ライフサイエンスコーパス: oestrogen

1 mbinatorial regulation of AXIN1 by RUNX1 and oestrogen.

2 sex differences in cell-cycle regulation by oestrogen.

3 boembolic complications associated with oral 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 ses, sex steroid hormones such as the potent oestrogen 17beta-oestradiol have been less well recogniz

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

8 We also demonstrated oestrogen administration improved endothelial function i

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

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

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

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

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

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

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

16 ker changes in the glucocorticoid, oxytocin, oestrogen and immune systems, as key biological mediator

17 that systemic factors (for example, insulin, oestrogen and inflammatory cytokines) and their intracel

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

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

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

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

22 platinum use, history of CNS metastases, and oestrogen and progesterone receptor status.

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

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

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

26 Oestrogen and progestogen have the potential to influenc

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

28 mately 75% of all breast cancers express the oestrogen and/or progesterone receptors.

29 st cancers that expressed hormone receptors (oestrogen and/or progesterone receptors; HR(+)) but did

30 like-to-like comparison between the prenatal oestrogens and androgens.

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

32 high prenatal testosterone and low prenatal oestrogen) and the age of lung cancer diagnosis.

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

34 the general (but erroneous) perception that oestrogens are 'female' hormones have probably prevented

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

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

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

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

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

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

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

42 In Parkinson disease (PD), for example, oestrogens can influence the severity of motor symptoms,

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

44 Endogenous oestrogen concentrations decline by 60% during the menop

45 esults for the first time show that prenatal oestrogens contribute to autism likelihood, extending th

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

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

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

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

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

51 ined treatment improves bone properties with oestrogen deficiency, a cardinal feature of osteoporosis

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

53 tumour risk in dogs and may be influenced by oestrogen deficiency-a risk factor for dementia and brai

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

55 NO bioavailability), but not consistently in oestrogen-deficient postmenopausal women.

56 of blood and lymphatic vessels, the overall oestrogen dependence and the associated sexual dimorphis

57 We suggest that lipoedema is an oestrogen-dependent disorder of adipose tissue, which is

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

59 evaluated the intersecting roles of ageing, oestrogen depletion and excess weight on altering cardia

60 ay help understand the roles that ageing and oestrogen depletion play in early (pre-HFpEF) disease de

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

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

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

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

65 mutations are associated with resistance to oestrogen deprivation therapy.

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

67 en fulvestrant in combination with continued oestrogen deprivation.

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

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

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

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

72 Oestrogen/ERalpha signalling promotes haematopoietic ste

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

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

75 -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

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

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

78 The loss of oestrogens further aggravates such changes by leading to

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

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

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

82 Oestrogen has been shown to play an important role in th

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

84 17alpha-ethinylestradiol (EE2), a synthetic oestrogen in oral contraceptives, is one of many pharmac

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

86 fferences, including the role of circulating oestrogens in transducing the aerobic exercise training

87 ean and obese women with PCOS likely because oestrogen increased NO availability.

88 high prenatal testosterone and low prenatal oestrogen inhibits lung development and may predispose i

89 the phenotypic sex of the medulla as long as oestrogen is provided.

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

91 Oestrogen levels increased during pregnancy, increasing

92 e) cells in gonadal chimeras, or by altering oestrogen levels of ZW and ZZ embryos.

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

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

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

96 indirect mechanisms, including modulation of oestrogen metabolism.

97 Prenatal oestrogens need to be investigated, as they play a key r

98 Oestrogen, often via oestrogen receptor alpha (ERalpha)

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

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

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

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

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

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

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

106 14.9) and 18 events in 17 (10.1%) men in the oestrogen-patch group (6.0-15.6).

