ライフサイエンスコーパス: tamoxifen

1 therapy, and the duration of treatment with tamoxifen).

2 ely after endocrine therapy is restricted to tamoxifen.

3 otor symptoms, and deep vein thromboses with tamoxifen.

4 e to staurosporine or the anti-estrogen drug tamoxifen.

5 erapy, and adjuvant hormone therapy, usually tamoxifen.

6 te for some women with contraindications for tamoxifen.

7 ith aromatase inhibitors (AIs) compared with tamoxifen.

8 1.24-2.12; P < .001; n = 918) compared with tamoxifen.

9 ss of KLF5 was achieved by administration of tamoxifen.

10 ia progression in the presence of vehicle or tamoxifen.

11 is the selective estrogen receptor modulator tamoxifen.

12 in TamR cells, especially when combined with tamoxifen.

13 ed women and women who were not treated with tamoxifen.

14 omen who used AIs only or sequentially after tamoxifen (1.26 [1.09-1.45]) vs tamoxifen (reference) as

15 ar between anastrozole (1323 women, 91%) and tamoxifen (1379 women, 93%); the side-effect profiles of

16 em to receive anastrozole (1449 analysed) or tamoxifen (1489 analysed).

17 ndomly assigned (1:1) to receive either oral tamoxifen 20 mg per day (with matching placebo in place

18 g once a day) or a sequential scheme of oral tamoxifen (20 mg once a day) followed by exemestane for

19 ion were randomly assigned to receive either tamoxifen (20 mg/day) or anastrazole (1 mg/day) for 5 ye

20 rtant target for the design of drugs such as tamoxifen (2a) and fulvestrant (5).

21 women were adherent for at least 4.5 years (tamoxifen: 65.2% v placebo: 74.0%; P < .001).

22 d concomitantly administered with vehicle or tamoxifen, a selective ER modulator that acts as a ERalp

23 Tamoxifen, a selective estrogen receptor modulator (SERM

24 se models of photoreceptor degeneration that tamoxifen, a selective estrogen receptor modulator and a

25 Tamoxifen, a selective estrogen receptor modulator appro

26 Tamoxifen, a small-molecule antagonist of the transcript

27 n macrophages in vitro, under the control of tamoxifen-activated Cre-ER(T) fusion protein, robustly i

28 he-art methods and a cardiomyocyte-specific, tamoxifen-activated, PKP2 knockout mouse to demonstrate

29 Because tamoxifen acts as an agonist in the postmenopausal endom

30 Upon tamoxifen administration at postnatal day 21, the floxed

31 itional Stat3 knockout allele and found that tamoxifen administration conferred a significant reducti

32 in 75% of mice as early as 2.5 months after tamoxifen administration.

33 cancer and distant recurrence compared with tamoxifen alone among the subset of patients who were at

34 plus OFS were more affected than patients on tamoxifen alone by hot flushes at 6 and 24 months, by lo

35 ian function suppression (OFS) compared with tamoxifen alone for the cohort of premenopausal patients

36 Without prior chemotherapy, patients on tamoxifen alone reported more vaginal discharge over the

37 sk; the benefit of tamoxifen plus OFS versus tamoxifen alone was apparent at the highest composite ri

38 CFI) was 67.1% (95% CI, 54.6% to 76.9%) with tamoxifen alone, 75.9% with tamoxifen plus OFS (95% CI,

39 estane plus OFS versus tamoxifen plus OFS or tamoxifen alone, reaching 10% to 15% at intermediate to

40 thout chemotherapy were randomly assigned to tamoxifen alone, tamoxifen plus ovarian function suppres

41 5-year BCFI with exemestane plus OFS versus tamoxifen alone.

42 ces large improvements in BCFI compared with tamoxifen alone.

43 Tamoxifen also rescued degeneration in a genetic (Pde6b(

44 Tamoxifen, an estrogen receptor (ER) antagonist, is the

45 In this study, we demonstrate that a tamoxifen analog, 6c, which more potently inhibits PKC t

46 These results demonstrate the utility of tamoxifen analogs in reducing AMPH effects on dopamine a

47 ssigned to the two treatment groups (1552 to tamoxifen and 1552 to anastrozole).

48 o determine the association between adjuvant tamoxifen and AI therapy and CBC risk within a general c

49 o determine the association between adjuvant tamoxifen and AI therapy and CBC risk within a general c

50 Given the similar efficacy of tamoxifen and anastrozole for women older than age 60 ye

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

52 fication and prediction of drug responses to tamoxifen and chemotherapy.

