ライフサイエンスコーパス: fulvestrant

1 her SERMs, such as raloxifene or ICI182,780 (Fulvestrant).

2 tase inhibitor [letrozole or anastrazole] or fulvestrant).

3 athways and blunting therapeutic response to fulvestrant.

4 of subsequent 28-day cycles) or placebo plus fulvestrant.

5 ifen, but has no effect on responsiveness to fulvestrant.

6 y tamoxifen, but not by the ER downregulator fulvestrant.

7 tive breast cancer most likely to respond to fulvestrant.

8 sitive metastatic breast cancer treated with fulvestrant.

9 urther promoted cell cycle arrest induced by fulvestrant.

10 s ER target gene promoter in the presence of fulvestrant.

11 ancer in monotherapy and in combination with fulvestrant.

12 ists tamoxifen, raloxifene, bazedoxifene, or fulvestrant.

13 rther potentiated tumor growth inhibition by fulvestrant.

14 d selective estrogen receptor down-regulator fulvestrant.

15 ion with letrozole or 4-hydroxytamoxifen and fulvestrant.

16 ected in resistance to the antiestrogen drug fulvestrant.

17 the cytocidal effects of both tamoxifen and fulvestrant.

18 oss determines resistance to the ER degrader fulvestrant.

19 as profoundly inhibited by the ER antagonist fulvestrant.

20 d after the start of endocrine therapy with fulvestrant.

21 ence of estrogen deprivation, tamoxifen, and fulvestrant.

22 strozole-alone group crossed over to receive fulvestrant.

23 h the effectiveness of adding palbociclib to fulvestrant.

24 stance to aromatase inhibitors, tamoxifen or fulvestrant.

25 resistant to the anti-estrogen tamoxifen and fulvestrant.

26 etrozole (0.42; 0.23-0.76), palbociclib plus fulvestrant (0.37; 0.23-0.59), ribociclib plus fulvestra

27 ients with a PIK3CA mutation, alpelisib plus fulvestrant (0.39; 0.22-0.66), and several chemotherapy-

28 vestrant (0.48; 0.31-0.74), abemaciclib plus fulvestrant (0.44; 0.28-0.70), everolimus plus exemestan

29 lvestrant (0.37; 0.23-0.59), ribociclib plus fulvestrant (0.48; 0.31-0.74), abemaciclib plus fulvestr

30 ed by an oestrogen receptor (ER) antagonist (fulvestrant, 1 mum), and inhibition of transcription (ac

31 zole or anastrozole (100%), tamoxifen (48%), fulvestrant (16%), and chemotherapy (68%).

32 resence of an oestrogen receptor antagonist, Fulvestrant 182,780 suggesting a direct translational re

33 Fulvestrant (250 mg + LD regimen) in combination with an

34 e design of drugs such as tamoxifen (2a) and fulvestrant (5).

35 omly assigned (1:1) to receive intramuscular fulvestrant 500 mg (day 1) every 28 days (plus a loading

36 therapy for advanced disease received either fulvestrant 500 mg (days 0, 14, 28, and every 28 days th

37 1 months]) have been reported previously for fulvestrant 500 mg and anastrozole, respectively.

38 However, the present results suggest fulvestrant 500 mg extends OS versus anastrozole.

39 Patients received fulvestrant 500 mg intramuscularly on day 1, followed by

40 ing on day 15 of cycle 1, plus intramuscular fulvestrant 500 mg on day 1 and day 15 of cycle 1 and da

41 h subsequent 21-day cycle, and intramuscular fulvestrant 500 mg on days 1, 15, and 29 and once every

42 The hazard ratio (95% CI) for OS with fulvestrant 500 mg versus anastrozole was 0.70 (0.50 to

43 ns (treated with intramuscular extended-dose fulvestrant 500 mg); cohort B comprised patients with HE

44 total, 205 patients were randomly assigned (fulvestrant 500 mg, n = 102; anastrozole, n = 103).

