ライフサイエンスコーパス: estrogen receptor

1 TiPARP promotes the degradation of c-Myc and estrogen receptor.

2 of G protein-coupled receptor 30 (GPR30), an estrogen receptor.

3 me 6 (rs6557168) near ESR1, which encodes an estrogen receptor.

4 oic acid receptor, farnesoid X receptor, and estrogen receptor.

5 Estrogen receptor 1 (ESR1) mutations have been identifie

6 affinity to melatonin receptor 1 (MT1R) and estrogen receptor 1 (ESR1).

7 shows how alternative 'supergene' alleles of Estrogen Receptor 1 are differentially expressed in spec

8 and CYP1B1 using TaqMan and imputed SNPs in estrogen receptor 1 using genome-wide markers.

9 f the amygdalohippocampal area (AHiPM), onto estrogen receptor 1-expressing (Esr1(+)) neurons in the

10 one receptors, such as androgen receptor and estrogen receptor(1-4), but mechanisms regulating its bi

11 hibition and morpholino knockdown of nuclear estrogen receptor 2b (esr2b) increased hepatocyte gene e

12 have associations with previously described estrogen receptor activated pathways of sexually dimorph

13 VULCAN analysis of estrogen receptor activation in breast cancer highlights

14 Differential estrogen-receptor activation regulates extracellular mat

15 which follows the steps of the Collaborative Estrogen Receptor Activity Prediction Project (CERAPP).

16 Mutations in ESR1 that confer constitutive estrogen receptor alpha (ER) activity in the absence of

17 Phosphorylation of estrogen receptor alpha (ER) at serine 118 (pS118-ER) oc

18 We generated genetic deletions of four estrogen receptor alpha (ER) bound enhancers that regula

19 ast cancer patients with tumors that express estrogen receptor alpha (ER) generally respond well to h

20 been thought to be functionally connected to estrogen receptor alpha (ER) in breast cancer.

21 Estrogen receptor alpha (ER) is a key oncogene in endome

22 Estrogen signaling through estrogen receptor alpha (ER) plays a major role in endom

23 e success of approved systemic therapies for estrogen receptor alpha (ER)-positive breast cancer, dru

24 vo tumor uptake compared with wild-type (WT)-estrogen receptor alpha (ER).

25 Estrogen receptor alpha (ER-alpha) forms a regulatory ne

26 itutive active/androstane receptor (CAR) KO, estrogen receptor alpha (ERalpha KO, phosphorylation-blo

27 Estrogen receptor alpha (ERalpha) activity is associated

28 GH-releasing hormone (GHRH) neurons express estrogen receptor alpha (ERalpha) and androgen receptor

29 environmental contaminant that can activate estrogen receptor alpha (ERalpha) and contribute to the

30 Approximately 70% of breast cancers express estrogen receptor alpha (ERalpha) and depend on this key

31 rficial spinal cord dorsal horn that express estrogen receptor alpha (ERalpha) and explored the behav

32 associates with transcriptional enhancers of estrogen receptor alpha (ERalpha) and that this associat

33 The development of tamoxifen and subsequent estrogen receptor alpha (ERalpha) antagonists represents

34 (CA12) is associated with the expression of estrogen receptor alpha (ERalpha) in breast cancer and i

35 Here, we ablate estrogen receptor alpha (ERalpha) in the medial basal hy

36 Estrogen receptor alpha (ERalpha) is a key transcription

37 Estrogen receptor alpha (ERalpha) is a ligand-dependent

38 Global estrogen receptor alpha (ERalpha) knockout (KO) mice exh

39 Early studies indicated that estrogen receptor alpha (ERalpha) might impact the progr

40 Estrogen receptor alpha (ERalpha) modulates gene express

41 t there is possible neuroendocrine action of estrogen receptor alpha (ERalpha) on the skeleton.

