ライフサイエンスコーパス: tamoxifen

1 cer for three decades until the discovery of tamoxifen.

2 95% CI, 1.11-2.04]) compared with the use of tamoxifen.

3 abolizers after receiving a standard dose of tamoxifen.

4 early-stage breast cancer receiving adjuvant tamoxifen.

5 lated in oligodendroglia upon treatment with tamoxifen.

6 haps reflecting a longer carryover effect of tamoxifen.

7 m mice with acute SPEM, induced by high-dose tamoxifen.

8 nts with early-stage breast cancer receiving tamoxifen.

9 ir favorable clinical benefits compared with tamoxifen.

10 positive, rendering TNBC cells targetable by tamoxifen.

11 P expression was eliminated using ER-cre and tamoxifen.

12 cytes in adult mice following treatment with tamoxifen.

13 cer cell dissemination more effectively than tamoxifen.

14 ed by reduced sensitivity to fulvestrant and tamoxifen.

15 prescription, 55% self-reported adherence to tamoxifen.

16 ed common targets regulated by both PAX2 and tamoxifen.

17 tion of new metastases more effectively than tamoxifen.

18 Is were matched to 3,874 patients continuing tamoxifen.

19 e and cardiovascular mortality compared with tamoxifen.

20 Tamoxifen 20 mg/day for 5 years is still considered stan

21 tane (25 mg/day), raloxifene (60 mg/day), or tamoxifen (20 mg/day).

22 atment with either an aromatase inhibitor or tamoxifen (8139 and 9783, respectively).

23 Because tamoxifen acts as an agonist in the postmenopausal endom

24 Whereas tamoxifen acts as an antiestrogen and ERalpha antagonist

25 Tamoxifen administered for 5 years at 20 mg/d is effecti

26 nown as Lztfl1) expression can be removed by tamoxifen administration, restoring normal gene expressi

27 letion causes estradiol hypersensitivity and tamoxifen agonism, explaining the poor prognosis associa

28 Compared with tamoxifen, AIs were associated with an increased risk of

29 26-mTmG reporter mice, in which low doses of tamoxifen allowed labeling of single-cell pericytes at h

30 The initial endocrine therapy was tamoxifen alone in the majority of the premenopausal wom

31 nefit of escalating endocrine therapy versus tamoxifen alone is minimal for those at low recurrence r

32 ppression (OFS) or tamoxifen plus OFS versus tamoxifen alone.

33 estane plus OFS versus tamoxifen plus OFS or tamoxifen alone.

34 The 6-month discontinuation rates of tamoxifen among poor, intermediate, normal, and ultrarap

35 There were 12 serious adverse events with tamoxifen and 16 with placebo, including one deep vein t

36 years), there were 14 neoplastic events with tamoxifen and 28 with placebo (11.6 v 23.9 per 1,000 per

37 cts of T were inhibited by the ER antagonist tamoxifen and aromatase inhibitor anastrazole and were i

38 r, rendering ERalpha modulator drugs such as tamoxifen and aromatase inhibitors ineffective.

39 ian cancer cell cultures in aqueous media by tamoxifen and BAY 11-7082 films shows similar behavior t

40 tid artery injury, we demonstrated that both tamoxifen and estradiol accelerated endothelial healing,

41 The Tamoxifen and Exemestane Trial (TEXT)/Suppression of Ova

42 s the activity of the endocrine therapeutics tamoxifen and fulvestrant by lowering circulating IGF1,

43 Both tamoxifen and fulvestrant increased MFE and aldehyde deh

44 Mechanistically, we establish that both tamoxifen and fulvestrant induce STAT3 phosphorylation.

45 by estradiol, an effect that was blocked by tamoxifen and not observed in ERalpha-negative cells.

46 osis and one stage I endometrial cancer with tamoxifen and one pulmonary embolism with placebo.