45 At data cutoff, 61.8% (fulvestrant 500 mg, n = 63) and 71.8% (anastrozole, n =

46 ts were randomly assigned (1:1:1) to receive fulvestrant (500 mg intramuscular injection on day 1, fo

47 Patients were randomly assigned (1:1) to fulvestrant (500 mg intramuscular injection; on days 0,

48 in combination with open-label intramuscular fulvestrant (500 mg on day 1, then 250 mg on days 15, 29

49 ting on day 1 of cycle 1, plus intramuscular fulvestrant (500 mg) on days 1 and 15 of cycle 1 and on

50 ing on day 15 of cycle 1, plus intramuscular fulvestrant (500 mg) on days 1 and 15 of cycle 1, and on

51 , we found that the addition of ICI 182,780 (Fulvestrant), a selective ER down-regulator, could compl

52 This effect of BPA was blocked by Fulvestrant, a full estrogen antagonist, while the effec

53 nist; letrozole, an aromatase inhibitor; and fulvestrant, a pure ER antagonist.

54 al agonist tamoxifen and the pure antagonist fulvestrant, affect the tumor stroma has not yet been el

55 zole alone, despite substantial crossover to fulvestrant after progression during therapy with anastr

56 % of the patients in group 1 crossed over to fulvestrant after progression.

57 enhanced the antitumor effect of BKM120 and fulvestrant against estrogen-deprived ER(+) xenografts b

58 strogen deprivation is no better than either fulvestrant alone or exemestane.

59 ng the original treatments to anastrozole or fulvestrant alone or the combination of anastrozole plus

60 rally every day (group 1), with crossover to fulvestrant alone strongly encouraged if the disease pro

61 ared with tumors treated with anastrozole or fulvestrant alone.

62 This prediction is tested using fulvestrant, an anti-estrogen too large to pass through

63 rfering RNA to AXL, estrogen deprivation, or fulvestrant, an ER antagonist, decreases AXL expression

64 MIF production was blocked by Fulvestrant, an estrogen receptor (ER) antagonist, and i

65 462 patients were randomised (230 to receive fulvestrant and 232 to receive anastrozole).

66 confirmation in the larger phase III FALCON (Fulvestrant and Anastrozole Compared in Hormonal Therapy

67 ion was not seen in tumors treated with both fulvestrant and anti-ErbB3.

68 Whereas both fulvestrant and doxorubicin induced BIK mRNA, only doxor

69 SEMA7A conferred primary tumor resistance to fulvestrant and induced lung metastases.

70 Acquired resistance to fulvestrant and palbociclib is a new challenge to treatm

71 d HE4-overexpressing ovarian cancer cells to fulvestrant and tamoxifen.

72 nd was accompanied by reduced sensitivity to fulvestrant and tamoxifen.

73 ast to ER mutations-resistance to tamoxifen, fulvestrant and the CDK4 and CDK6 inhibitor palbociclib.

74 verexpression abrogated growth inhibition by fulvestrant and/or the PI3K inhibitor BKM120 in 3 ER(+)

75 rtib 400 mg plus intramuscular standard-dose fulvestrant); and cohort D comprised patients with AKT1

76 AKT activities, resistance to tamoxifen and fulvestrant, and hormone-independent growth.

77 The combination of abemaciclib, fulvestrant, and trastuzumab significantly improved prog

78 e selective estrogen-receptor down-regulator fulvestrant, as compared with anastrozole alone, as firs

79 cancer cell lines (NCI60) in the presence of fulvestrant, as well as the baseline gene expression of

80 Fulvestrant binds and accelerates degradation of estroge

81 In contrast, the full ER antagonist fulvestrant blocks the ability of ER to inhibit p53-medi

82 diating resistance to the pure anti-estrogen fulvestrant both in vitro and in vivo.

83 of the endocrine therapeutics tamoxifen and fulvestrant by lowering circulating IGF1, insulin and le

84 The latter genes suggest that resistance to fulvestrant can be overcome by drugs targeting the PI3K

85 is to establish if addition of pictilisib to fulvestrant can improve progression-free survival in oes

86 or-positive with intramuscular standard-dose fulvestrant); cohort C comprised patients with AKT1 muta

87 ximum double endocrine treatment with 250 mg fulvestrant combined with oestrogen deprivation is no be

88 e mice was inhibited by both anastrozole and fulvestrant compared with the control tumors.

