ライフサイエンスコーパス: antiestrogen

1 cancer cells was no longer inhibited by this antiestrogen.

2 to cell cycle progression in the presence of antiestrogen.

3 ld and that this upregulation was reduced by antiestrogen.

4 Ralpha and the activation was blocked by the antiestrogen.

5 to the acrylic acid side chain used in many antiestrogens.

6 s in the same culture during the exposure to antiestrogens.

7 of estrogen derivatives called nonsteroidal antiestrogens.

8 ensitive to the growth inhibitory effects of antiestrogens.

9 acquired resistance to clinically important antiestrogens.

10 es and lignans, can act as weak estrogens or antiestrogens.

11 onists from selective ER modulators and pure antiestrogens.

12 sufficient to partly restore sensitivity to antiestrogens.

13 sults, but NAs act as potent antiandrogen or antiestrogens.

14 s in the presence or absence of estrogens or antiestrogens.

15 ll cycle arrest effect by tamoxifen and pure antiestrogens.

16 ent one mechanism by which DTACs function as antiestrogens.

17 ynthetase heavy subunit (GCSh) expression by antiestrogens.

18 and that this down-regulation is reversed by antiestrogens.

19 cell growth can be effectively inhibited by antiestrogens.

20 d crystallography of planar estrogens or TPE antiestrogens.

21 hat HE4 overexpression induces resistance to antiestrogens.

22 r-alpha gene, sensitizing the tumor cells to antiestrogens.

23 hormone deprivation and become resistant to antiestrogens.

24 A novel class of pure antiestrogens, 1,1-dichloro-2,2,3-triarylcyclopropanes (

25 , 2-methoxyestradiol, catecholestrogens, the antiestrogen 4-hydroxytamoxifen (OHT), and dietary flavo

26 significantly better than inhibition by the antiestrogen 4-hydroxytamoxifen alone, whereas a combina

27 Because there is now a clinical need for new antiestrogens (AE) against these mutant ERs, we describe

28 Radiation therapy (RT) and antiestrogen agents reduce the risk of IBTR and are cons

29 PELP1/pRb interaction could be modulated by antiestrogen agents.

30 c approach based on combination therapy with antiestrogen and anti-RET in luminal breast cancer.

31 proliferation can be effectively blocked by antiestrogen and ovariectomy, indicating that the induce

32 We also observed that antiestrogen and the HER-2/neu antagonist, Herceptin (Tr

33 chanisms involved appeared to be similar for antiestrogens and aromatase inhibitors, the most signifi

34 Blocking estrogen receptors with antiestrogens and blocking estrogen synthesis with aroma

35 vation of the UPR and reduced sensitivity to antiestrogens and chemotherapeutics in estrogen receptor

36 Therefore, therapy combining antiestrogens and MEK inhibitors may be ineffective in s

37 sing cancers typically display resistance to antiestrogens and poor prognosis.

38 progression and suggests that combination of antiestrogens and VEGF inhibitors may prolong tamoxifen

39 sistance to the growth inhibiting effects of antiestrogens, and (c) chromosomal instability.

40 r that lost transcriptomal responsiveness to antiestrogens as a consequence of genetic abnormalities

41 grow by 4-hydroxytamoxifen, as well as other antiestrogens, as partial agonists.

42 This study has produced structurally novel antiestrogens based on a simple adamantyl core structure

43 tamoxifen, to the estrogen receptor (ER) and antiestrogen binding site (AEBS), which are commonly pre

44 rmaldehyde conjugate is mediated by both the antiestrogen binding site and estrogen receptor.

45 ty to tightly bind the estrogen receptor and antiestrogen binding sites.