47 34 patients received vorinostat, tamoxifen and pembrolizumab with no excessive toxicity a

48 The USPSTF found convincing evidence that tamoxifen and raloxifene and adequate evidence that arom

49 Tamoxifen and raloxifene were associated with increased

50 improvement with exemestane plus OFS versus tamoxifen and reached 10% across composite risks; for ta

51 The development of tamoxifen and subsequent estrogen receptor alpha (ERalph

52 in complex with the anti-breast cancer drug tamoxifen and the other in complex with the cholesterol

53 ing therapies, including the partial agonist tamoxifen and the pure antagonist fulvestrant, affect th

54 to the selective estrogen receptor modulator tamoxifen and to aromatase inhibitors that lower circula

55 nts with breast cancer who were treated with tamoxifen and were diagnosed from 2005 to 2012; they wer

56 ntly involved in drug metabolism of codeine, tamoxifen, and citalopram.

57 wth in the presence of estrogen deprivation, tamoxifen, and fulvestrant.

58 as demonstrated by oxygenating benzydamine, tamoxifen, and thioanisole, drug-related compounds known

59 se lines using a sensitive Ai14 reporter and tamoxifen application either by a systemic injection, or

60 tions of endoxifen, the active metabolite of tamoxifen, are a better predictor of tamoxifen efficacy

61 resistant to the estrogen receptor modulator tamoxifen as a result of increased autophagy and decreas

62 Data on low-dose tamoxifen as an alternative to the standard dose for bot

63 Patients who were not treated, who received tamoxifen as endocrine therapy, or who were treated with

64 y identify patients who do not take adjuvant tamoxifen as prescribed and are at risk for poorer outco

65 oxazone, and acetaminophen) and the prodrug (tamoxifen) as P450 substrates, reveal that P450 ERAD dis

66 in the breast, we compared ERalpha sites in tamoxifen-associated endometrial cancers with publicly a

67 The ERalpha-binding sites in tamoxifen-associated endometrial tumors differed from th

68 Tamoxifen at 5 mg/d for 3 years can halve the recurrence

69 can-expressing chondrocytes by administering tamoxifen at 8-weeks of age.

70 Plp-CreER (T2) :Rosa26 (tdTomato) mice with tamoxifen at P2 and P3.

71 absolute difference (between exemestane and tamoxifen) at 10 years in the population that was estrog

72 om tamoxifen to AIs with patients continuing tamoxifen between 1998 and 2016.

73 ormonal therapy with aromatase inhibitors or tamoxifen between April 1, 1998, and February 29, 2016.

74 After withdrawal of tamoxifen, BrdU-positive ZCs reappeared.

75 ositive patients are frequently treated with tamoxifen, but resistance is common.

76 an aromatase inhibitor after 2 to 3 years of tamoxifen can lead to sustained benefits in terms of red

77 CreER(T2/+); IKKalpha(f/f) mice treated with tamoxifen (cKO).

78 Mechanistically, PAX2 and tamoxifen coexert an antitumoral effect by maintaining h

79 Tamoxifen decreased contralateral breast events by 75% (

80 Tamoxifen decreased IL-5 and IL-13 production and BAL eo

81 We report that tamoxifen decreases the levels of hypoxia-inducible fact

82 fluorescent protein using mice expressing a tamoxifen-dependent Cre recombinase under the control of

83 ether metabolizer status was associated with tamoxifen discontinuation and prognosis for breast cance

84 lapse-free survival (censored at the time of tamoxifen discontinuation; RFSt) by Cox regression analy

85 ed association might call for individualized tamoxifen dosage.

86 Novel melatonin-tamoxifen drug conjugates may be promising to treat BC a

87 These melatonin-tamoxifen drug conjugates show promise as novel anticanc

88 nation of either CDK2 or EZH2 inhibitor with tamoxifen effectively suppresses tumor growth and marked

89 lite of tamoxifen, are a better predictor of tamoxifen efficacy than CYP2D6 genotypes.