89 midex) trial, which compared exemestane with fulvestrant-containing regimens in patients with prior s

90 er the selective oestrogen receptor degrader fulvestrant could improve progression-free survival comp

91 Treatment with fulvestrant decreased (18)F-FFNP, (18)F-FES, and (18)F-F

92 ertib in combination with the ER antagonist, fulvestrant, decreased MCF7 xenograft growth in ovariect

93 Here we observe that fulvestrant decreases ER(+) breast cancer growth compare

94 Addition of palbociclib to fulvestrant demonstrated efficacy in all biomarker group

95 ng the LRIG1 mutant were poorly sensitive to fulvestrant, despite effective ERalpha downregulation.

96 Although addition of pictilisib to fulvestrant did not significantly improve progression-fr

97 Adding lapatinib to fulvestrant does not improve PFS or OS in advanced ER-po

98 ATION: The safety profile of buparlisib plus fulvestrant does not support its further development in

99 on following treatment with the antiestrogen fulvestrant enhances PI3K/mTOR-mediated cell survival.

100 exposure to tamoxifen (T-series sublines) or fulvestrant (F-series sublines) and sublines unselected

101 The Fulvestrant First-Line Study Comparing Endocrine Treatme

102 strozole alone or sequential anastrozole and fulvestrant for the treatment of HR-positive metastatic

103 ly, the tumors treated with anastrozole plus fulvestrant from the beginning had only just doubled the

104 Anastrozole plus fulvestrant from the beginning or in sequence was associ

105 D, and MCF-7:2A cells; however, only BZA and fulvestrant (FUL) inhibited the growth of hormone-indepe

106 ble (22.4 to not estimable) in the CDKI plus fulvestrant group (difference not estimable; HR 0.58, 95

107 16 (7%) of 228 patients in in the fulvestrant group and 11 (5%) of 232 patients in the ana

108 onths (95% CI 14.8-23.5) in the placebo plus fulvestrant group and not estimable (22.4 to not estimab

109 gression-free survival between the CDKI plus fulvestrant group and the placebo plus fulvestrant group

110 ree survival was significantly longer in the fulvestrant group than in the anastrozole group (hazard

111 was 16.6 months (95% CI 13.83-20.99) in the fulvestrant group versus 13.8 months (11.99-16.59) in th

112 erse events were arthralgia (38 [17%] in the fulvestrant group vs 24 [10%] in the anastrozole group)

113 zole group) and hot flushes (26 [11%] in the fulvestrant group vs 24 [10%] in the anastrozole group).

114 plus fulvestrant group and the placebo plus fulvestrant group was 6.9 months in favour of the CDKI g

115 d 1:1:1 to the abemaciclib, trastuzumab, and fulvestrant (group A), abemaciclib and trastuzumab (grou

116 Pure anti-estrogen fulvestrant has been shown to be a promising ER antagoni

117 Fulvestrant has superior efficacy and is a preferred tre

118 One drug of this class, fulvestrant, has been approved as a third line treatment

119 Antiestrogens including tamoxifen and fulvestrant have been evaluated as chemotherapeutics for

120 CBR was similar for fulvestrant HD (n = 102) and anastrozole (n = 103), 72.5

121 rsus anastrozole (median TTP not reached for fulvestrant HD v 12.5 months for anastrozole; hazard rat

122 First-line fulvestrant HD was at least as effective as anastrozole

123 Fulvestrant HD was generally well tolerated, with a safe

124 e (ORR) was also similar between treatments: fulvestrant HD, 36.0%; anastrozole, 35.5%.

125 ration of OR and CB also numerically favored fulvestrant HD.

126 was abolished not only by the ER antagonist fulvestrant (ICI 182,780) but also by JNJ 16259685, and

127 Moreover, the estrogen receptor antagonist fulvestrant (ICI 182,780) did not block effects of 17bet

128 oactivation at the AP-1 site is augmented by fulvestrant (ICI 182,780).

129 an be activated by the estrogen-antagonists, fulvestrant (ICI) and 4OHT.