46 ase-containing protein complex that binds to antiestrogen-bound ERalpha and contributes to negative r

47 Induction was blocked by an antiestrogen but also by the chelation of intracellular

48 positive breast cancers initially respond to antiestrogens but eventually become estrogen independent

49 estrogen receptor-positive and treated with antiestrogens, but aberrant signaling networks can induc

50 proximately two thirds had received adjuvant antiestrogens, but only eight individuals had received a

51 a show that NSCLC cells respond to estrogens/antiestrogens by altering endogenous gene expression and

52 Antiestrogens can worsen angioedema symptoms.

53 p2 prevented growth arrest of MCF-7 cells by antiestrogen, coinciding with decreased p27Kip1 expressi

54 Since antiestrogens compete with estrogens for binding to ER,

55 Antiestrogen compounds exhibit a variety of different ef

56 that the combination of SIRT1 inhibitors and antiestrogen compounds may offer more effective treatmen

57 ding to p53 and inhibited p21 transcription, antiestrogens decreased ERalpha recruitment and induced

58 Thus, antiestrogens define an important and well-understood cl

59 brane where it transduces both estrogen- and antiestrogen-dependent activation of the mitogen-activat

60 2 can phosphorylate MTA1s, but not ER, in an antiestrogen-dependent manner and that estrogen stimulat

61 amoxifen, and Combined trial, addition of an antiestrogen did not decrease efficacy of the AI.

62 f ERalpha was reflected in resistance to the antiestrogen drug fulvestrant.

63 al and clinical evidence links resistance to antiestrogen drugs in breast cancer cells with the overe

64 also resensitized LCC9 cells (resistant) to antiestrogen drugs.

65 Heregulin beta1 or estradiol abrogate antiestrogen effects by increasing Cks1 expression, down

66 -resistant cells to determine the effect of antiestrogens/ERalpha on regulating autophagy and unfold

67 atively high proportion of previous adjuvant antiestrogen exposure.

68 icate superiority of aromatase inhibitors to antiestrogens for breast cancer prevention.

69 icate superiority of aromatase inhibitors to antiestrogens for breast cancer prevention.Oncogene adva

70 noids may be most useful in combination with antiestrogens for more effective prevention of breast ca

71 estrogen agonist displaces a SNAPFL-labeled antiestrogen from the ligand binding pocket of a terbium

72 The antiestrogen fulvestrant (ICI 182,780) causes immobiliza

73 Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only).

74 In MCF7 cells, pure antiestrogen fulvestrant also induces BIK mRNA and apopt

75 B3 upregulation following treatment with the antiestrogen fulvestrant enhances PI3K/mTOR-mediated cel

76 The pure antiestrogen fulvestrant inhibited the estradiol-stimula

77 Treatment with the pure antiestrogen fulvestrant to block ERalpha disrupted the

78 ression can be delayed by combining the pure antiestrogen fulvestrant with the nonsteroidal aromatase

79 Although growth was inhibited by the antiestrogen fulvestrant, the IC50 was 100-fold higher t

80 rowth and differentiation (17beta-estradiol, antiestrogens fulvestrant and tamoxifen, progestin R5020

81 he role of miRNAs in resistance to the 'pure antiestrogen' fulvestrant, using fulvestrant-resistant M

82 Antiestrogens had failed to fulfill their promise as pos

83 4-hydroxytamoxifen, these concentrations of antiestrogens had no significant effect on the growth of

84 While antiestrogens have been available since the early 1970s,

85 Though antiestrogenic in the breast, some antiestrogens have estrogen-like actions in other tissue

86 motor symptoms are common adverse effects of antiestrogen hormone treatment in conventional breast ca

87 or vasomotor symptoms secondary to long-term antiestrogen hormone use in patients with breast cancer.

88 nificantly less active than ZOHT or the pure antiestrogen ICI 182,780 (faslodex) in stimulating trans

89 n of ML20 cells in media containing the pure antiestrogen ICI 182,780 was also markedly inhibited upo

90 on was totally blocked by 100 nmol/L of pure antiestrogen ICI 182,780, implying estrogen receptor (ER

91 s were abolished in the presence of the pure antiestrogen ICI 182,780, indicating that the classic es

92 d cathepsin D mRNAs that were blocked by the antiestrogen ICI 182,780.