90 ed trial comparing adjuvant letrozole versus tamoxifen (either treatment received for 5 years) and th

91 Chronic treatment with 17beta-estradiol and tamoxifen elicited differential gene expression profiles

92 ts ER(+) breast cancer more effectively than tamoxifen even in the presence of estradiol, mainly by a

93 TG (Rox-Lox-tdTomato-eGFP) mice treated with Tamoxifen expressed tdTomato+ in cardiomyocytes with rar

94 of treatment with an aromatase inhibitor or tamoxifen followed by an aromatase inhibitor, were rando

95 emestane alone and sequential treatment with tamoxifen followed by exemestane are reasonable options

96 usal patients were enrolled and had received tamoxifen for a median time of 0.37 years (range, 0.23 t

97 adjuvant endocrine therapy should be offered tamoxifen for an initial duration of five years; those w

98 Efficacy of letrozole versus tamoxifen for contralateral breast cancer varied signifi

99 rs of aromatase inhibitors with new users of tamoxifen for each of the study outcomes (myocardial inf

100 as-in contrast to ER mutations-resistance to tamoxifen, fulvestrant and the CDK4 and CDK6 inhibitor p

101 Compared with tamoxifen, fulvestrant significantly affected inflammato

102 Tamoxifen has been used for many years to target estroge

103 h poor and ultrarapid CYP2D6 metabolizers of tamoxifen have a worse prognosis for breast cancer compa

104 Moreover, PAX2 and tamoxifen have an additive effect and both induce coding

105 Men who have completed five years of tamoxifen, have tolerated therapy, and still have a high

106 breast cancers are successfully treated with tamoxifen; however, a significant number of patients dev

107 Serum assessment of tamoxifen identified 16.0% of patients (n = 188) below t

108 breast cancer was higher for raloxifene than tamoxifen in 1 trial after long-term follow-up (RR, 1.24

109 content during development of resistance to tamoxifen in breast cancer is driven by multiple signals

110 ole of CYP2C19 polymorphisms and response to tamoxifen in breast cancer patients and, consequently, C

111 d with anti-estrogen therapies, particularly tamoxifen in premenopausal women.

112 ses ER(+) breast cancer growth compared with tamoxifen in the presence of physiologic levels of estra

113 Treatment with tamoxifen increases liver cytotoxic T cell accumulation

114 However, tamoxifen-independent Cre recombination precluded determ

115 ors that arise in the presence or absence of tamoxifen, indicating divergent enhancer activity for tu

116 Here we show that mice with tamoxifen-induced adult-onset ablation of P/Q channel al

117 Here, we report that tamoxifen-induced conditional deletion of TSPO in reside

118 fl); Hcn4(CreERt2)) developed AV block while tamoxifen-induced conduction system deletion of Tjp1 dis

119 Mice with tamoxifen-induced conduction system-specific deletion of

120 Furthermore, tamoxifen-induced deletion of EGFR from epithelial cells

121 Tamoxifen-induced deletion of Fbxo7, after myelination u

122 Here we show that tamoxifen-induced deletion of Slc8b1 in adult mouse hear

123 fasting and a fasting-mimicking diet prevent tamoxifen-induced endometrial hyperplasia.

124 ction of beta1 integrin-blocking antibody or tamoxifen-induced endothelial cell-specific deletion of

125 Upon tamoxifen-induced expression of CNG channels, rods recov

126 ck-in mouse strain was generated that allows tamoxifen-induced expression of the homologous Card14(E1

127 Constitutive or tamoxifen-induced inhibition of NF-kappaB in SSCs rescue

128 Tamoxifen-induced loss of ZO-1 led to atrioventricular (

129 Despite global Lamc1 gene deletion in tamoxifen-induced mutant mice, there was minimal change

130 zed for H pylori colonization in vivo during tamoxifen-induced SPEM or after decrease of stomach acid

131 cal action potential (AP) mapping ex vivo in tamoxifen-induced STIM1(flox/flox)-Cre(tg)(/-) (STIM1-KD

132 Tamoxifen induces autophagy-dependent NET formation in C

133 Here, we have employed a tamoxifen inducible BACE1 conditional Knock-out (cKO) mo

134 orated with CAG-CRE plasmids or crossed with tamoxifen inducible CAG-CRE-ER(T2) or nestin-CRE-ER(T2)