42 More than 75% of breast cancers are estrogen receptor alpha (ERalpha) positive (ER+), and re

43 ng nodules are estrogen dependent and retain estrogen receptor alpha (ERalpha) reactivity, but have d

44 Estrogen receptor alpha (ERalpha) regulates gene transcr

45 The DNA-binding sites of estrogen receptor alpha (ERalpha) show great plasticity

46 nding and transcriptional activation through estrogen receptor alpha (ERalpha) to that of 17beta-estr

47 s missense mutation in the gene encoding the estrogen receptor alpha (ERalpha) was previously identif

48 otein 14-3-3sigma and a peptide derived from Estrogen Receptor alpha (ERalpha), an important breast c

49 The classical estrogen receptor alpha (ERalpha), but not ERbeta, in th

50 e-negative breast cancer (TNBC), which lacks estrogen receptor alpha (ERalpha), progesterone receptor

51 Herein, we investigated the estrogen receptor alpha (ERalpha)-mediated EA of six new

52 Obesity is a risk factor for postmenopausal estrogen receptor alpha (ERalpha)-positive (ER(+)) breas

53 ourse of estradiol (E2) stimulation in human estrogen receptor alpha (ERalpha)-positive breast cancer

54 ling pathways that include the estrogen (E2)-estrogen receptor alpha (ERalpha).

55 ene has captured ESR1, the gene that encodes estrogen receptor alpha (ERalpha); as a result, this gen

56 Normal osteoblasts express estrogen receptor alpha (ERalpha); however, osteosarcoma

57 In addition to known CYP3A4 TFs, estrogen receptor alpha (ESR1) emerges as key TF with th

58 Here we identify estrogen receptor alpha (Esr1)-expressing cells in the p

59 egulation of gene expression (SATB1) and the estrogen receptor alpha (ESR1).

60 uR1, depending on its activation by membrane estrogen receptor alpha (mERalpha; during diestrus) vers

61 itro cellular toxicity, devoid of detectable estrogen receptor alpha affinity, displays high aqueous

62 gamma agonist) and 17beta-estradiol (E2; an estrogen receptor alpha agonist) nearly abolished TDCIPP

63 cellular pathway in both tissues, including estrogen receptor alpha and peroxisome proliferator acti

64 In the MG there was overexpression of estrogen receptor alpha and progesterone receptor, loss

65 cells within the AVPV/PeN highly co-express estrogen receptor alpha as well as glucocorticoid recept

66 of pharmacology and demonstrated the desired estrogen receptor alpha degrader-antagonist profile and

67 Estrogen receptor alpha gene (ESR1) mutations occur freq

68 Estrogen receptor alpha is required for oviductal transp

69 Metastatic, antiestrogen resistant estrogen receptor alpha positive (ER+) breast cancer is

70 vity of oestrogen signalling is mediated via estrogen receptor alpha within the left gonad epithelium

71 /progenitor activity, elevated expression of estrogen receptor alpha, and increased DNA damage in cel

72 ns, including HSP70 (heat-shock protein 70), estrogen receptor alpha, and RNA helicase A.

73 e expression and proliferation are driven by estrogen receptor alpha, and targeting this transcriptio

74 Dysregulation of hypothalamic-pituitary estrogen receptor alpha-mediated signaling causes episod

75 hat could be suppressed by inhibitors of the estrogen receptors alpha and beta, fibroblast growth fac

76 thelial cells through mechanisms mediated by estrogen-receptor alpha (ERalpha).

77 Estrogen receptor -alpha signaling increased IL-33 relea

78 It acts as an ER (estrogen receptor) alpha antagonist in ER-positive breas

79 ally required for response to two classes of estrogen receptor-alpha (ER) antagonists.