93 endent because they were blocked by the pure antiestrogen ICI 182,780.

94 nsfectants, grew in the presence of the pure antiestrogen ICI 182,780.

95 translocation of IRS-1 was blocked with the antiestrogen ICI 182,780; (3) nuclear IRS-1 colocalized

96 wth factor (EGF) in the presence of the pure antiestrogen ICI 182780 (Faslodex; fulvestrant).

97 d by these AhR ligands were inhibited by the antiestrogen ICI 182780 and by the transfection of a sma

98 When exposed to the antiestrogen ICI 182780, these cells accumulate in G(1)

99 hin this class of molecules is the steroidal antiestrogen ICI182,780 (faslodex), recently approved fo

100 r p21(WAF1/CIP1) is regulated by estrogen or antiestrogen in an antiestrogen-resistant MCF-7 derivati

101 expression and proliferation by estrogen and antiestrogen in ERalpha-negative breast cancer cells.

102 receptor modulator (SERM), which acts as an antiestrogen in the mammary tissue and displays estrogen

103 ggest that LYN mutations mediate escape from antiestrogens in a subset of ER(+) breast cancers.

104 y, has been reported to induce resistance to antiestrogens in breast cancer cell lines.

105 inhibition on the emergence of resistance to antiestrogens in breast cancer models.

106 iving the cell fate decisions in response to antiestrogens in ER(+) breast cancer cells, both in vitr

107 he cellular and molecular changes induced by antiestrogens in the context of a uniform clonal backgro

108 and estrogens has led to the development of antiestrogens, in particular tamoxifen, to inhibit the a

109 Antiestrogens include agents such as tamoxifen, toremife

110 Antiestrogens including tamoxifen and fulvestrant have b

111 Antiestrogens induce both cytostasis (cell cycle arrest)

112 on of XBP1(S) prevents cell cycle arrest and antiestrogen-induced cell death through the mitochondria

113 antly, the expression of Smad4 inhibits both antiestrogen-induced luciferase activity and estrogen do

114 ncreased cell migration and invasion; caused antiestrogen insensitivity; and promoted metastasis of b

115 We previously reported that antiestrogen-liganded estrogen receptor beta (ERbeta) tr

116 We previously reported that antiestrogen-liganded estrogen receptor beta (ERbeta) tr

117 th Smad4, and the interaction was induced by antiestrogen ligands such as tamoxifen, raloxifene, and

118 angular TPE complexes as "estrogen-like" or "antiestrogen-like" complexes, respectively.

119 y which cell and tissue selective effects of antiestrogens may be achieved.

120 gens for binding to ER, clinical response to antiestrogens may be affected by exogenous estrogenic ex

121 tagonists such as tamoxifen, suggesting that antiestrogens may be beneficial in the treatment of CF l

122 tagonists such as tamoxifen, suggesting that antiestrogens may be beneficial in the treatment of CF l

123 that early pharmacological intervention with antiestrogens may diminish persistent pubertal gynecomas

124 elial growth factor (anti-VEGF) therapy with antiestrogens may prevent or delay the development of en

125 The data suggest that antiestrogens may represent pharmacological targets to i

126 To search for new antiestrogens more effective in treating breast cancers,

127 The effects of estrogen and antiestrogens on p21 transcription were diametrically op

128 Treatment with an antiestrogen or ERalpha knockdown abolished basal and es

129 ase, luminobasal cells expand in response to antiestrogen or estrogen withdrawal therapies.

130 duction of PDCD4 expression by RAR-agonists, antiestrogen or HER2/neu antagonist in breast cancer cel

131 uccessfully treated by adjuvant therapy with antiestrogens or aromatase inhibitors.

