of an oestrogen receptor antagonist, Fulvestrant 182,780 sugge

157 The discovery of oestrogen receptor beta (ERbeta/ESR2) was a landmark dis

158 In addition, oestrogen receptor beta ligand treatment caused an incre

159 Oestrogen receptor beta ligand treatment of experimental

160 ings show a direct neuroprotective effect of oestrogen receptor beta ligand treatment on oligodendroc

161 resent study we investigated the capacity of oestrogen receptor beta ligand treatment to affect callo

162 inated axons with intact nodes of Ranvier in oestrogen receptor beta ligand-treated mice.

163 se mutations in patients receiving selective oestrogen receptor degrader (SERD) therapy.

164 We investigated whether the selective oestrogen receptor degrader fulvestrant could improve pr

165 simultaneously increased Ca(2+) currents via oestrogen receptor ERalpha.

166 use pancreatic beta-cells from wild-type and oestrogen receptor ERbeta-/- mice, we found that exposur

167 ncer overall, and by tumour histology and by oestrogen receptor expression.

168 dentify recurrent rearrangements between the oestrogen receptor gene ESR1 and its neighbour CCDC170,

169 target the dependence of this subtype on the oestrogen receptor have substantial activity, yet the de

170 Oestrogens and oestrogen receptor ligands are promising treatments to p

171 Tamoxifen is a selective oestrogen receptor modulator widely used for the treatme

172 We assessed the effectiveness of selective oestrogen receptor modulators (SERMs) on breast cancer i

173 e prevention trials comparing four selective oestrogen receptor modulators (SERMs; tamoxifen, raloxif

174 s (log P ~4-7), comprising several selective oestrogen receptor modulators and a modified testosteron

175 rapy (aromatase inhibitors only vs selective oestrogen receptor modulators only vs both therapies), a

176 as an additional subgroup, characterised as oestrogen receptor negative and androgen receptor positi

177 nal candidate, rs4442975, is associated with oestrogen receptor positive (ER+) disease with an odds r

178 esponse to endocrine therapy and survival in oestrogen receptor positive breast cancer is a significa

179 sponders and non-responders in patients with oestrogen receptor positive breast cancer.

180 g LINC00160 expressions and interaction with oestrogen receptor signalling.

181 involved axillary lymph nodes, tumour stage, oestrogen receptor status, type and timing of systemic t

182 TRIM24 binds chromatin and oestrogen receptor to activate oestrogen-dependent genes

183 ch tumour cells do not express the genes for oestrogen receptor, progesterone receptor and HER2 (also

184 cers and to establish if these are linked to oestrogen receptor, progesterone receptor, and human epi

185 ta will be available for how factors such as oestrogen receptor, progesterone receptor, HER2, and ind

186 Oestrogen receptor-alpha (ER) is the defining and drivin

187 ime, we present a genome-wide global view of oestrogen receptor-alpha (ERalpha) binding events in the

188 or (PR) expression is used as a biomarker of oestrogen receptor-alpha (ERalpha) function and breast c

189 ified a direct interaction between Hippo and oestrogen receptor-alpha (ERalpha) signalling.

190 opoietic stem cells expressed high levels of oestrogen receptor-alpha (ERalpha).

191 se range of transcription factors, including oestrogen receptor-alpha (ERalpha).

192 ation-associated breast cancer originates in oestrogen receptor-alpha-negative (ER(-)) progenitors in

193 -oestradiol, which induces proliferation via oestrogen receptor-beta (ER-beta), the catecholoestradio

194 actions enriched for both enhancer marks and oestrogen receptor-binding sites.

195 the adult virgin gland is restricted to the oestrogen receptor-expressing luminal cell lineage.

196 Our data also demonstrate that the oestrogen receptor-expressing, milk and basal cell subpo

197 s carrying EBV encoding a conditional EBNA3C-oestrogen receptor-fusion revealed that this epigenetic

198 =0.05), but no effect was noted for invasive oestrogen receptor-negative breast cancer (HR 1.05 [95%

199 tingham-HES; n=1650), Nottingham early stage oestrogen receptor-negative breast cancer adjuvant chemo

200 In patients with oestrogen receptor-negative breast cancer with high SPAG

201 oxic chemotherapy sensitivity, especially in oestrogen receptor-negative breast cancer.