130 g ER action using targeted therapies such as fulvestrant (ICI) is often effective, later emergence of

131 eration in micromolar 4-hydroxytamoxifen and fulvestrant/ICI 182,780 (ICI).

132 nds, including estrogen, tamoxifen (OHT) and fulvestrant (ICI182780; ICI) in breast carcinoma cell li

133 -2 function and reverses antagonists such as fulvestrant/ICI182780 (ICI) or 4-hydoxytamoxifen (OHT) i

134 rivation (LTED) and subsequent resistance to fulvestrant (ICIR).

135 ated whether the addition of capivasertib to fulvestrant improved progression-free survival in patien

136 ty to confer resistance to the anti-estrogen fulvestrant in 2 ER(+) breast cancer cell lines.

137 and both potency and efficacy comparable to fulvestrant in cell lines resistant to endocrine therapy

138 f the disease progressed, or anastrozole and fulvestrant in combination (group 2).

139 g approach with the steroidal anti-oestrogen fulvestrant in combination with continued oestrogen depr

140 trate novel effects of the pure antiestrogen fulvestrant in ER(+) breast cancer and evaluate its effe

141 from the PALOMA3 (Palbociclib Combined With Fulvestrant in Hormone Receptor-Positive HER2-Negative M

142 owed a pharmacological profile comparable to fulvestrant in its ability to degrade ERalpha in both MC

143 ive in inhibition of cell proliferation than fulvestrant in MCF-7 cells.

144 d the efficacy and safety of buparlisib plus fulvestrant in patients with advanced breast cancer who

145 cy of the pan-PI3K inhibitor buparlisib plus fulvestrant in patients with advanced breast cancer, inc

146 e 3-hydroxypropylamide was as efficacious as fulvestrant in suppressing cell proliferation and gene e

147 In the patients treated with fulvestrant in the second-line setting and beyond (n=155

148 e not associated with clinical resistance to fulvestrant in this study.

149 Both tamoxifen and fulvestrant increased MFE and aldehyde dehydrogenase (AL

150 Like DHEA, GPER agonists G-1 and fulvestrant increased pri-miR-21 in a GPER- and ERalpha3

151 strate that 17beta-estradiol, tamoxifen, and fulvestrant induce nuclear and nucleolar translocation o

152 ically, we establish that both tamoxifen and fulvestrant induce STAT3 phosphorylation.

153 n of the FGFR TKI erdafitinib to palbociclib/fulvestrant induced complete responses of FGFR1-amplifie

154 counteracted the effects of E2 depletion or fulvestrant-induced cell death, thus also conferring hor

155 lpha, but not its F domain, is essential for fulvestrant-induced ERalpha-CK8 and CK18 interactions.

156 by small interference RNAs partially blocked fulvestrant-induced receptor degradation.

157 inant-negative p53 effectively inhibited the fulvestrant induction of BIK mRNA, protein, and apoptosi

158 were corroborated in a zebrafish model where fulvestrant inhibited neutrophil- and macrophage-depende

159 y a week off over 28-day cycles) plus 500 mg fulvestrant (intramuscular injection on days 1 and 15 of

160 Fulvestrant is a potent selective estrogen receptor degr

161 Fulvestrant is a selective estrogen receptor antagonist.

162 Fulvestrant is a selective estrogen receptor downregulat

163 Fulvestrant is a steroid-based, selective estrogen recep

164 Fulvestrant is an antiestrogen that leads to estrogen re

165 Fulvestrant is an estrogen receptor (ER) antagonist admi

166 When fulvestrant is combined with palbociclib (a cyclin-depen

167 nical pharmacology to the intramuscular SERD fulvestrant is described.

168 The clinical SERD fulvestrant is hampered by intramuscular administration

169 The clinical potential of fulvestrant is limited by poor physicochemical features,

170 reverse the insensitivity to anastrozole or fulvestrant is to combine the two agents.