132 ls and ER+ tumors with an acquired resistant antiestrogen phenotype were both shown to overexpress GR

133 calization of PELP1 modulates sensitivity to antiestrogens, potentiates tumorigenicity, presumably vi

134 e1-null mice with either an anticoagulant or antiestrogen prevented the fetal loss phenotype.

135 It was recently demonstrated that antiestrogens prevented prostate cancer (PRCA) in men.

136 Antiestrogens produced an ER-dependent increase of up to

137 n signaling and plays a critical role in the antiestrogen-provoked breast cancer cell apoptosis.

138 Newer treatment strategies, such as the antiestrogen raloxifene, have shown promising results; h

139 on on the action of estradiol (E(2)) and two antiestrogens, raloxifene and 4-hydroxytamoxifen, in est

140 F-7, T47D, and ZR-75-1), a model of acquired antiestrogen resistance (MCF7/LCC9; estrogen receptor po

141 n receptor positive), and a model of de novo antiestrogen resistance (MDA-MB-231; estrogen receptor n

142 k-associated substrate)/BCAR1 (breast cancer antiestrogen resistance 1 gene) are associated with aggr

143 ated that the adaptor molecule breast cancer antiestrogen resistance 3 (BCAR3) promotes adhesion disa

144 tor coactivator or corepressor expression in antiestrogen resistance also is unclear, and understandi

145 These data identify a novel mechanism of antiestrogen resistance and implicate IRF-1 as a key com

146 nts confer ERalpha constitutive activity and antiestrogen resistance and suggest that ligand-binding

147 d in human breast cancers, can contribute to antiestrogen resistance by altering p21(WAF1/CIP1) regul

148 Further, they confer antiestrogen resistance by altering the conformational d

149 Thus, the apparent acquisition of antiestrogen resistance by MCF-7 cells reflects selectio

150 Whether antiestrogen resistance can be conferred by a switch fro

151 Three out of four antiestrogen resistance cell lines (Tam/MCF-7, ICI/MCF-7

152 se studies suggest that AND-34/BCAR3 induces antiestrogen resistance in breast cancer cell lines by a

153 T-1 interactions might abrogate FGF-mediated antiestrogen resistance in breast cancers.

154 suggest that PKC-delta plays a major role in antiestrogen resistance in breast tumor cells and thus p

155 Furthermore, antiestrogen resistance in cells overexpressing BCAR1/BC

156 lity to interact, we show that BCAR3-induced antiestrogen resistance in MCF7 breast cancer cells crit

157 titutively active form of Rac1, also induced antiestrogen resistance in ZR-75-1 cells.

158 Antiestrogen resistance is a major clinical problem in t

159 igated scaffolding protein that also confers antiestrogen resistance is the SH2 domain-containing pro

160 (ICI) is often effective, later emergence of antiestrogen resistance limits clinical use.

161 Essentially, two forms of antiestrogen resistance occur: de novo resistance and ac

162 ation might be useful to define and overcome antiestrogen resistance of breast cancer.

163 rmone-driven development of neoplasia and to antiestrogen resistance of breast cancers.

164 ted ERalpha degradation likely contribute to antiestrogen resistance seen in ERalphaY537S and ERalpha

165 ene expression in the onset of breast cancer antiestrogen resistance, and an improved understanding o

166 previously implicated in the development of antiestrogen resistance, this finding implicates ELF5 as

167 tein, p130(Cas) (also known as breast cancer antiestrogen resistance-1; BCAR1), that plays a role in

168 cated in tamoxifen resistance, breast cancer antiestrogen resistance-3 (BCAR3), has also been shown t

169 The Cas-binding protein BCAR3 (breast cancer antiestrogen resistance-3) is expressed at high levels i

170 Loss of IRF-1 regulation appears specific to antiestrogen resistance-resistant cells induce IRF-1 mRN

171 sponse, and contribute to the development of antiestrogen resistance.