80 -GAP (GTPase-activating protein), is also an estrogen receptor-alpha (ER) transcriptional co-represso

81 d unclear whether estrogen signaling through estrogen receptor-alpha (ER-alpha, Esr1) or ER-beta (Esr

82 p) on neutralizing epigenetic aberrations in estrogen receptor-alpha (ERalpha) leading to enhanced an

83 o differentiates primary tumors to a benign, Estrogen Receptor-alpha (ERalpha) positive, Rictor-negat

84 or glucose homeostasis primarily through the estrogen receptor-alpha (ERalpha), but the respective im

85 Here we report that estrogen receptor-alpha (ERalpha)-expressing neurons in

86 Estrogen receptor-alpha (ESR1) expression was essentiall

87 pply our method to dissect the regulation of estrogen receptor-alpha activation in breast cancer to i

88 of this study was to determine the effect of estrogen receptor-alpha gene (ESR1) mutations at the tyr

89 e used the approach to probe the mobility of estrogen receptor-alpha in the vicinity of an integrated

90 is associated with poor patient outcomes in estrogen receptor-alpha-positive (ERalpha(+)) breast can

91 reased autophagy and decreased expression of estrogen receptor-alpha.

92 athways, and with other receptors, including estrogen receptor and human epidermal growth factor rece

93 resistance to competition are seen with the estrogen receptor and its DNA response elements.

94 ausal women with stage cT2 to 4b, any N, M0; estrogen receptor and progesterone receptor greater than

95 vealing an unexpected similarity between the estrogen receptor and the beta-tubulin taxane binding po

96 Computational results identified estrogen receptors and 17-beta-hydroxysteroid dehydrogen

97 breast cancers (TNBCs) lack progesterone and estrogen receptors and do not have amplified human epide

98 Finally, we describe how ERs (estrogen receptors) and RAGE (receptor for advanced glyc

99 very-low-density lipoprotein, vitellogenin, estrogen receptor, and thyroid hormone receptor, demonst

100 ): androgen receptor antagonist (flutamide); estrogen receptor antagonist (fulvestrant); TES suppleme

101 d small effects on cAMP levels but G protein estrogen receptor antagonists had little effect on respo

102 ent candidate genes, including those for the estrogen receptors, aromatases, and vitellogenins.

103 riptional output, as evidenced by changes in estrogen receptor-associated eRNA expression and stronge

104 Estrogen receptor beta (ERbeta) is expressed in microgli

105 Disagreements about the phenotype of estrogen receptor beta (ERbeta) knockout mouse, created

106 While estrogen receptor beta (ERbeta) may impact the progressi

107 Recent studies suggest that estrogen receptor beta (ERbeta), may function as a tumor

108 hat are potent and selective agonists of the estrogen receptor beta, and that are selectively cytotox

109 and its receptor, oxytocin and its receptor, estrogen receptor beta, serotonin receptors (Htr1a, Htr2

110 In EAE, remyelination was induced with estrogen receptor-beta (ERbeta) ligand treatment, and up

111 Herein, using growth-regulating estrogen receptor binding 1 (GREB1) as an ERalpha target

112 ptor-associated eRNA expression and stronger estrogen receptor binding at active enhancers after GRHL

113 trate that GRHL2 is recruited to a subset of estrogen receptor binding sites and regulates transcript

114 n to lineage-specific transcription factors, estrogen receptor binding sites were also found to have

115 by androgen receptor (AR) but suppression by estrogen receptor, both of which were dependent on hepat

116 C/inositol trisphosphate receptor (IP3R) and estrogen receptor co-regulation in spinal cord yielded C

117 cancer highlights the key components of the estrogen receptor complex alongside a novel interaction

118 input to KNDy cells, as well as identify the estrogen receptor content and peptidergic phenotype of a

119 p3(L351PneoR) knock-in crossed to inducible (estrogen receptor Cre-CreT) mice were incubated with lip

120 Fulvestrant is a potent selective estrogen receptor degrader (SERD), which degrades the ER

121 clic indazoles as a novel class of selective estrogen receptor degrader antagonists.

122 a series of tricyclic indazoles as selective estrogen receptor degraders (SERD) and antagonists for t

123 We investigated the effect of BP-3 and PP on estrogen receptor-dependent transactivation and DNA dama

124 ase inhibitor anastrozole plus the selective estrogen-receptor down-regulator fulvestrant, as compare

125 The majority of breast cancers expresses the estrogen receptor (ER(+)) and is treated with anti-estro

126 Immunohistochemistry on 134 estrogen receptor (ER(+)) primary breast cancer samples

127 example, aryl hydrocarbon receptor (AhR) or estrogen receptor (ER) activities.