171 Fulvestrant is unique among approved ER therapeutics due

172 Fulvestrant is used in only postmenopausal patients, and

173 tive estrogen receptor (ER) degrader (SERD), fulvestrant, is effective in metastatic breast cancer, b

174 Mechanistically, we find that fulvestrant-like antagonists suppress ER transcriptional

175 sease were open-label randomly assigned to a fulvestrant loading dose (LD) regimen followed by monthl

176 cells, and by blocking ERalpha activity with fulvestrant, LRIG1 is decreased thus permitting ErbB3 ac

177 ther group received ED plus the antiestrogen fulvestrant (MCF7 wt only).

178 Importantly, LRIG1 overexpression improved fulvestrant-mediated growth inhibition, whereas cells ex

179 In cells with acquired resistance to fulvestrant, miR-221/222 expression was essential for ce

180 A third inhibitor, fulvestrant, moderately delayed hair cell regeneration b

181 atment with OSI-906 and the ER downregulator fulvestrant more effectively suppressed hormone-independ

182 urred included aromatase inhibitor (n = 36), fulvestrant (n = 21), and tamoxifen (n = 15).

183 progression-free survival (PFS) after taking fulvestrant (n = 45) compared with exemestane (n = 18; h

184 o receive buparlisib (n=576) or placebo plus fulvestrant (n=571).

185 he growth inhibitory effect of tamoxifen and fulvestrant on shPTEN cells, suggesting that cotargeting

186 ted with immune response and were altered by fulvestrant only.

187 Cotreatment with either fulvestrant or anastrazole completely abolished the impr

188 or with E2+KB-R4973 (an INCX inhibitor), E2+fulvestrant or E2 with apex myocytes.

189 nd investigators were aware of assignment to fulvestrant or exemestane, but not of assignment to anas

190 ancer patients randomized either to the SERD fulvestrant or fulvestrant plus a pan-PI3K inhibitor.

191 ant ER MBC might respond to standard-of-care fulvestrant or other selective ER degraders when combine

192 Inhibition of both ERs with fulvestrant or selective antagonism of ERbeta, but not E

193 o plus an aromatase inhibitor, 1296 received fulvestrant plus a CDKI, and 652 received fulvestrant pl

194 randomized either to the SERD fulvestrant or fulvestrant plus a pan-PI3K inhibitor.

195 In all, 514 women were randomly assigned to fulvestrant plus anastrozole (experimental arm; n = 258)

196 as recorded between the patients assigned to fulvestrant plus anastrozole and fulvestrant plus placeb

197 ts were reported: 36 in patients assigned to fulvestrant plus anastrozole, 22 in those assigned to fu

198 randomisation: 243 were assigned to receive fulvestrant plus anastrozole, 231 to fulvestrant plus pl

199 ths (95% CI 3.4-5.4) in patients assigned to fulvestrant plus anastrozole, 4.8 months (3.6-5.5) in th

200 28 days) plus daily oral anastrozole (1 mg); fulvestrant plus anastrozole-matched placebo; or daily o

201 ed patients to receive either anastrozole or fulvestrant plus anastrozole.

202 e arthralgia (three in the group assigned to fulvestrant plus anastrozole; seven in that assigned to

203 igible and were randomly assigned to receive fulvestrant plus capivasertib (n=69) or fulvestrant plus

204 .33; P = .37); median PFS was 4.7 months for fulvestrant plus lapatinib versus 3.8 months for fulvest

205 521 patients were randomly assigned, 347 to fulvestrant plus palbociclib and 174 to fulvestrant plus

206 ree-survival events had occurred (145 in the fulvestrant plus palbociclib group and 114 in the fulves

207 occurred in 44 patients (13%) of 345 in the fulvestrant plus palbociclib group and 30 (17%) of 172 p

208 occurred in 251 (73%) of 345 patients in the fulvestrant plus palbociclib group and 38 (22%) of 172 p

209 ival was 9.5 months (95% CI 9.2-11.0) in the fulvestrant plus palbociclib group and 4.6 months (3.5-5

210 se events were neutropenia (223 [65%] in the fulvestrant plus palbociclib group and one [1%] in the f

211 Fulvestrant plus palbociclib improved PFS compared with

212 which compared fulvestrant plus placebo with fulvestrant plus palbociclib in patients with progressio

213 Fulvestrant plus palbociclib was associated with signifi

214 assigned to fulvestrant plus anastrozole and fulvestrant plus placebo (hazard ratio 1.00, 95% CI 0.83

215 eive fulvestrant plus capivasertib (n=69) or fulvestrant plus placebo (n=71).