172 [XBP1(S)], is a key UPR component mediating antiestrogen resistance.

173 radiol signaling and may contribute to local antiestrogen resistance.

174 eins involved in cell adhesion/migration and antiestrogen resistance.

175 ated c-Myc expression has been implicated in antiestrogen resistance.

176 study the molecular mechanisms that control antiestrogen resistance.

177 IFN regulatory factor-1 (IRF-1) in acquired antiestrogen resistance.

178 he ACTR-E2F1 pathway as a novel mechanism in antiestrogen resistance.

179 oach to exploring the mechanistic aspects of antiestrogen resistance.

180 AR1, ultimately potentiating BCAR1-dependent antiestrogen resistance.

181 a key role for ERK1/2 in BCAR1/BCAR3-induced antiestrogen resistance.

182 that the BCAR3-related NSP3 can also promote antiestrogen resistance.

183 y mutated pathway in breast cancer, promotes antiestrogen resistance.

184 nes were constitutively active and partially antiestrogen resistant.

185 acquired fulvestrant resistance, we compared antiestrogen-resistant and -sensitive breast cancer cell

186 strated that XBP1 expression is increased in antiestrogen-resistant breast cancer cell lines and is c

187 27 gene and created estrogen-independent and antiestrogen-resistant breast cancer cells that still ma

188 proliferation in antiestrogen-sensitive and antiestrogen-resistant breast cancer cells.

189 Preclinical tumor models of antiestrogen-resistant breast cancer often remain sensit

190 The development of targeted therapies for antiestrogen-resistant breast cancer requires a detailed

191 Antiestrogen-resistant breast cancers often show increas

192 h factor receptor signaling is implicated in antiestrogen-resistant breast tumors suggesting that abr

193 ntent and function are maintained in all the antiestrogen-resistant cell lines.

194 ER+ antiestrogen-resistant cells and ER+ tumors with an acqu

195 methylation, was more frequently observed in antiestrogen-resistant cells compared with gene inactiva

196 Emergence of antiestrogen-resistant cells in MCF-7 cells during suppr

197 The p21 levels in the antiestrogen-resistant cells increased when c-Myc expres

198 ificant Pol II binding changes in E2-treated antiestrogen-resistant cells.

199 of PKC isoforms in four different models of antiestrogen-resistant cells.

200 nhibited estrogen- and Tam-induced growth in antiestrogen-resistant cells.

201 This is a first report of a mouse model of antiestrogen-resistant ER-positive breast cancers, and c

202 utations lead to a constitutively active and antiestrogen-resistant ERalpha.

203 nd MEK inhibitors may be ineffective in some antiestrogen-resistant estrogen receptor-positive breast

204 naling components and abrogate FGF-1-induced antiestrogen-resistant growth.

205 regulated by estrogen or antiestrogen in an antiestrogen-resistant MCF-7 derivative.

206 rmone-dependent MCF7 breast cancer cells and antiestrogen-resistant MCF7 breast cancer cells before a

207 dent breast cancers to estrogen-independent, antiestrogen-resistant, and metastatic breast cancers ar

208 nsights into how molecular signaling affects antiestrogen responsiveness and strongly suggest that a

209 the role of XBP1 and the UPR in estrogen and antiestrogen responsiveness in breast cancer.

210 unctional significance of IRF-1 in affecting antiestrogen responsiveness in estrogen receptor-positiv

211 Nonsteroidal antiestrogens selectively turn on or turn off estrogen t

212 R expression with tamoxifen, suggesting that antiestrogen selects for ER-negative tumor cells and tha

213 r liver receptor homolog-1 (LRH-1, NR5A2) in antiestrogen-sensitive and -resistant breast cancer cell

214 We used antiestrogen-sensitive and -resistant cells to determine

215 s of genes involved in cell proliferation in antiestrogen-sensitive and antiestrogen-resistant breast

216 many population doublings ago, not from the antiestrogen-sensitive cells in the same culture during

217 cell line is a model of estrogen-dependent, antiestrogen-sensitive human breast cancer.