202 The association is stronger for oestrogen receptor-negative disease (OR 0.34, 95% CI 0.2

203 oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p<0.01 for both com

204 oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than

205 who did not receive chemotherapy (Nottingham-oestrogen receptor-negative-ACT cohort: HR 0.37, 95% CI

206 cer adjuvant chemotherapy cohort (Nottingham-oestrogen receptor-negative-ACT; n=697), the Nottingham

207 mutations in breast cancer, specifically in oestrogen receptor-positive (ER(+)) tumours.

208 tion of phenotypes in concordance with human oestrogen receptor-positive (ER+) breast cancer samples,

209 lationship between mutations and response of oestrogen receptor-positive (ER+) breast cancer to aroma

210 ions leading to the more aggressive forms of oestrogen receptor-positive (ER+) breast cancers is of c

211 patients were enrolled on the basis of their oestrogen receptor-positive and HER2-negative biomarker

212 2 study, postmenopausal women with advanced oestrogen receptor-positive and HER2-negative breast can

213 ression-free survival in women with advanced oestrogen receptor-positive and HER2-negative breast can

214 atest reduction in risk was seen in invasive oestrogen receptor-positive breast cancer (HR 0.66 [95%

215 al evidence of growth-inhibitory activity in oestrogen receptor-positive breast cancer cells and syne

216 Poor-prognosis oestrogen receptor-positive breast cancer is characteris

217 n three genomic regions focally amplified in oestrogen receptor-positive breast cancer, 8p11-12, 11q1

218 issue, aberrant production of which promotes oestrogen receptor-positive breast cancer.

219 ive disease (OR 0.34, 95% CI 0.21-0.54) than oestrogen receptor-positive disease (OR 0.63, 95% CI 0.4

220 enous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen r

221 trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen r

222 cells and also, although at lower levels, in oestrogen receptor-positive luminal cells.

223 dose (1.7 micromol kg(-1), 1 T), but not in oestrogen receptor-positive MCF-7 tumours.

224 gible patients with histologically confirmed oestrogen receptor-positive or progesterone receptor-pos

225 nhances oestrogen-dependent transcription in oestrogen receptor-positive tumour cells and promotes th

226 e increased risk appears largely confined to oestrogen receptor-positive tumour risk.

227 ant can improve progression-free survival in oestrogen receptor-positive, endocrine-resistant breast

228 menopausal women aged 18 years or older with oestrogen receptor-positive, HER2-negative breast cancer

229 st-line treatment of patients with advanced, oestrogen receptor-positive, HER2-negative breast cancer

230 ifen metabolites that most strongly bind the oestrogen receptor.

231 stmenopausal women with early stage hormone (oestrogen) receptor-positive invasive breast cancer were

232 expression profiling studies have shown that oestrogen-receptor (ER)-positive and ER-negative breast

233 Three patients with oestrogen-receptor (ER)-positive, human epidermal growth

234 culating tumour cells in women with advanced oestrogen-receptor (ER)-positive/human epidermal growth

235 ks, and stratified by previous chemotherapy, oestrogen-receptor and progesterone-receptor status, and

236 PI3K, AKT, and HER2, and a new generation of oestrogen-receptor degraders.

237 Two selective oestrogen-receptor modulators--tamoxifen and raloxifene-

238 ssociated with bone relapse in patients with oestrogen-receptor negative breast cancer.

239 east cancer, especially if the recurrence is oestrogen-receptor negative.

240 es of disease-free survival according to the oestrogen-receptor status of the primary tumour were not

241 known prognostic factors (age, nodal status, oestrogen-receptor status, grade, and tumour size).

242 axillary lymph nodes, clinical tumour stage, oestrogen-receptor status, type and timing of systemic t

243 zoledronic acid on DFS were not affected by oestrogen-receptor status.

244 significantly more effective for women with oestrogen-receptor-negative ILRR (pinteraction=0.046), b

245 ence single normal and tumour nuclei from an oestrogen-receptor-positive (ER(+)) breast cancer and a

246 o oestrogen-deprivation therapy is common in oestrogen-receptor-positive (ER+) breast cancer.

