ライフサイエンスコーパス: fulvestrant

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

2 the pure antiestrogen ICI 182780 (Faslodex; fulvestrant).

3 urther promoted cell cycle arrest induced by fulvestrant.

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

5 ists tamoxifen, raloxifene, bazedoxifene, or fulvestrant.

6 rther potentiated tumor growth inhibition by fulvestrant.

7 d selective estrogen receptor down-regulator fulvestrant.

8 ion with letrozole or 4-hydroxytamoxifen and fulvestrant.

9 ected in resistance to the antiestrogen drug fulvestrant.

10 the cytocidal effects of both tamoxifen and fulvestrant.

11 as profoundly inhibited by the ER antagonist fulvestrant.

12 and PUMA mRNA, only BIK mRNA was induced by fulvestrant.

13 nstitutively expressed BIK mRNA even without fulvestrant.

14 ch as tamoxifen, toremifene, raloxifene, and fulvestrant.

15 , with efficacy end points slightly favoring fulvestrant.

16 athways and blunting therapeutic response to fulvestrant.

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

18 resistant to the anti-estrogen tamoxifen and fulvestrant.

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

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

21 tive breast cancer most likely to respond to fulvestrant.

22 sitive metastatic breast cancer treated with fulvestrant.

23 /d; n = 18), or letrozole (10 microg/d) plus fulvestrant (1 mg/d; n = 5).

24 ed s.c. daily with vehicle (control; n = 6), fulvestrant (1 mg/d; n = 7), letrozole (10 microg/d; n =

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

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

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

28 receive either an intramuscular injection of fulvestrant 250 mg once monthly or a daily oral dose of

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

30 ase were randomly assigned to receive either fulvestrant (250 mg, via intramuscular injection, once m

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

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

33 1 months]) have been reported previously for fulvestrant 500 mg and anastrozole, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

47 nduced by estrogen starvation or exposure to fulvestrant, a pure antiestrogen that competes with the

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

49 % of the patients in group 1 crossed over to fulvestrant after progression.

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

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

52 essing tumor growth than either letrozole or fulvestrant alone or sequential therapies with tamoxifen

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

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

55 ared with tumors treated with anastrozole or fulvestrant alone.

56 In MCF7 cells, pure antiestrogen fulvestrant also induces BIK mRNA and apoptosis.

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

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

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

60 mization to progression) was 19.0 months for fulvestrant and 10.8 months for anastrozole.

61 462 patients were randomised (230 to receive fulvestrant and 232 to receive anastrozole).

62 .14; P =.43); median TTP was 5.4 months with fulvestrant and 3.4 months with anastrozole.

63 te for the overall population was 31.6% with fulvestrant and 33.9% with tamoxifen, and 33.2% and 31.1

64 able disease > or = 24 weeks) were 42.2% for fulvestrant and 36.1% for anastrozole (95% CI, -4.00% to

65 ximately 78%), median TTP was 8.2 months for fulvestrant and 8.3 months for tamoxifen (hazard ratio,

66 growth factor, and striking overlaps between fulvestrant and all-trans-retinoic acid.

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

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

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

70 s, combined treatment with ER down-regulator fulvestrant and letrozole, prevented increases in erbB-2

71 there was no significant difference between fulvestrant and tamoxifen for the primary end point of t

72 erentiation (17beta-estradiol, antiestrogens fulvestrant and tamoxifen, progestin R5020, antiprogesti

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

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

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

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

77 Fulvestrant binds and accelerates degradation of estroge

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

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

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

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

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

83 patients, DOR was significantly greater for fulvestrant compared with anastrozole; the ratio of aver

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

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

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

87 tamoxifen, and statistical noninferiority of fulvestrant could not be demonstrated.

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

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

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

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

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

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

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

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

96 cyclodextrin, the ER antagonist ICI 182,780 [fulvestrant (Faslodex)], and two inhibitors of PI-3 kina

97 ptor (EGFR) pathways using an ER antagonist, fulvestrant ("Faslodex"), and the selective EGFR tyrosin

98 ol (E2), the pure ER antagonist ICI 182,780 (fulvestrant, Faslodex), or epidermal growth factor, whic

99 The Fulvestrant First-Line Study Comparing Endocrine Treatme

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

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

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

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

104 16 (7%) of 228 patients in in the fulvestrant group and 11 (5%) of 232 patients in the ana

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

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

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

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

109 ients with hormone receptor-positive tumors, fulvestrant had similar efficacy to tamoxifen and was we

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

111 Fulvestrant has superior efficacy and is a preferred tre

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

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

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

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

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

117 Fulvestrant HD was generally well tolerated, with a safe

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

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

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

121 The antiestrogen fulvestrant (ICI 182,780) causes immobilization of estro

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

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

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

125 blocked by the estrogen receptor antagonist fulvestrant (ICI-182,780, Faslodex) but was unaffected b

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

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

128 -2 function and reverses antagonists such as fulvestrant/ICI182780 (ICI) or 4-hydoxytamoxifen (OHT) i

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

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

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

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

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

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

135 gned to examine the efficacy and toxicity of fulvestrant in patients with disease progression on a th

136 e of exemestane, letrozole, anastrozole, and fulvestrant in postmenopausal women.