128 ions in the presence or absence of selective estrogen receptor (ER) agonists (ERalpha /PPT or ERbeta:

129 ted greater expression of the IL-4Ralpha and estrogen receptor (ER) alpha compared with macrophages f

130 Activating mutations in the estrogen receptor (ER) alpha-gene (ESR1) result in const

131 Estrogen receptor (ER) and progesterone receptor (PR) ar

132 The highly selective estrogen receptor (ER) beta ligand chloroindazole (IndCl

133 the molecular mechanism of estrogens at the estrogen receptor (ER) complex by different types of est

134 The clinical steroidal selective estrogen receptor (ER) degrader (SERD), fulvestrant, is

135 rous/menstrual cycle, dynamically modulating estrogen receptor (ER) expression, activity, and traffic

136 The estrogen receptor (ER) is a validated target for the tre

137 ination with conjugated estrogens) selective estrogen receptor (ER) modulator (SERM) that could move

138 ination with conjugated estrogens) selective estrogen receptor (ER) modulator (SERM), bazedoxifene (B

139 Tamoxifen is the most prescribed selective estrogen receptor (ER) modulator in patients with ER-pos

140 Estrogen receptor (ER) positive breast cancer is frequen

141 Estrogen receptor (ER) positive breast cancers often con

142 same interactions, but for invasive cancer, estrogen receptor (ER) positive cancer and with broader

143 g RNA-seq data, with a Jaccard score 0.8 for estrogen receptor (ER) positive samples.

144 Limited knowledge of the changes in estrogen receptor (ER) signaling during the transformati

145 nts were selected by the following criteria: estrogen receptor (ER) status, lymph node invasion, recu

146 etween parity and breast cancer according to estrogen receptor (ER) status, with an increased risk of

147 amined separately, and further classified by estrogen receptor (ER) status.

148 elationships when stratified by breast tumor estrogen receptor (ER) status.

149 ction was assessed among treatment, BMI, and estrogen receptor (ER) status.

150 alcium are associated with decreased risk of estrogen receptor (ER)+ and ER- breast cancer, and of tr

151 static site, and have applied this system to estrogen receptor (ER)+ breast cancer.

152 Here we focus on the response of Estrogen Receptor (ER)+ post-menopausal breast cancer tu

153 cused on a subclass of EDCs that impacts the estrogen receptor (ER), a pivotal transcriptional regula

154 eventy percent of breast cancers express the estrogen receptor (ER), and agents that target the ER ar

155 NBC) in which the three major receptors i.e. estrogen receptor (ER), progesterone receptor (PR) and h

156 Estrogen receptor (ER), progesterone receptor (PR), and

157 for total invasive breast cancer risk and by estrogen receptor (ER), progesterone receptor (PR), and

158 n disproportionally, including those lacking estrogen receptor (ER), progesterone receptor, and HER2

159 an aggressive breast cancer subtype lacking estrogen receptor (ER), progesterone receptor, and human

160 Nevertheless, the estrogen receptor (ER)-balanced subset for gene-centerin

161 ith asthma exhibited increased expression of estrogen receptor (ER)-beta, which upon activation down-

162 our gene modules associated with survival in estrogen receptor (ER)-negative and one in ER-positive d

163 TRPM8 mRNA predict poor clinical outcome in estrogen receptor (ER)-negative breast cancer patients,

164 rall breast cancer risk variants, and 17 for estrogen receptor (ER)-negative breast cancer, several w

165 Limited data exist for estrogen receptor (ER)-positive (+) breast cancer among

166 Responses to immunotherapy are uncommon in estrogen receptor (ER)-positive breast cancer and to dat

167 Gene expression profiling in estrogen receptor (ER)-positive breast cancer MCF-7 cell

168 Estrogen receptor (ER)-positive breast cancer recurrence

169 e preferred treatment for certain women with estrogen receptor (ER)-positive breast cancer, but evide

170 , is the most frequently mutated oncogene in estrogen receptor (ER)-positive breast cancer.