135 Using the tamoxifen inducible Hnf1b:CreER(T2) (H) transgenic mouse

136 itutively-activated Acvr1 (caAcvr1) carrying tamoxifen-inducible Cre driven by a ubiquitin promotor a

137 advantage of the progeny of mice expressing tamoxifen-inducible Cre recombinase (Cre-ERT2) under the

138 We generated mice with tamoxifen-inducible Cre recombinase (CreERT2) in the Anx

139 ty in vivo, the SPP gene was deleted using a tamoxifen-inducible Cre recombinase driven by the ubiqui

140 Cell type-specific tamoxifen-inducible Cre recombinase transgenes were used

141 The tamoxifen-inducible Cre system is a popular transgenic m

142 Finally, the Hexb locus was employed for tamoxifen-inducible Cre-mediated gene manipulation in mi

143 We generated Epm2a-deficient LD mice with tamoxifen-inducible Cre-mediated Gys1 knockout.

144 IV-derived Bdnf transcripts ("p4-cells") for tamoxifen-inducible Cre-mediated recombination (AAV8-p4B

145 s and at different stages of degeneration by tamoxifen-inducible cre-mediated recombination.

146 scleraxis (Scx)-expressing tenocytes using a tamoxifen-inducible Cre-recombinase system and caused te

147 e have generated transgenic mouse models for tamoxifen-inducible de novo expression of Ags in LCs but

148 We found that tamoxifen-inducible deletion of the mammalian iron expor

149 First, we utilized a tamoxifen-inducible EC-specific YY1 deficient mouse mode

150 eries and lung vascular endothelial cells of tamoxifen-inducible endothelial cell-specific NRP1 knock

151 We used a tamoxifen-inducible EphA4 conditional KO mouse to achiev

152 Tamoxifen-inducible Foxm1 deletion suppressed the capaci

153 Tamoxifen-inducible genetic lineage tracing of mature ad

154 disruption of Mcl1 (Mcl1(DeltaIEC) mice) or tamoxifen-inducible IEC-specific disruption of Mcl1 (i-M

155 n and HD progression, we crossed conditional tamoxifen-inducible IKKbeta knockout mice with R6/1 HD m

156 This hypothesis was tested by generating tamoxifen-inducible knockout mouse models of Cyp26b1 alo

157 deletion of DLX3 in adult epidermis using a tamoxifen-inducible Krt14-cre/ERT system.

158 technology and generated a cardiac-specific, tamoxifen-inducible MCUB mutant mouse (CAG-CAT-MCUB x MC

159 Utilizing a cardiomyocyte-specific and tamoxifen-inducible MerCreMer recombinase (MCM), 3 mouse

160 by cardiac-specific deletion of ACC2 using a tamoxifen-inducible model (ACC2 iKO).

161 Plp1-Cre Trpa1fl/fl mice with a tamoxifen-inducible specific deletion of TRPA1 in Schwan

162 Here, we generated mice with tamoxifen-inducible Thy1-Cre mediated ERalpha inactivati

163 Here, we generated mice with tamoxifen-inducible, epidermis-specific alpha3 knockout

164 Mice with a tamoxifen-inducible, hepatocyte-specific Atg5 knockout w

165 d murine SMCs in vitro and in iSM-Gprc5b-KO (tamoxifen-inducible, SMC-specific knockout) mice under c

166 Here, we describe a tamoxifen-inducible, time-course ChIP-seq approach to me

167 from Nestin-positive progenitors labeled by tamoxifen induction at embryonic day 10.5.

168 enrolled up to a maximum of 12 months after tamoxifen initiation.

169 inal ganglia (TG) and by 99% in the liver of tamoxifen-injected mice, while SPP protein expression wa

170 acts of different doses of a single systemic tamoxifen injection on the testis and the wider endocrin

171 d mice using standard Cre-Lox technology and tamoxifen injections.