216 g-rank p=0.98), or between those assigned to fulvestrant plus placebo and exemestane (0.95, 0.79-1.14

217 ciclib group and 4.6 months (3.5-5.6) in the fulvestrant plus placebo group (hazard ratio 0.46, 95% C

218 t plus palbociclib group and one [1%] in the fulvestrant plus placebo group), anaemia (ten [3%] and t

219 strant plus palbociclib group and 114 in the fulvestrant plus placebo group); median follow-up was 8.

220 ib group and 38 (22%) of 172 patients in the fulvestrant plus placebo group.

221 ib group and 30 (17%) of 172 patients in the fulvestrant plus placebo group.

222 plus palbociclib improved PFS compared with fulvestrant plus placebo in both ESR1 mutant (HR, 0.43;

223 s in progression-free survival compared with fulvestrant plus placebo in patients with metastatic bre

224 ter Endocrine Failure) trial, which compared fulvestrant plus placebo with fulvestrant plus palbocicl

225 receive fulvestrant plus anastrozole, 231 to fulvestrant plus placebo, and 249 to exemestane.

226 nt plus anastrozole, 22 in those assigned to fulvestrant plus placebo, and 29 in those assigned to ex

227 e, 4.8 months (3.6-5.5) in those assigned to fulvestrant plus placebo, and 3.4 months (3.0-4.6) in th

228 t in progression-free survival compared with fulvestrant plus placebo, irrespective of the degree of

229 7 to fulvestrant plus palbociclib and 174 to fulvestrant plus placebo.

230 estrant plus lapatinib versus 3.8 months for fulvestrant plus placebo.

231 ed fulvestrant plus a CDKI, and 652 received fulvestrant plus placebo.

232 plus anastrozole; seven in that assigned to fulvestrant plus placebo; eight in that assigned to exem

233 strogen receptor coactivator MED1 sensitized fulvestrant resistance breast cancer cells to fulvestran

234 l as MCF-7 cells with acquired tamoxifen and fulvestrant resistance expressed elevated levels of T-be

235 ion into the role of miR-221/222 in acquired fulvestrant resistance, a clinically important problem,

236 tly expressed microRNAs (miRNAs) in acquired fulvestrant resistance, we compared antiestrogen-resista

237 ntributed to estrogen-independent growth and fulvestrant resistance, whereas TGF-beta-mediated growth

238 so conferring hormone-independent growth and fulvestrant resistance.

239 imization of BETi using growth inhibition in fulvestrant-resistant (MCF-7:CFR) cells was confirmed in

240 hat distinguished fulvestrant-sensitive from fulvestrant-resistant ERalpha(+)/PR(+) tumors before cha

241 a requirement for ERRalpha in tamoxifen- and fulvestrant-resistant MCF-7 cells, with pharmacologic in

242 o the 'pure antiestrogen' fulvestrant, using fulvestrant-resistant MCF7-FR cells and their drug-sensi

243 eracted to kill estrogen receptor (ER)+, ER+ fulvestrant-resistant, HER2+, or triple-negative mammary

244 ne expression score and its correlation with fulvestrant response was measured in a panel of 20 breas

245 al breast tumors with the antiendocrine drug fulvestrant resulted in increased ErbB3 expression and P

246 ells transduced with FGFR1 were resistant to fulvestrant +/- ribociclib or palbociclib.

247 a profile was identified that distinguished fulvestrant-sensitive from fulvestrant-resistant ERalpha

248 Fulvestrant treatment of estradiol (E2)- and fulvestrant-sensitive MCF7 cells resulted in increased e

249 As second-line therapy, fulvestrant should be administered at 500 mg with a load

250 However, fulvestrant shows poor pharmacokinetic properties in hum

251 Compared with tamoxifen, fulvestrant significantly affected inflammatory proteins

252 Fulvestrant significantly inhibited macrophage and neutr

253 However, fulvestrant suffers from poor pharmaceutical properties

254 MCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocri

255 Together, these results suggest that fulvestrant targets ER(+) breast cancer more effectively

256 t (flutamide); estrogen receptor antagonist (fulvestrant); TES supplementation; aromatase inhibitor (

257 with the estrogen receptor alpha antagonist fulvestrant (Tfm, n=8), or physiological testosterone in

258 breast cancer, despite the use of a dose of fulvestrant that was below the current standard.