171 The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crosso

172 Greater than 50% of estrogen receptor (ER)-positive breast cancers coexpress

173 surable radiographic and biologic changes in estrogen receptor (ER)-positive DCIS.

174 aging agent to quantify CDK4/6 expression in estrogen receptor (ER)-positive human epidermal growth f

175 CDK4/6 inhibitors are used to treat estrogen receptor (ER)-positive metastatic breast cancer

176 1.11) for all, 0.78 (95% CI: 0.60, 0.99) for estrogen receptor (ER)-positive, and 2.01 (95% CI: 1.41,

177 As ILC is nearly always (95%) estrogen receptor (ER)-positive, ER-targeting PET tracer

178 ly two thirds of all breast cancer cases are estrogen receptor (ER)-positive.

179 to develop PRSs, optimized for prediction of estrogen receptor (ER)-specific disease, from the larges

180 How different estrogen receptor (ER)-targeting therapies, including th

181 a across a variety of targets, including the estrogen receptor (ER).

182 y, particularly against tumors driven by the estrogen receptor (ER).

183 ibuted to estrogen-induced apoptosis via the estrogen receptor (ER).

184 468, 4T1 (triple-negative cells), and MCF-7 (estrogen receptor (ER)/progesterone receptor (PR)-positi

185 epatic gluconeogenesis through activation of estrogen receptor (ER)alpha-phosphoinositide 3-kinase-Ak

186 Estrogen receptors (ER) are activated by the steroid hor

187 has detected pharmaceuticals, hormones, and estrogen-receptor (ER)-, glucocorticoid receptor (GR)-,

188 noma (LSCC) responds to 17beta-estradiol via estrogen-receptor (ER, transcribed from ESR1) dependent

189 T3 correlated with worse clinical outcome in estrogen receptor+ (ER+) breast cancers.

190 Importantly, we found that the classical estrogen receptors ERalpha and ERbeta were robustly expr

191 s most often studied in terms of the nuclear estrogen receptors ERalpha and ERbeta.

192 or (GPER) but not by agonists of the classic estrogen receptors ERalpha/ERbeta, whereas the opposite

193 Tamoxifen is an antagonist of estrogen receptor (ERalpha), a transcription factor expr

194 OVSAHO and COV362 express moderate levels of estrogen receptor (ERalpha), which translated into impro

195 Reduced ESR1 (estrogen receptor, ERalpha) expression is observed in mu

196 ol) regulate neuronal function by binding to estrogen receptors (ERs), including ERalpha and GPER1, a

197 ogen-responsive gene expression analyses and estrogen receptor (ESR) immunofluorescence staining of e

198 al blockade of estrogen synthesis or nuclear estrogen receptor (ESR) signaling enhanced liver size an

199 sequencing transcripts were associated with estrogen receptor (ESR1) in the TCGA breast cancer cohor

200 eously promoted expression and activation of estrogen receptor (ESR1/ER) and its target genes (PGR, K

201 ugh previous studies revealed populations of estrogen receptor-expressing neurons in primary afferent

202 Type 1 estrogen receptor-expressing neurons in the ventrolatera

203 s, where soft microenvironments downregulate estrogen receptor expression and upregulate autophagy, t

204 ceptor signaling despite the conservation of estrogen receptor expression.

205 own.Objectives: To determine whether the ER (estrogen receptor) facilitates the development of pulmon

206 Activation of the membrane estrogen receptor G-protein-coupled estrogen receptor (G

207 GATA-binding protein 1 (GATA-1) fused to the estrogen receptor (GATA-1-ER) and therefore undergo eryt

208 ing evidence suggests that G-protein-coupled estrogen receptor (GPER) activation mimics effects of 17

209 escued by an agonist of the G-protein-linked estrogen receptor (GPER) but not by agonists of the clas

210 membrane estrogen receptor G-protein-coupled estrogen receptor (GPER) in ovariectomized mice via the

211 ential contribution of the G protein-coupled estrogen receptor (GPER) to innate defense against infec

212 is also an agonist of the G protein-coupled estrogen receptor (GPER), a GPCR ubiquitously expressed

213 Unlike canonical estrogen receptors, GPER activation is associated with r

214 We measured levels of G-protein-coupled estrogen receptor (GPER1) in HCC and nontumor liver tiss

215 human epidermal growth factor receptor 2 and estrogen receptor had an impact on preoperative SLN visu

216 nstrating widespread epigenetic silencing of estrogen receptor in human osteosarcomas.