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

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

139 to estrogen and up-regulated in response to fulvestrant in vitro, suggesting that the EGFR pathway i

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

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

142 mall interfering RNA effectively blocked the fulvestrant-induced breast cancer cell apoptosis.

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

144 uct in fluorescence microscopy revealed that fulvestrant-induced cytoplasmic localization of newly sy

145 Furthermore, fulvestrant-induced ERalpha degradation was not observed

146 To investigate the in vivo role of H12 in fulvestrant-induced ERalpha immobilization/degradation,

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

148 only the ERalpha H12 mutant was resistant to fulvestrant-induced immobilization to the nuclear matrix

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

150 rmediate filament proteins are necessary for fulvestrant-induced receptor turnover.

151 We suggest that fulvestrant induces ERalpha to interact with CK8 and CK1

152 In this study we tested the hypothesis that fulvestrant induces specific nuclear matrix protein-ERal

153 ontrast to doxorubicin or gamma-irradiation, fulvestrant induction of BIK mRNA is not a direct effect

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

155 The pure antiestrogen fulvestrant inhibited the estradiol-stimulated prolifera

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

157 Fulvestrant is a selective estrogen receptor antagonist.

158 Fulvestrant is a selective estrogen receptor downregulat

159 Fulvestrant is a steroid-based, selective estrogen recep

160 Fulvestrant is a well-tolerated treatment and has effica

161 The estrogen receptor downregulator fulvestrant is also an option after treatment with aroma

162 Fulvestrant is an antiestrogen that leads to estrogen re

163 Fulvestrant is an estrogen receptor (ER) antagonist admi

164 nical pharmacology to the intramuscular SERD fulvestrant is described.

165 The clinical SERD fulvestrant is hampered by intramuscular administration

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

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

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

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

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

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

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

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

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

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

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

177 Fulvestrant neither affected the stability of the BIK mR

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

179 trogen and 10 ng/mL EGF and either 1 mumol/L fulvestrant or 1 mumol/L gefitinib alone or in combinati

180 Cotreatment with either fulvestrant or anastrazole completely abolished the impr

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

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

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

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

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

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

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

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

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

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

191 28 days) plus daily oral anastrozole (1 mg); fulvestrant plus anastrozole-matched placebo; or daily o

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

193 .33; P = .37); median PFS was 4.7 months for fulvestrant plus lapatinib versus 3.8 months for fulvest

194 521 patients were randomly assigned, 347 to fulvestrant plus palbociclib and 174 to fulvestrant plus

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

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

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

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

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

200 Fulvestrant plus palbociclib improved PFS compared with

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

202 Fulvestrant plus palbociclib was associated with signifi

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

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

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

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

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

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

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

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

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

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

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

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

215 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

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

217 7 to fulvestrant plus palbociclib and 174 to fulvestrant plus placebo.

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

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

220 Fulvestrant represents an additional treatment option fo

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

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

223 Fulvestrant resistance was characterized by pronounced u

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

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

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

227 so conferring hormone-independent growth and fulvestrant resistance.

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

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

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

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

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

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

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

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

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

237 However, fulvestrant suffers from poor pharmaceutical properties

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

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

240 ugh growth was inhibited by the antiestrogen fulvestrant, the IC50 was 100-fold higher than for paren

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

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

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

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

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

246 Tumor volumes of the fulvestrant-treated group had doubled in 10 weeks.

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

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

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

250 compared with 49% and 32% for gefitinib and fulvestrant treatment alone, respectively.

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

252 Fulvestrant treatment caused ERalpha degradation in CK8.

253 Fulvestrant treatment increased phosphorylation of all E

254 Tamoxifen and fulvestrant treatment inhibited estradiol-induced ER tra

255 Fulvestrant treatment of estradiol (E2)- and fulvestrant

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

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

258 ulvestrant resistance breast cancer cells to fulvestrant treatment.

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

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

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

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

263 files associated with acquired resistance to fulvestrant versus tamoxifen.

264 Fulvestrant was administered intramuscularly at a dose o

265 Fulvestrant was as effective as anastrozole in terms of

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

267 Fulvestrant was at least as effective as anastrozole, wi

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

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

270 Thus, the combination of letrozole plus fulvestrant was more effective in suppressing tumor grow

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

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

273 Fulvestrant was well tolerated.

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

275 The relative responses to gefitinib and fulvestrant were similar regardless of ER and EGFR expre

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

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

278 e delayed by combining the pure antiestrogen fulvestrant with the nonsteroidal aromatase inhibitor le

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