53 ression of Ovarian Function Trial (SOFT) and Tamoxifen and Exemestane Trial (TEXT).

54 7S cells were resistant to the anti-estrogen tamoxifen and fulvestrant.

55 Tamoxifen and raloxifene are selective estrogen receptor

56 in Lgr5-positive ISCs upon administration of tamoxifen and SPDEF upon administration of tetracycline.

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

58 , and who filled 2 or more prescriptions for tamoxifen and/or an aromatase inhibitor.

59 changes by treating tumor-bearing mice with tamoxifen and/or linoleic acid.

60 ed ET, which was evenly split between AI and tamoxifen, and no significant differences were observed

61 on of PUER to the nucleus in the presence of tamoxifen, and we speculate that remodeler recruitment m

62 ologic symptoms were significant only in the tamoxifen arm (OR, 0.77; 95% CI, 0.62 to 0.97; P = .024)

63 Adherence to tamoxifen, aromatase inhibitors (AIs), and overall AET (

64 Mammography, chemotherapy, tamoxifen, aromatase inhibitors, and trastuzumab.

65 tective effects warrant the consideration of tamoxifen as a drug suitable for being repurposed to tre

66 Use of tamoxifen as a therapeutic intervention mitigated smoke-

67 onductivity detection of the anticancer drug tamoxifen as well as its metabolites.

68 tween FOXA1 and ERalpha in breast cancer and tamoxifen-associated endometrial cancer.

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

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

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

72 llin-Cre-ER(T2)mice, which were treated with tamoxifen (at days 1, 3, 5, and 7), to deleteLpcat3speci

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

74 absolute difference (between exemestane and tamoxifen) at 10 years of 4.0% (95% CI, 1.2% to 6.7%), a

75 including caffeine, paracetamol, ibuprofen, tamoxifen, BAY 11-7082 and fluorescein, with accuracy on

76 g, 6c, which more potently inhibits PKC than tamoxifen but lacks affinity for the estrogen receptor,

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

78 clinical and preclinical data indicates that tamoxifen can modulate multiple cellular processes indep

79 as generated, in which the administration of tamoxifen causes mutant astrocytes to fail in the assemb

80 zed trials have found that therapy including tamoxifen citrate and aromatase inhibitors (AIs) reduces

81 en were grouped by endocrine therapy status (tamoxifen citrate only, AI only, both, or neither).

82 , 0.50-0.91; P = .01) independent of age and tamoxifen citrate use.

83 the long-term effect of 2 years of adjuvant tamoxifen compared with no systemic treatment (control)

84 y higher in the 3 months after initiation of tamoxifen compared with the risk before therapy (HR, 5.5

85 Using a tamoxifen-dependent conditional Blimp-1 knockout mixed b

86 l complexes along with p38MAPK and Skp2 in a tamoxifen-dependent manner leading to TOT-dependent gene

87 loyed a lineage-tracing strategy that uses a tamoxifen-dependent, promoter-driven cre to mark early c

88 hen Rec8 is activated in arrested oocytes by tamoxifen despite cohesin synthesis.

89 ating the addition of ovarian suppression to tamoxifen did not show an overall clinical benefit for o

90 while controlling for genetic background and tamoxifen effects.

91 From our screening, tamoxifen emerges as a potent inducer of OPC differentia

92 receive 1 mg oral anastrozole or 20 mg oral tamoxifen every day for 5 years.

93 After 5 years of median follow-up, the Tamoxifen Exemestane Adjuvant Multinational (TEAM) trial

94 ss the active form of Kras in chief cells on tamoxifen exposure.

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

96 stane monotherapy and a sequential scheme of tamoxifen followed by exemestane in postmenopausal patie

97 ausal serum estradiol (E2), and had received tamoxifen for >/= 1 year were treated with letrozole (2.

98 aromatase inhibitors are more effective than tamoxifen for preventing recurrence in postmenopausal wo

99 5 years of treatment with anastrozole versus tamoxifen for reducing subsequent occurrence of breast c

100 g per day (with matching placebo in place of tamoxifen) for 5 years.

101 rombosis or embolism--a known side-effect of tamoxifen-for which there were 17 grade 4 or worse event

102 er-free interval events occurred: 122 in the tamoxifen group and 90 in the anastrozole group (HR 0.73

103 The tamoxifen group had higher levels of hot flashes (P = .0

104 .0001) were significantly more severe in the tamoxifen group than in the anastrozole group.