217 Rather, DBH expression correlated with estrogen receptor in the female rat brains for this estr

218 he NuRD complex, mediating regulation of the estrogen receptor in triple-negative breast cancer cells

219 le assembly and raises the possibility of an estrogen receptor-independent mechanism for inhibiting c

220 t and 17beta-Estradiol (E2) as an agonist of Estrogen Receptors, known predisposing factor for hormon

221 the rate-limiting enzyme aromatase, but not estrogen receptors, measured by qPCR changes across the

222 hrough sustained co-activation of metabolic, estrogen receptor-mediated nociceptive, and autoimmune s

223 The selective estrogen receptor modulator (SERM) toremifene was previo

224 Selective estrogen receptor modulator drug molecules of triphenyle

225 It also produced a selective estrogen receptor modulator effect as assessed by measur

226 east cancer cells were more resistant to the estrogen receptor modulator tamoxifen as a result of inc

227 is of a precursor of raloxifene, a selective estrogen receptor modulator.

228 SCs) into myofibroblasts is inhibited by the estrogen-receptor modulator, tamoxifen, which activates

229 When using selective estrogen receptor modulators (SERMs) in cancer therapy,

230 of 2,400 compounds, we noted that selective estrogen receptor modulators (SERMs) potently stabilize

231 Evaluation of nine selective estrogen receptor modulators (SERMs) via cellular and bi

232 The selective estrogen receptor modulators (SERMs), including 4-hydrox

233 biological parameters such as polyploidy and estrogen receptor negative status.

234 In estrogen receptor-negative (ER(-)) and triple-negative b

235 s match existing subtypes of amplified-HER2, estrogen receptor-negative human tumors by molecular exp

236 e effect was more marked in PTGS2-low and/or estrogen receptor-negative tumors.

237 max predict response to four cycles of PT in estrogen receptor-negative, HER2-positive breast cancer.

238 urring estrogen estetrol and Selective Human Estrogen-Receptor Partial Agonists are being evaluated i

239 pe of tumor cells through stimulation of the estrogen receptor pathway.

240 ined a molecular pathway where an unexpected estrogen receptor, phosphodiesterase 3A, allows its part

241 ne therapy resistance frequently develops in estrogen receptor positive (ER+) breast cancer, but the

242 lbociclib is a new challenge to treatment of estrogen receptor positive (ER+) breast cancer.

243 rs that may contribute to the progression of estrogen receptor positive breast cancer.

244 A set of predominantly estrogen receptor positive tumors (ER + 85%) and their n

245 l samples from breast cancer patients across estrogen receptor positive, Her2-overexpressing, and tri

246 tors are the mainstay of hormonal therapy in estrogen receptor positive, postmenopausal breast cancer

247 otein expression as markers of recurrence in estrogen receptor- positive (ER+) breast cancer tissue.

248 st had ductal carcinoma (95%), and most were estrogen receptor-positive (97%).

249 ration was lower in TNBC cells compared with estrogen receptor-positive (ER + ) cells, and that both

250 Approximately 70% of all breast cancers are estrogen receptor-positive (ER(+) breast cancer), and en

251 Estrogen receptor-positive (ER(+)) breast cancer is the

252 Estrogen receptor-positive (ER(+)) breast cancers freque

253 transcription factor FOXA1 are a hallmark of estrogen receptor-positive (ER(+)) breast cancers.