172 Here, we tested whether tamoxifen is able to accelerate endothelial healing and

173 Tamoxifen is also an agonist of the G protein-coupled es

174 Tamoxifen is an antagonist of estrogen receptor (ERalpha

175 ha in endothelial cells, while the effect of tamoxifen is mediated by the nuclear actions of ERalpha

176 However, tamoxifen is not an inert inducer of recombination, but

177 Resensitization to tamoxifen is restored only by reducing eIF4E expression

178 Tamoxifen is the most prescribed selective estrogen rece

179 Tamoxifen is used to prevent and treat estrogen receptor

180 Tamoxifen is widely prescribed as adjuvant therapy in pa

181 we found that focal eye drop application of tamoxifen led to an exclusive Cre-activation in pericyte

182 We found that a single dose of tamoxifen less than 10% of the mean dose used for recomb

183 five years; those with a contraindication to tamoxifen may be offered a gonadotropin-releasing hormon

184 Breast cancer patients treated with tamoxifen may experience recurrence due to endocrine res

185 hen mice were given BrdU at the same time as tamoxifen, more than 90% of cells were labeled in all ga

186 nhibitor (n = 36), fulvestrant (n = 21), and tamoxifen (n = 15).

187 were less likely to be adherent in both the tamoxifen (odds ratio [OR], 0.57; 95% CI, 0.37 to 0.86;

188 eased the response of breast cancer cells to tamoxifen on soft substrata.

189 cision revealed acute deleterious effects of tamoxifen on striated muscles, including a transient dow

190 ATAC sample collection that consisted of the tamoxifen or anastrozole arms of the ATAC trial.

191 al BrdU-positive population, acute injury by tamoxifen or chronic injury by H pylori infection result

192 eveloped resistance to aromatase inhibitors, tamoxifen or fulvestrant.

193 n select experiments, mice were administered tamoxifen or vehicle pellets for 21 days prior to challe

194 ere supplemented with 17beta-estradiol (E2), tamoxifen, or left untreated.

195 We studied mice in homeostasis or with tamoxifen- or H pylori-induced SPEM.

196 rease in frequency of daily hot flashes with tamoxifen (P = .02).

197 BCFI was 79.2% (95% CI, 66.2% to 87.7%) with tamoxifen plus OFS and 81.6% (95% CI, 69.8% to 89.2%) wi

198 improvement with exemestane plus OFS versus tamoxifen plus OFS of 5.1%, and STEPP analysis showed im

199 t recurrence with exemestane plus OFS versus tamoxifen plus OFS or tamoxifen alone.

200 e plus ovarian function suppression (OFS) or tamoxifen plus OFS versus tamoxifen alone.

201 and reached 10% across composite risks; for tamoxifen plus OFS versus tamoxifen, the maximum improve

202 Of 188 patients who did not adhere to the tamoxifen prescription, 55% self-reported adherence to t

203 Tamoxifen prevents the recurrence of breast cancer and i

204 ll survival among women who had not received tamoxifen previously was longer with the combination the

205 0.58 to 0.92); among women who had received tamoxifen previously, overall survival was similar in th

206 s including AY9944 and the chemotherapy drug tamoxifen promoted clearance of Zika virus and multiple

207 Here we report that tamoxifen promotes mechanical quiescence in hepatic stel

208 The USPSTF found that the benefits of taking tamoxifen, raloxifene, and aromatase inhibitors to reduc

209 Tamoxifen, raloxifene, and aromatase inhibitors were ass

210 ing evidence that risk-reducing medications (tamoxifen, raloxifene, or aromatase inhibitors) provide

211 ne use of risk-reducing medications, such as tamoxifen, raloxifene, or aromatase inhibitors, in women

212 prescribe risk-reducing medications, such as tamoxifen, raloxifene, or aromatase inhibitors, to women

213 In 8 RCTs (n = 54 651), tamoxifen (relative risk [RR], 0.69 [95% CI, 0.59-0.84];

214 cardiotoxicity as sequential treatments with tamoxifen remains unknown.