105 there were 17 grade 4 or worse events in the tamoxifen group versus four in the anastrozole group.

106 oup and 603 (26.2%) of 2,305 patients in the tamoxifen group.

107 Tamoxifen has shown great success in the treatment of br

108 fere with stem cell differentiation, whereas tamoxifen has significant effects.

109 ce (67 recurrences for anastrozole vs 77 for tamoxifen; HR 0.89 [95% CI 0.64-1.23]).

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

111 t-4 enhanced tumor growth in the presence of tamoxifen in mice in vivo.

112 ook this trial to compare anastrozole versus tamoxifen in postmenopausal women with ductal carcinoma

113 are the efficacy of anastrozole with that of tamoxifen in postmenopausal women with hormone-receptor-

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

115 trial that investigated the effectiveness of tamoxifen in reducing the risk of breast cancer among wo

116 d when ER signalling was inhibited either by tamoxifen in vitro or letrozole in human subjects.

117 hepatic gene expression changes elicited by tamoxifen in wild-type mice were abrogated in ERalpha-AF

118 demonstrated that simvastatin combined with tamoxifen increased TamR cell apoptosis and inhibited xe

119 -td tomato (Col2-Cre-ERT2) mice treated with tamoxifen indicated that the same Col2 expressing chondr

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

121 However, postnatal tamoxifen induced targeting of nestin(+) cells in nes-cr

122 as well as mice with constitutive (cGOF) or tamoxifen-induced (icGOF) cardiac-specific Kir6.1 GOF su

123 nsity of viable astrocytes even 1 year after tamoxifen-induced Cox10 gene targeting.

124 Deletion of ARL13b in adult mice via tamoxifen-induced Cre/loxP recombination indicated that

125 We also show that tamoxifen-induced cytotoxicity is modulated by isoform-s

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

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

128 rhans cells and macrophages within 3 days of tamoxifen-induced DLX3 ablation.

129 Tamoxifen-induced inactivation of Sox2 demonstrates the

130 with vehicle-treated controls, kidneys with tamoxifen-induced Wnt1 expression from proximal tubules

131 ited the flexibility of our system, enabling tamoxifen inducible conditional gene ablation while cont

132 ess this question, we have generated a novel tamoxifen-inducible cardiomyocyte-specific Runx1-deficie

133 Using a newly engineered tamoxifen-inducible Cbl and Cbl-b deletion model with a

134 Tamoxifen-inducible chondrocyte-targeted glucocorticoid

135 enerated by breeding GR(flox/flox) mice with tamoxifen-inducible collagen 2a1 Cre (Col2a1-CreER(T2))

136 (periostin) gene-targeted mice containing a tamoxifen-inducible Cre for cellular lineage-tracing ana

137 of the trefoil factor 1 (Tff1) gene and the tamoxifen-inducible Cre recombinase (CreERT2)-coding seq

138 We generated mice that express tamoxifen-inducible Cre recombinase under control of the

139 broblasts or myofibroblasts with 2 different tamoxifen-inducible Cre recombinase-expressing gene-targ

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

141 uring DNA replication in fetal oocytes using tamoxifen-inducible Cre.

142 ckout phenotype in vitro and in vivo using a tamoxifen-inducible CRISPR targeting strategy demonstrat

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

144 oped transgenic mouse strains that allow for tamoxifen-inducible deletion of Lrp1 specifically within

145 Using a mouse model with tamoxifen-inducible endothelial cell-restricted disrupti

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

147 Here we developed a tamoxifen-inducible liver cancer mouse model with a defi

148 Here we address this question using a tamoxifen-inducible Lkb1 knockout (KO) mouse model: Rosa

149 ion on a Cbl-b null background, as well as a tamoxifen-inducible mammary stem cell (MaSC)-specific Cb

150 n in a new experimental setting, we used the tamoxifen-inducible mb1-CreER(T2) mouse strain to delete

151 etically engineered mouse model in which the tamoxifen-inducible p53ER(TAM) fusion protein was expres

152 idney tissue from mice with kidney-specific, tamoxifen-inducible Pkd1 deletion demonstrated higher ex

153 poly(I:C)-induced lung inflammation using a tamoxifen-inducible versican-deficient mouse model (Vcan

