ライフサイエンスコーパス: antiestrogen

1 Ralpha and the activation was blocked by the antiestrogen.

2 cancer cells was no longer inhibited by this antiestrogen.

3 to cell cycle progression in the presence of antiestrogen.

4 ld and that this upregulation was reduced by antiestrogen.

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

6 of estrogen derivatives called nonsteroidal antiestrogens.

7 ensitive to the growth inhibitory effects of antiestrogens.

8 to the acrylic acid side chain used in many 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 s in the presence or absence of estrogens or antiestrogens.

13 ll cycle arrest effect by tamoxifen and pure antiestrogens.

14 ent one mechanism by which DTACs function as antiestrogens.

15 ynthetase heavy subunit (GCSh) expression by antiestrogens.

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

17 efit from treatment with PI3K inhibitors and antiestrogens.

18 sufficient to partly restore sensitivity to antiestrogens.

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

20 d crystallography of planar estrogens or TPE antiestrogens.

21 hat HE4 overexpression induces resistance to antiestrogens.

22 ived (LTED) breast cancer cells resistant to antiestrogens.

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

24 hormone deprivation and become resistant to antiestrogens.

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

26 , 2-methoxyestradiol, catecholestrogens, the antiestrogen 4-hydroxytamoxifen (OHT), and dietary flavo

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

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

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

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

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

32 Whereas tamoxifen acts as an antiestrogen and ERalpha antagonist in breast cancer but

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

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

35 lation in vivo caused complete resistance to antiestrogen and, partially, anti-VEGF therapies.

36 In 3D monocultures, antiestrogens and antiandrogens induced anoikis by abrog

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

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

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

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

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

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

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

44 the responses of ER+ cancers to estrogen and antiestrogens are poorly understood, particularly in the

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

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

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

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

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

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

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

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

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

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

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

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

57 Antiestrogens can worsen angioedema symptoms.

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

59 Antiestrogen compounds exhibit a variety of different ef

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

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

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

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

64 2 can phosphorylate MTA1s, but not ER, in an antiestrogen-dependent manner and that estrogen stimulat

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

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

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

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

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

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

71 atively high proportion of previous adjuvant antiestrogen exposure.

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

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

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

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

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

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

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

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

80 ndings demonstrate novel effects of the pure antiestrogen fulvestrant in ER(+) breast cancer and eval

81 The pure antiestrogen fulvestrant inhibited the estradiol-stimula

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

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

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

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

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

87 Antiestrogens had failed to fulfill their promise as pos

88 4-hydroxytamoxifen, these concentrations of antiestrogens had no significant effect on the growth of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 Antiestrogens including tamoxifen and fulvestrant have b

112 Antiestrogens induce both cytostasis (cell cycle arrest)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 ndeed, CDK4/6 inhibitors in combination with antiestrogens produce a significant benefit in patients

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Whether antiestrogen resistance can be conferred by a switch fro

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

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

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

151 Furthermore, antiestrogen resistance in cells overexpressing BCAR1/BC

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

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

154 Antiestrogen resistance is a major clinical problem in t

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

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

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

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

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

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

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

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

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

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

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

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

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

168 radiol signaling and may contribute to local antiestrogen resistance.

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

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

171 study the molecular mechanisms that control antiestrogen resistance.

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

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

174 oach to exploring the mechanistic aspects of antiestrogen resistance.

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

176 AR1, ultimately potentiating BCAR1-dependent antiestrogen resistance.

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

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

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

180 Metastatic, antiestrogen resistant estrogen receptor alpha positive

181 nes were constitutively active and partially antiestrogen resistant.

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

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

184 27 gene and created estrogen-independent and antiestrogen-resistant breast cancer cells that still ma

185 sequently different apoptotic effects on the antiestrogen-resistant breast cancer cells.

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

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

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

189 Antiestrogen-resistant breast cancers often show increas

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 Nonsteroidal antiestrogens selectively turn on or turn off estrogen t

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

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

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

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

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

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

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

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

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

219 Moreover, antiestrogens show efficacy as chemopreventive agents in

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

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

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

223 Antiestrogens such as tamoxifen are widely used in the c

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

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

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

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

228 imary xenograft tumors were resistant to the antiestrogen tamoxifen (Tam) as well as to estradiol (E(

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

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

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

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

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

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

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

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

237 Options include the antiestrogen tamoxifen, estrogen deprivation with aromat

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

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

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

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

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

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

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

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

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

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

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

249 Fulvestrant is an antiestrogen that leads to estrogen receptor degradation

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

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

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

253 ently overcome cell cycle arrest mediated by antiestrogen therapeutics.

254 Although antiestrogen therapies targeting estrogen receptor (ER)

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

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

257 profiles and worse outcome in patients given antiestrogen therapies.

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

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

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

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

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

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

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

265 Current antiestrogen therapy for breast cancer is limited by the

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

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

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

269 Antiestrogen therapy induces the unfolded protein respon

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

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

272 Prior neoadjuvant/adjuvant antiestrogen therapy was allowed.

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

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

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

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

277 -positive metastatic breast cancer following antiestrogen therapy.

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

279 following cisplatin, ionizing radiation, and antiestrogen therapy.

280 hormone deprivation and become resistant to antiestrogen therapy.

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

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

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

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

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

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

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

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

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

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

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

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

293 s expression did not uniformly decrease with antiestrogen treatments.

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 By contrast, the test TPE derivatives act as antiestrogens with a free para-hydroxyl on the phenyl ri

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