215 ol accelerated endothelial healing, but only tamoxifen required the presence of the underlying medial

216 Tamoxifen requires the transcription factor paired box 2

217 th deficient ERalpha expression that confers tamoxifen resistance in vivo.

218 However, tamoxifen resistance is responsible for a large proporti

219 breast cancer cell growth and contributes to tamoxifen resistance of these cells.

220 highlights an important mechanism conferring tamoxifen resistance via both ERalpha dependent and inde

221 Furthermore, tamoxifen resistance was conferred by phosphorylation in

222 was the high levels of FOXM1 that conferred Tamoxifen resistance.

223 can increase uterine cancer risk and induce tamoxifen resistance.

224 and FOXM1, and significantly associated with tamoxifen resistance.

225 anslation regulated by eIF4E, contributes to tamoxifen resistance.

226 We show that in vitro development of tamoxifen-resistance is associated with increased sensit

227 In summary, we show that tamoxifen-resistance is associated with sensitivity to O

228 f ERBB-signaling, which is a known driver of tamoxifen-resistance.

229 e survival of tamoxifen-sensitive (TamS) and tamoxifen-resistant (TamR) breast cancer cells.

230 mic compartments showed higher alteration in tamoxifen-resistant breast cancer cells.

231 utic proof of principle for FEN1 blockade in tamoxifen-resistant breast cancer.

232 RISPR/Cas knockout of Sox9 reduces growth of tamoxifen-resistant breast tumours in vivo.

233 lpha function and inhibited proliferation of tamoxifen-resistant cell lines as well as ex vivo-cultur

234 er, a significant number of patients develop tamoxifen-resistant disease.

235 port that HNRNPA2/B1 expression is higher in tamoxifen-resistant LCC9 breast cancer cells as compared

236 e further assessed for their actions against tamoxifen-resistant MCF-7 cells and a patient-derived xe

237 C4 and C5 inhibited tamoxifen-resistant MCF-7 cells with equal potency (IC(5

238 linked) for their effects on BC cell (MCF-7, tamoxifen-resistant MCF-7, mouse mammary carcinoma, MDA-

239 alpha function and inhibits proliferation of tamoxifen-resistant tumor cells.

240 PS) and adenosine triphosphate (ATP), or 4OH-tamoxifen, respectively.

241 In placebo-controlled trials, tamoxifen (risk ratio [RR], 0.69 [95% CI, 0.59-0.84]; 4

242 ansferase (OGT) activity for the survival of tamoxifen-sensitive (TamS) and tamoxifen-resistant (TamR

243 breast cancer cells as compared to parental, tamoxifen-sensitive MCF-7 cells.

244 itivity, single-channel open probability and tamoxifen sensitivity.

245 fter a median follow-up of 24.2 months since tamoxifen serum assessment, patients who were biochemica

246 n of biochemical nonadherence was based on a tamoxifen serum level < 60 ng/mL, assessed 1 year after

247 However, the mCol1a1 environment enabled tamoxifen-stimulated growth of pulmonary metastases and

248 transcription and this effect is enhanced by tamoxifen, suggesting that they converge on repression o

249 K68Q) expressing cells exhibit resistance to tamoxifen (Tam) and cells selected for Tam resistance ex

250 ft tumors were resistant to the antiestrogen tamoxifen (Tam) as well as to estradiol (E(2)) withdrawa

251 Tamoxifen (TAM) inducible Cre recombinase system is an e

252 Long-term estrogen deprivation (LTED) with tamoxifen (TAM) or aromatase inhibitors leads to endocri

253 used Rosa(creERT2) IL-4Ralpha(-/lox) mice, a tamoxifen (TAM)-inducible IL-4Ralpha knockdown model to

254 mposite risks; for tamoxifen plus OFS versus tamoxifen, the maximum improvement was approximately 3.5