218 responsiveness in estrogen receptor-positive antiestrogen-sensitive models (MCF-7, T47D, and ZR-75-1)

219 Knockdown of GRP78 restored antiestrogen sensitivity in resistant cells, and overexp

220 GRP78 and beclin-1 synergistically restored antiestrogen sensitivity in resistant cells.

221 Moreover, antiestrogens show efficacy as chemopreventive agents in

222 The estrogen and antiestrogen signaling pathways mediated by hER-alpha36

223 In contrast, the bypass of antiestrogen signaling resulted in continued proliferati

224 ed resistance phenotype, with a switch to an antiestrogen-stimulated growth being a minor phenotype.

225 with the coactivator GRIP1 and suppressed by antiestrogens such as tamoxifen and ICI 182,780.

226 Antiestrogens such as tamoxifen are widely used in the c

227 prognosis and treatment responsiveness with antiestrogens, such as tamoxifen.

228 ed cell cycle progression in the presence of antiestrogen, suggesting that the decrease in p21 is nec

229 omparison with estrogen withdrawal (E2W) and antiestrogens Tam and faslodex.

230 ially TAM responsive develop tumors that are antiestrogen/TAM resistant (TAM-R).

231 -TFII, but not COUP-TFI, is reduced in three antiestrogen/TAM-R cell lines derived from TAM-sensitive

232 been reported to be more effective than the antiestrogen tamoxifen (Tam) in treating breast cancer.

233 The use of the antiestrogen tamoxifen (TAM) is associated with an incre

234 ssociated with the failure to respond to the antiestrogen tamoxifen and poor prognosis, highlighting

235 downregulates miR-515-5p levels, whereas the antiestrogen tamoxifen causes a decrease in SK1, which i

236 pression was correlated with response to the antiestrogen tamoxifen in both patients and in vitro-der

237 The antiestrogen tamoxifen is a well-tolerated, effective tr

238 itive breast cancer who are treated with the antiestrogen tamoxifen will either not respond to initia

239 ule Cas has been linked to resistance to the antiestrogen tamoxifen, both in tissue culture and in hu

240 Options include the antiestrogen tamoxifen, estrogen deprivation with aromat

241 inical response in patients treated with the antiestrogen tamoxifen, whereas promoter methylation of

242 n of Mdm-2 oncoprotein and resistance to the antiestrogen tamoxifen.

243 ts with ER(+) breast cancer treated with the antiestrogen tamoxifen.

244 sitivity to growth inhibition induced by the antiestrogens Tamoxifen and Faslodex in a manner indepen

245 events underlying acquired resistance to the antiestrogens tamoxifen and fulvestrant, we established

246 e of 17beta-estradiol and derepressed by the antiestrogens tamoxifen and ICI 182780 in a promoter-spe

247 The antiestrogen, tamoxifen (TMX), has been shown to functio

248 ncer cell lines with HDAC inhibitors and the antiestrogen, tamoxifen, resulted in synergistic antitum

249 rone, and androstadienedione, as well as the antiestrogen, testolactone.

250 tarvation or exposure to fulvestrant, a pure antiestrogen that competes with the natural estrogens fo

251 de novel evidence that endoxifen is a potent antiestrogen that functions in part by targeting ERalpha

252 Fulvestrant is an antiestrogen that leads to estrogen receptor degradation

253 n production through aromatase inhibitors or antiestrogens that compete for hormone binding.

254 f phosphatidylinositol 3-kinase (PI 3-K), by antiestrogens, the protein tyrosine kinase inhibitor, ge

255 One subclass of antiestrogens, the selective estrogen receptor down-regu

256 ently overcome cell cycle arrest mediated by antiestrogen therapeutics.