247 These include a high-risk, oestrogen-receptor-positive 11q13/14 cis-acting subgroup

248 has been made in identifying the drivers of oestrogen-receptor-positive breast cancer and the mechan

249 Distinct phenotypes in oestrogen-receptor-positive breast cancer are associated

250 e bank from all postmenopausal patients with oestrogen-receptor-positive breast cancer from whom the

251 Oestrogen-receptor-positive breast cancer is the most co

252 for postmenopausal women with node-positive, oestrogen-receptor-positive breast cancer showed that ch

253 is prognostic for women with node-negative, oestrogen-receptor-positive breast cancer treated with t

254 correlate the variable clinical features of oestrogen-receptor-positive breast cancer with somatic a

255 therapy for late recurrence in patients with oestrogen-receptor-positive breast cancer would be clini

256 e replacement therapy, either overall or for oestrogen-receptor-positive disease.

257 Patients with oestrogen-receptor-positive ILRR received adjuvant endoc

258 patients with early stage breast cancer and oestrogen-receptor-positive tumours.

259 tissue was available from 665 patients with oestrogen-receptor-positive, N0 breast cancer for BCI an

260 h early and late recurrence in patients with oestrogen-receptor-positive, node-negative (N0) disease

261 (beta-ARs) and independently of the classic oestrogen receptors (ERs).

262 ly, CB sparks the constitutive activation of oestrogen receptors alpha (ERalpha) in AI-resistant cell

263 r4.1 and glutamate transporter 1 via genomic oestrogen receptors.

264 ptors (beta-AR) and independently of classic oestrogen receptors.

265 ify a cohort of breast cancer-associated and oestrogen-regulated lncRNAs, and investigate the role of

266 These sex-specific effects may occur via oestrogen regulation of ADCYAP1R1.

267 eviously published data, suggest how loss of oestrogen regulation of AP-2gamma may contribute to the

268 orepressor, it functions as a coactivator of oestrogen-related receptor alpha (ERRalpha) in brown adi

269 Esrrb (oestrogen-related receptor beta) is a transcription fact

270 R1 mRNA is induced with fear conditioning or oestrogen replacement in rodent models.

271 ort for the 'critical window' hypothesis for oestrogen replacement therapy benefit.

272 clear guidelines for the timing and dose of oestrogen replacement.

273 Oestrogen-replacement therapy, primarily via the transde

274 ment for osteoporosis, systemic steroids, or oestrogen-replacement therapy.

275 A single SNP in a putative oestrogen response element within ADCYAP1R1, rs2267735,

276 co-operative binding of LRH-1 and ERalpha at oestrogen response elements controls the expression of o

277 -regulated genes by LRH-1 through binding to oestrogen response elements, as exemplified by the TFF1/

278 ta form heterodimers binding DNA at specific oestrogen-responsive elements (EREs) to regulate gene tr

279 DNA hypermethylation occurs predominantly at oestrogen-responsive enhancers and is associated with re

280 analysis of LRH-1-regulated genes identified oestrogen-responsive genes as the most highly enriched G

281 response elements controls the expression of oestrogen-responsive genes.

282 rs of the ovary are rare, hormonally active, oestrogen-secreting tumours of the ovary existing in two

283 sequences-some of which are progesterone and oestrogen sensitive-between individual copies.

284 toward the construction of a rapid, portable oestrogen sensor that is not restricted to use to the la

285 velopment and that it functions by mediating oestrogen signalling.

286 nd grade I evidence for 4 medical exposures (oestrogen, statin, antihypertensive medications and non-

287 prevented the loss of bone caused by loss of oestrogens, suggesting that decreasing H2O2 production i

288 Here we report an essential role for the oestrogen sulfotransferase (EST or SULT1E1), a conjugati

289 s mediate placental uptake of substrates for oestrogen synthesis as well as clearing waste products a

290 which is consistent with the effects of anti-oestrogen treatment in breast cancer prevention, and sug

291 monal blockade or acceleration of puberty by oestrogen treatment led to increased or decreased surviv

292 d monoallelic-repression of IGFBP5 following oestrogen treatment.

293 t its effects were normalized with 4 days of oestrogen treatment.

294 discuss the latest findings on the impact of oestrogen upon various cellular components of the immune

295 macteric symptoms in terms of the effects of oestrogen use for about 5 years on breast cancer inciden

296 14, 2009), we assessed long-term effects of oestrogen use on invasive breast cancer incidence, tumou

297 We aimed to assess the influence of oestrogen use on longer term breast cancer incidence and

298 , we noted breast cancer risk reduction with oestrogen use was concentrated in women without benign b

299 l method to quantitatively detect vertebrate oestrogens using an oestrogen binding protein (EBP1) pre

300 plate, we revealed potential interactions of oestrogen with the pore loop hERG mutation (G604S).