255 In breast cancer, nonadherence to tamoxifen therapy after surgery constitutes a major obst

256 Self-reported nonadherence to tamoxifen therapy was collected at the same time through

257 Using a ubiquitous tamoxifen (TMX)-inducible Cre ( UBC-Cre/ER(T2)) line cro

258 nction and fibrosis was studied in mice with tamoxifen (Tmx)-inducible deletion of ER chaperone Grp78

259 Following administration of tamoxifen to 8-12-wk-old mice, an upregulation of Sftpc(

260 We then pretreated alphaDKRC::RLTG mice with Tamoxifen to activate the reporter before sham or reperf

261 tch, in a 1:2 ratio, patients switching from tamoxifen to AIs with patients continuing tamoxifen betw

262 y tumor, it fostered the agonist activity of tamoxifen to increase proliferation and AP-1 activity.

263 Mice were given tamoxifen to induce Cre recombinase.

264 iven intraperitoneal injections of high-dose tamoxifen to induce SPEM or gavaged with H pylori (PMSS1

265 ted in developed tumors by administration of tamoxifen to mice.

266 hinery, this study highlights repurposing of tamoxifen to potentiate host defense in CGD patients.

267 in the absence of ligand or presence of 4OH-tamoxifen (TOT).

268 Potent drugs for breast cancer treatment are Tamoxifen, Trastuzumab, Paclitaxel, etc.

269 X2 contributes to better clinical outcome in tamoxifen treated ER-positive breast cancer patients by

270 Tamoxifen- treated patients with recurrence or non-recur

271 There were no deaths in the ultralow-risk tamoxifen-treated arm at 15 years, and these patients ha

272 a1 (Aldh1a1) mRNA in the liver compared with tamoxifen-treated controls.

273 everity of demyelination was similar between tamoxifen-treated mice and vehicle-treated controls.

274 FEN1 levels were predictive of outcome in tamoxifen-treated patients, and FEN1 played a causal rol

275 n of FEN1, which is predictive of outcome in tamoxifen-treated patients, effectively blocks ERalpha f

276 umably originate, and (b) temporally through tamoxifen treatment after birth.

277 Delayed tamoxifen treatment demonstrated ongoing CNS recruitment

278 Following tamoxifen treatment, Dicer mRNA expression was significa

279 ssary and sufficient to confer resistance to tamoxifen treatment, identifying SLC7A5 as a potential t

280 educed in tumors of patients with relapse to tamoxifen treatment.

281 moderate levels of PAX2 in combination with tamoxifen treatment.

282 uld not be included in clinical decisions on tamoxifen treatment.

283 ive breast cancer patients and resistance to tamoxifen treatment.

284 PAX2-tamoxifen upregulated genes are also enriched with PAX2

285 C and may help offset the adverse effects of tamoxifen usage alone due to the presence of melatonin.

286 tified by pathological node status, previous tamoxifen use, and lowest bone mineral density T score i

287 ization was stratified according to adjuvant tamoxifen use.

288 rate of biochemical nonadherence to adjuvant tamoxifen using serum assessment and to examine its effe

289 Tamoxifen was administered at 4 months and disease progr

290 Tamoxifen was associated with higher risk of endometrial

291 % CI, 0.53-0.73]; 2 trials [n = 16 929]) and tamoxifen was associated with lower risk for nonvertebra

292 thromboembolic events compared with placebo; tamoxifen was associated with more events than raloxifen

293 Finally, tamoxifen was more effective than anastrazole at reducin

294 e monotherapy comparison of letrozole versus tamoxifen, we found a 9% relative reduction in the hazar

295 nts with breast cancer treated with adjuvant tamoxifen were included.

296 , octreotide, thalidomide, lenalidomide, and tamoxifen) were described in a few case reports and seri

297 nhibited by the estrogen-receptor modulator, tamoxifen, which activates a G-protein-coupled receptor

298 y exogenous treatment with autophagy inducer tamoxifen, which rescued the NET formation defect in Min

299 Tamoxifen, with half a century of safe clinical use, mig

300 After 3 months' recovery (no tamoxifen), ZCs became the predominant BrdU-labeled popu