254 ation or overexpression has been reported in estrogen receptor-positive (ER(+)) endocrine-resistant m

255 Over 70% of human breast cancers are estrogen receptor-positive (ER(+)), most of which expres

256 y is prognostic among women with early-stage estrogen receptor-positive (ER+) and human epidermal gro

257 expression levels are elevated in metastatic estrogen receptor-positive (ER+) and TNBC clinical tissu

258 Tamoxifen is used to prevent and treat estrogen receptor-positive (ER+) breast cancer (BC); how

259 Estrogen receptor-positive (ER+) breast cancer can recur

260 ) is a validated target for the treatment of estrogen receptor-positive (ER+) breast cancer.

261 ly and has been shown to be overexpressed in estrogen receptor-positive (ER+) breast cancers.

262 HDACIs) may overcome endocrine resistance in estrogen receptor-positive (ER+) metastatic breast cance

263 proximately two-fold increase in the rate of estrogen receptor-positive breast cancer (hazard ratio,

264 ) inhibitors are an established treatment in estrogen receptor-positive breast cancer and are current

265 ene transcript was increased in both luminal estrogen receptor-positive breast cancer and basal tripl

266 derate benefit in reducing risk for invasive estrogen receptor-positive breast cancer in postmenopaus

267 tors are the mainstay of hormonal therapy in estrogen receptor-positive breast cancer, although the r

268 ed to nuclear receptor RORgamma, compared to estrogen receptor-positive breast cancer.

269 ated the use of anastrozole for reduction of estrogen receptor-positive breast cancers in postmenopau

270 Seventy-six percent had estrogen receptor-positive HER2-negative disease.

271 Eligibility included endocrine-refractory, estrogen receptor-positive metastatic breast cancer.

272 One patient-derived xenograft, the estrogen receptor-positive model T126, was chosen to gen

273 ger and were less likely to have stage I and estrogen receptor-positive tumors.

274 t with a tumor-suppressive role for PADI4 in estrogen receptor-positive tumors.

275 Estrogen receptor-positive/human epidermal growth factor

276 common alterations of the SWI/SNF complex in estrogen-receptor-positive (ER(+)) breast cancer.

277 rs (AIs) are used as an adjuvant therapy for estrogen-receptor-positive breast cancer and are associa

278 M1-mediated resistance to PI3K inhibition in estrogen-receptor-positive breast cancer.

279 ccount for underlying tumor heterogeneity by estrogen receptor, progesterone receptor and human epide

280 ed age; nodal status; tumor size; grade; and estrogen receptor, progesterone receptor, and Ki-67 labe

281 No differences were detected in estrogen receptor, progesterone receptor, beta-catenin,

282 Breast cancer lacking estrogen receptors, progesterone receptors and HER2 rece

283 patients had triple-negative breast cancer (estrogen receptor/progesterone receptor < 10%), and five

284 3), prostaglandin-E2 and interaction between estrogen receptor-related alpha, flightless-1 (FLII) and

285 groups, induce various conformations of the estrogen receptor's ligand-binding domain, which in turn

286 r to identify potential co-regulators of the estrogen receptor's transcriptional response.

287 During early vertebrate development, estrogen receptor signaling is critical for many differe

288 in regulating eRNA transcription as part of estrogen receptor signaling.

289 xifen has been used for many years to target estrogen receptor signalling in breast cancer cells.

290 l phenotypes such as breast tumor status and estrogen receptor status (AUC = 0.999, 0.94 respectively

291 For newly diagnosed breast cancer, estrogen receptor status (ERS) is a key molecular marker

292 pes, including intrinsic molecular subtypes, estrogen receptor status, and TP53 mutation.

293 invasive breast carcinoma according to tumor estrogen receptor status.

294 ; OS and PFS were also analyzed according to estrogen-receptor status.

295 ed in hormone replacement therapy can target estrogen receptors that have become resistant to breast

296 upted functional interactions of mGluR5 with estrogen receptors that switch the normally positive eff

297 androgen receptor (AR) or indirectly via the estrogen receptor through aromatase conversion to estrad

298 d to schistosome eggs, and downregulation of estrogen receptor was predicted in urothelial cells expo

299 demethylating agents caused reexpression of estrogen receptor, which promoted therapeutic differenti

300 Meningiomas often express estrogen receptors, which were linked to higher prolifer