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

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

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

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

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

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

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

114 Mechanically stimulated stromal oestrogen production enhances oestrogen-dependent transc

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

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

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

118 A significant proportion of patients with oestrogen receptor (ER) positive breast cancers (BC) dev

119 Stronger associations with survival in oestrogen receptor (ER) positive disease were observed.

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

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

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

123 1, was significantly associated with risk of oestrogen receptor (ER)-negative breast cancer (odds rat

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

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

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

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

128 Women with early-stage oestrogen receptor (ER)-positive (ER(+)) breast cancer w

129 herapy improves clinical outcome in advanced oestrogen receptor (ER)-positive breast cancer, however

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

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

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

133 d >=18 years) with histologically confirmed, oestrogen receptor (ER)-positive, HER2-negative, stage I

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

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

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

137 5 nm) but not the beta- (DPN, 5 nm) subtype oestrogen receptor (ERalpha/ERbeta) upregulated I(Ca,L)

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

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

140 o-endoscopic imaging of neurons positive for oestrogen receptor 1 (ESR1) in either the medial preopti

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

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

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

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

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

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

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

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

149 Oestrogen receptor alpha (ERalpha) is a nuclear receptor

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

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

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

153 cally, the differential interactions between oestrogen receptor alpha and other oncogenic transcripti

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

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

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

157 Vitamin D receptor, oestrogen receptor and mineralocorticoid receptor modula

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

159 by ERBB2), activation of hormone receptors (oestrogen receptor and progesterone receptor) and/or BRC

160 sources and the model was further tested in oestrogen receptor and progesterone receptor-labelled im

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

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

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

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

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

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

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

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

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

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

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

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

173 e new standard of care for HER2-positive and oestrogen receptor negative breast cancer, even for pati

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

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

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

177 g LINC00160 expressions and interaction with oestrogen receptor signalling.

178 M0 disease and those with incomplete data on oestrogen receptor status, progesterone receptor status,

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

180 The oestrogen receptor targets LLGL2 expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

194 =0.05), but no effect was noted for invasive oestrogen receptor-negative breast cancer (HR 1.05 [95%

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

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

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

198 D comprised patients with AKT1 mutations and oestrogen receptor-negative cancer or PTEN mutation (tre

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

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

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

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

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

204 081), especially in participants known to be oestrogen receptor-positive (0.22, 0.78-0.65, p<0.0001).

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

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

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

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

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

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

211 2 study, postmenopausal women with advanced oestrogen receptor-positive and HER2-negative breast can

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

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

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

215 Invasive oestrogen receptor-positive breast cancer was reduced by

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

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

218 C comprised patients with AKT1 mutations and oestrogen receptor-positive cancer (treated with oral ca

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 l to improve outcomes in women with operable oestrogen receptor-positive primary breast cancer.

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

227 (treated with oral neratinib 240 mg, and if oestrogen receptor-positive with intramuscular standard-

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

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

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

231 Oncology Group performance status of 0-2 and oestrogen receptor-positive, HER2-negative, metastatic o

232 IRT1 and orthologous sirtuins coactivate the oestrogen receptor/ER and the worm steroid receptor DAF-

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

234 ow-up is especially important for those with oestrogen-receptor (ER)-positive breast cancers, which c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 jority (about 75%) of breast cancers express oestrogen receptors (ERs)(3), and patients with these tu

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

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

259 CAV1, the matrix metalloproteinase MMP14 and oestrogen receptors.

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

261 ading to decreased expression of 'classical' oestrogen-regulated genes and was accompanied by reduced

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

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

264 a (PGC1alpha), the cofactor and activator of oestrogen-related receptor alpha (ERRalpha).

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

266 rast, two interventions are not recommended: oestrogen replacement therapy (Level A2) and acetylcholi

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

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

269 Oestrogen-replacement therapy, primarily via the transde

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

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

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

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

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

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

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

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

278 ory adipokine secretions, such as leptin and oestrogen secretions.

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

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

281 o show that the cortex-promoting activity of oestrogen signalling is mediated via estrogen receptor a

282 velopment and that it functions by mediating oestrogen signalling.

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

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

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

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

287 f a fasting-mimicking diet as an adjuvant to oestrogen therapy in hormone-receptor-positive breast ca

288 ne-receptor-positive breast cancer receiving oestrogen therapy, cycles of a fasting-mimicking diet ca

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

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

291 d monoallelic-repression of IGFBP5 following oestrogen treatment.

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

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

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

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

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

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

298 In addition, oestrogen, which is essential for ductal elongation duri

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

300 In women, reductions in circulating oestrogens with menopause interact with ageing processes