259 08 induces more complete ER degradation than fulvestrant, the only approved selective ER degrader (SE

260 However, after prolonged fulvestrant therapy, acquired resistance eventually occu

261 promotes growth, survival, and resistance to fulvestrant, thus suggesting ErbB3 as a target for breas

262 The addition of fulvestrant to anastrozole was associated with increased

263 Treatment with the pure antiestrogen fulvestrant to block ERalpha disrupted the interaction o

264 e mechanism by which ErbB3 is upregulated in fulvestrant-treated cells is unknown.

265 ng LRIG1 and maintaining low ErbB3 levels in fulvestrant-treated cells.

266 B downregulator, was decreased in a panel of fulvestrant-treated luminal breast cancer cells.

267 erm tamoxifen-treated MCF-7 cells by 80% and fulvestrant-treated MCF-7 cells by 70%.

268 In first-line fulvestrant-treated patients (n=396), the median progres

269 Depletion of ErbB3 in fulvestrant-treated tumor cells reduced PI3K/mTOR signal

270 nistic studies indicated that combination of fulvestrant treatment and MED1 knockdown is able to coop

271 Fulvestrant treatment caused ERalpha degradation in CK8.

272 Fulvestrant treatment for 28 d significantly reduced tum

273 Fulvestrant treatment increased phosphorylation of all E

274 Fulvestrant treatment induced a similar early metabolic

275 Tamoxifen and fulvestrant treatment inhibited estradiol-induced ER tra

276 Fulvestrant treatment of estradiol (E2)- and fulvestrant

277 estrogen and for ethanol vehicle control or fulvestrant treatment, a selective ER degrader.

278 how a consistent pattern of increases during fulvestrant treatment, and progression-free survival is

279 urface presentation were increased following fulvestrant treatment, focusing our attention on protein

280 ulvestrant resistance breast cancer cells to fulvestrant treatment.

281 umors was significantly reduced after 7 d of fulvestrant treatment; however, this reduction did not o

282 ks of treatment, whereas the anastrozole and fulvestrant treatments alone resulted in 9- and 12-fold

283 NAs in resistance to the 'pure antiestrogen' fulvestrant, using fulvestrant-resistant MCF7-FR cells a

284 their responses to the cytostatic effects of fulvestrant varied greatly, and their remarkably diversi

285 ogression (TTP) was significantly longer for fulvestrant versus anastrozole (median TTP not reached f

286 files associated with acquired resistance to fulvestrant versus tamoxifen.

287 The combination of capivasertib and fulvestrant warrants further investigation in phase 3 tr

288 Fulvestrant was administered intramuscularly at a dose o

289 the CDK4 and CDK6 inhibitor palbociclib and fulvestrant was associated with significant improvements

290 e expression score that predicts response to fulvestrant was developed.

291 ines, whose transcriptomal responsiveness to fulvestrant was largely lost.

292 ensitivity of each patient to treatment with fulvestrant was predicted based on the RNA profile of th

293 own-regulation of SNAT2 by the ER antagonist fulvestrant was reverted in hypoxia.

294 The combination of anastrozole and fulvestrant was superior to anastrozole alone or sequent

295 esistance to the antiestrogens tamoxifen and fulvestrant, we established drug-resistant sublines from

296 ed with the CDK4/6 inhibitor ribociclib plus fulvestrant, we identified FGFR1 as a mechanism of drug

297 te p53-binding sequence, was not affected by fulvestrant when tested by reporter assay.

298 rapeutically by combining the ER-antagonist, fulvestrant with MEKi.

299 abemaciclib plus trastuzumab with or without fulvestrant with standard-of-care chemotherapy of physic

300 alone or the combination of anastrozole plus fulvestrant would reduce tumor growth.