257 Although antiestrogen therapies targeting estrogen receptor (ER)

258 though ER-positive tumors usually respond to antiestrogen therapies, 30% of them do not.

259 nespimycin (a heat shock protein inhibitor), antiestrogen therapies, and an antibody-drug conjugate (

260 (P < .0001), younger age (P < .008), and no antiestrogen therapy (P < .02).

261 negative, with ERalpha+ tumors responding to antiestrogen therapy and having a better prognosis.

262 ned Cox regression analysis identified prior antiestrogen therapy as a significant factor in the HER2

263 y significant higher likelihood of receiving antiestrogen therapy compared with non-navigated control

264 the prevalence of BMD abnormalities, whether antiestrogen therapy decreased BMD, and if treatment wit

265 YStat5 was associated with increased risk of antiestrogen therapy failure as measured by univariate C

266 of active Stat5 in tumors is associated with antiestrogen therapy failure in patients.

267 Current antiestrogen therapy for breast cancer is limited by the

268 storing ERalpha expression and responding to antiestrogen therapy in a subset of breast cancers.

269 ggest that these data warrant the testing of antiestrogen therapy in females with CF and propose an a

270 ceived included the following: initiation of antiestrogen therapy in patients with hormone receptor-p

271 Antiestrogen therapy induces the unfolded protein respon

272 on estrogen for continued tumor growth, then antiestrogen therapy may be effective in the treatment o

273 mains unanswered, but predicting response to antiestrogen therapy requires only measurement of ERalph

274 Prior neoadjuvant/adjuvant antiestrogen therapy was allowed.

275 ptor/progesterone receptor-positive disease, antiestrogen therapy with an aromatase inhibitor is a re

276 While ERalpha-dependent cancers respond to antiestrogen therapy, Her-2/neu-overexpressing cancers t

277 tic lung lesions, is frequently treated with antiestrogen therapy, i.e., progesterone and/or oophorec

278 Among participants eligible for antiestrogen therapy, navigated participants (n = 380) h

279 inhibition by p21 and p27, and resistance to antiestrogen therapy.

280 following cisplatin, ionizing radiation, and antiestrogen therapy.

281 hormone deprivation and become resistant to antiestrogen therapy.

282 y than non-navigated participants to receive antiestrogen therapy.

283 ophagy to determine cell fate in response to antiestrogen therapy.

284 are resistant to and others are worsened by antiestrogen therapy; the data suggest that hER-alpha36

285 vely with increased disease-free survival in antiestrogen-treated breast cancer patients.

286 duced cytoplasmic localization of p27Kip1 in antiestrogen-treated cells and prevented accumulation of

287 le c-Myc expression, we demonstrated that in antiestrogen-treated cells, the elevated mRNA and protei

288 sitive AQUA quantification of Nuc-pYStat5 in antiestrogen-treated patients (cohort V; n = 97) identif

289 growth-inhibitory mechanism associated with antiestrogen treatment of breast cancer.

290 Adjusting for tumor characteristics and antiestrogen treatment, HF-negative women assigned to th

291 ot significantly attenuated by DNA damage or antiestrogen treatment, indicating that the protein may

292 prognosis, ER negativity, and resistance to antiestrogen treatment.

293 oming drug resistance to currently available antiestrogen treatments, all of which target the hormone

294 Antiestrogen unresponsiveness appears to be the major ac

295 Furthermore, autophagy induction by antiestrogens was prosurvival but did not prevent ERalph

296 bjected to estrogen starvation or exposed to antiestrogens, we characterized changes in the gene expr

297 tes are transformed from an estrogen into an antiestrogen when the 11beta-side chain is increased in

298 Loss of IRF1 promoted resistance to antiestrogens, whereas combined silencing of ATG7 and IR

299 ssed and predict that a brief treatment with antiestrogens will boost FR-alpha expression by passive

300 t combining autophagy or UPR inhibitors with antiestrogens would reduce the development of resistance