154 the p.Gly131Glu patients mirrored defects in tamoxifen-inducible VPS33B-deficient Vps33b(fl/fl)-ER(T2

155 We generated mice with tamoxifen-inducible, pancreatic acinar cell-specific Sec

156 ever, HIF1alpha/2alpha dKO produced with the tamoxifen-inducible, satellite cell-specific Pax7(CreER)

157 eficiency in the forebrain at 23 weeks after tamoxifen induction demonstrate profound brain atrophy,

158 ificant concerns about the widespread use of tamoxifen induction of recombination, and highlight the

159 Two to three weeks after tamoxifen induction, Aldh1l1-Cre/ERT2 selectively target

160 ight reduction and died within 6 weeks after tamoxifen induction.

161 tic knockout approaches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of

162 Although tamoxifen inhibits the progression of breast cancer, it

163 acutely deleted in intestinal epithelium via Tamoxifen injection in Tritrichomonas muris (Tm) infecte

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

165 Pax6 deficiency, achieved by tamoxifen injection, caused progressive hyperglycemia.

166 T2) in early cartilage cells with a one-time tamoxifen injection.

167 (placebo IQ-OR, 1.46; 95% CI, 1.13 to 1.87; tamoxifen IQ-OR, 1.25; 95% CI, 0.96 to 1.64; P for heter

168 astrozole are intolerable, then switching to tamoxifen is a good alternative.

169 Tamoxifen is a well-established drug and is thus a promi

170 Tamoxifen is a widely applied therapy in breast cancer t

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

172 Resensitization to tamoxifen is restored only by reducing eIF4E expression

173 tes that selective ERalpha-AF1 activation by tamoxifen is sufficient to elicit metabolic protection,

174 Tamoxifen is the most widely used adjuvant chemotherapeu

175 Although ER blockade with drugs such as tamoxifen is very effective, a major clinical limitation

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

177 herapy arm (n = 318), followed by sequential tamoxifen-letrozole (n = 189), letrozole-tamoxifen (n =

178 Tamoxifen may be suitable for clinical study as a potent

179 Purpose Endoxifen is a tamoxifen metabolite with potent antiestrogenic activity

180 n = 189), letrozole-tamoxifen (n = 176), and tamoxifen monotherapy (n = 106).

181 umors and were randomized to either a 5-year tamoxifen monotherapy arm or a 5-year letrozole monother

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

183 ial tamoxifen-letrozole (n = 189), letrozole-tamoxifen (n = 176), and tamoxifen monotherapy (n = 106)

184 = 564) were randomly assigned to 2 years of tamoxifen (n = 276) or no systemic treatment (n = 288).

185 undred sixteen patients (exemestane, n = 86; tamoxifen, n = 30; median age, 44 years; median E2, 51 p

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

187 e, we describe the ER-independent effects of tamoxifen on tumor metabolism.

188 ) and stroke (adjusted, 0.97 [0.70-1.33]) as tamoxifen-only users (reference).

189 aromatase inhibitors (AIs), and overall AET (tamoxifen or AIs) was assessed using the medication poss

190 suppression may be administered with either tamoxifen or an aromatase inhibitor.

191 ve breast cancer, adjuvant OFS combined with tamoxifen or exemestane produces large improvements in B

192 tamoxifen were randomly assigned to continue tamoxifen or switch to exemestane to complete a total of

193 uppression to standard adjuvant therapy with tamoxifen or with an aromatase inhibitor improved diseas

194 whites when they initiated AET therapy with tamoxifen (OR, 0.54; 95% CI, 0.31 to 0.93) after adjusti

195 m the large publicly available International Tamoxifen Pharmacogenomics Consortium (ITPC) dataset.

196 In addition, Tamoxifen plays an important role in biomedical research

197 % to 76.9%) with tamoxifen alone, 75.9% with tamoxifen plus OFS (95% CI, 64.0% to 84.4%), and 83.2% w

198 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

199 s, the benefit of exemestane plus OFS versus tamoxifen plus OFS in 5-year BCFI ranged from 5% to 15%;

200 5-year BCFI with exemestane plus OFS versus tamoxifen plus OFS or tamoxifen alone, reaching 10% to 1

201 diate to high composite risk; the benefit of tamoxifen plus OFS versus tamoxifen alone was apparent a

202 Patients on tamoxifen plus OFS were more affected than patients on t

203 discharge over the 5 years than patients on tamoxifen plus OFS.

204 randomly assigned to exemestane plus OFS or tamoxifen plus OFS.

205 on trial showed improved disease control for tamoxifen plus ovarian function suppression (OFS) compar

206 y were randomly assigned to tamoxifen alone, tamoxifen plus ovarian function suppression (OFS), or ex

207 ting in significantly lower levels than with tamoxifen plus triptorelin at all time points.

208 In a light-induced degeneration model, tamoxifen prevented onset of photoreceptor apoptosis and

209 .3% (95% CI, 13.4% to 43.1%) including prior tamoxifen progression (n = 3).

210 tially after tamoxifen (1.26 [1.09-1.45]) vs tamoxifen (reference) as well nonhormone users (1.18 [1.

211 We show that the effects of tamoxifen rely on modulation of the estrogen receptors E

212 Acquired tamoxifen resistance (TamR) remains a major challenge in

213 at DSCAM-AS1 mediates tumour progression and tamoxifen resistance and identify hnRNPL as an interacti

214 Oct-4, a phenomenon that appears to underlie tamoxifen resistance in breast cancer cells and in xenog

215 ility, and phosphorylation therefore promote tamoxifen resistance in ER(+) breast cancer through sele

216 ecifically translationally up-regulated with tamoxifen resistance include Runx2, which inhibits ER si

217 iption and translation studies, we show that tamoxifen resistance involves selective mRNA translation

218 However, tamoxifen resistance is responsible for a large proporti

219 The mechanism of acquiring tamoxifen resistance remains elusive, and no effective d

220 SOX9 as an ER-regulated gene associated with tamoxifen resistance was validated in a unique set of cl

221 UPR-regulated genes associated with tamoxifen resistance, including the oncogenic chaperone

222 independent ER activities and contributes to tamoxifen resistance.

223 ated insulin receptor (InsR) is expressed in tamoxifen-resistant (TamR) breast cancer cells.

224 s still lacking effective therapies, such as tamoxifen-resistant breast cancer and melanoma.

225 -76 nM, mimicking E2 in inhibiting growth of tamoxifen-resistant breast cancer cell lines.

226 , also suppressing early-stage metastasis of tamoxifen-resistant breast cancer cells in a zebrafish x

227 ho-mimetic proteins, tamoxifen-sensitive and tamoxifen-resistant breast cancer cells, a tamoxifen-res

228 Through the analysis of the ER cistrome in tamoxifen-resistant breast cancer cells, we have uncover

229 antisense intergenic RNA) is upregulated in tamoxifen-resistant breast cancer tissues compared to th

230 enograft models of endocrine-independent and tamoxifen-resistant breast cancer, and in contrast to E2

231 Tamoxifen-resistant but not tamoxifen-sensitive patient

232 and patient derived xenografts, including a tamoxifen-resistant model and those that harbor ERalpha

233 As everolimus is approved for tamoxifen-resistant or relapsing estrogen receptor-posit

234 d tamoxifen-resistant breast cancer cells, a tamoxifen-resistant patient-derived xenograft model, pat

235 Tamoxifen-resistant translational reprogramming is shown

236 Two years of adjuvant tamoxifen resulted in a long-term survival benefit in pr

237 Overall, OFS added to tamoxifen resulted in worse endocrine symptoms and sexua

238 luminal cell-like state and sensitization to tamoxifen, resulting in abrogation of mammary tumor grow

239 lecule inhibitors, phospho-mimetic proteins, tamoxifen-sensitive and tamoxifen-resistant breast cance

240 ot sensitive to IGF1R inhibition, whereas in tamoxifen-sensitive parental cancer cells, the presence

241 Tamoxifen-resistant but not tamoxifen-sensitive patient ER(+) breast cancer specimen

242 Silencing Runx2 significantly restores tamoxifen sensitivity.

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

244 In ovariectomized wild-type mice, tamoxifen significantly reduced food intake and totally

245 ely, our work presents a novel mechanism for tamoxifen-specific gene activation by ER, secondary to i

246 We reported that although tamoxifen stimulated miR-29b-1/a transcription in tamoxi

247 tomy and radiation enrolled in the Stockholm tamoxifen (STO-3) trial, 1976 to 1990.

248 cancer in the four-arm option to 5 years of tamoxifen (Tam), letrozole (Let), or the agents in seque

249 ibitory responses to an estrogen antagonist, tamoxifen (TAM), via at least in part, epigenetic reacti

250 ifen stimulated miR-29b-1/a transcription in tamoxifen (TAM)-resistant breast cancer cells, ectopic e

251 ere vehicle (Veh, satellite cell-replete) or tamoxifen (Tam, satellite cell-depleted) treated at 4 mo

252 significant at least 5 years after stopping tamoxifen therapy (RR per year of use, 0.85; 95% CI, 0.7

253 ation, with risk progressively decreasing as tamoxifen therapy duration increased.

254 ation, with risk progressively decreasing as tamoxifen therapy duration increased.

255 risk decreased significantly with increasing tamoxifen therapy duration.

256 Tamoxifen therapy for estrogen receptor-positive breast

257 for 5 years as up-front monotherapy or after tamoxifen therapy is the treatment of choice for hormone

258 In addition, AI use without tamoxifen therapy was associated with reduced CBC risk (

259 Conclusions and Relevance: Tamoxifen therapy was associated with reduced CBC risk d

260 Tamoxifen therapy was associated with reduced CBC risk d

261 sults Cholesterol levels were reduced during tamoxifen therapy.

262 rmore, we demonstrate that administration of tamoxifen to demyelinated rats in vivo accelerates remye

263 vant endocrine therapy after 2 to 3 years of tamoxifen to exemestane was associated with clinically r

264 for, but >40% of publications that have used tamoxifen to generate conditional knockouts have not rep

265 ich blocked gastric cell proliferation, plus tamoxifen to induce SPEM.

266 cytochrome P-450 2D6 gene (CYP2D6), oxidizes tamoxifen to its most active metabolites.

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

268 and/or transdifferentiation, we administered tamoxifen to Ren1cCreERxRs-tdTomato-R CoRL reporter mice

269 ations in Kras or Braf The administration of tamoxifen to the resulting adult Tg(Tff1-CreERT2);Kras(L

270 er, long-term treatment can lead to acquired tamoxifen (TOT) resistance and relapse.

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

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

273 breast cancer and endometrial cancer only in tamoxifen-treated breast cancer patients.

274 rgence of endometrial cancer, exclusively in tamoxifen-treated patients.

275 een density reduction and survival, both for tamoxifen-treated women and women who were not treated w

276 YP2D6 genotype and breast cancer survival in tamoxifen-treated women.

277 drug metabolizing enzymes in the efficacy of tamoxifen treatment of breast cancer is subject to subst

278 phic analysis reveals that within 2 weeks of tamoxifen treatment, double-knockout hearts leads to exc

279 ositive primary tumors who received adjuvant tamoxifen treatment, FOXC1 expression is associated with

280 on density reduction was larger than that of tamoxifen treatment.

281 gnaling, either by hormone deprivation or by tamoxifen treatment.

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

283 h respect to hormone replacement therapy and tamoxifen treatment.

284 und and quantify Cre activity upon different tamoxifen treatments in several organs.

285 Adjuvant tamoxifen use and AI therapy were treated as time-depend

286 Exposures: Adjuvant tamoxifen use and AI therapy were treated as time-depend

287 Among those surviving at least 5 years, tamoxifen use for at least 4 years was estimated to prev

288 nt users, the relative risk (RR) per year of tamoxifen use was 0.76 (95% CI, 0.64-0.89), with an esti

289 criptomic data of 47 endometrial tumors from tamoxifen users and 64 endometrial tumors from nonusers.

290 alpha profiles of 10 endometrial tumors from tamoxifen users with those of six endometrial tumors fro

291 and Methods Women were randomly assigned to tamoxifen versus placebo (20 mg/day; n = 4,279).

292 health scores (mean severity score 46.72 for tamoxifen vs 45.85 for anastrozole; p=0.20), mental heal

293 After 2 years of tamoxifen vs no systemic therapy, regardless of hormone

294 y analysis of a randomized clinical trial of tamoxifen vs no systemic therapy, with more than 20-year

295 The selective estrogen receptor modulator tamoxifen was also administered during smoke exposure in

296 estrogen receptor-positive tumors (n = 362), tamoxifen was associated with a marginal reduction in CM

297 (upper 95% CI <1.25), but its superiority to tamoxifen was not (p=0.49).

298 disease free after 2 to 3 years of adjuvant tamoxifen were randomly assigned to continue tamoxifen o

299 Patients assigned to tamoxifen were switched after 2.5-3.0 years to exemestan

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