ライフサイエンスコーパス: endocrine therapy

1 r target the ER directly (overall labeled as endocrine therapy).

2 rs; 10% stage III, 40% had received adjuvant endocrine therapy).

3 t cancer and the mechanisms of resistance to endocrine therapy.

4 apy) and had completed 4-6 years of adjuvant endocrine therapy.

5 uently in breast cancer that is resistant to endocrine therapy.

6 ve breast cancers undergoing radiotherapy or endocrine therapy.

7 erapy, postmastectomy radiation therapy, and endocrine therapy.

8 can occur despite appropriate treatment with endocrine therapy.

9 e pharmacodynamics of combination HDACIs and endocrine therapy.

10 receptor-positive breast cancer who received endocrine therapy.

11 breast cancers and is the primary target of endocrine therapy.

12 ) remains a major challenge in breast cancer endocrine therapy.

13 therapy, postsurgical radiation therapy, and endocrine therapy.

14 e to complete a total of 5 years of adjuvant endocrine therapy.

15 conferring poor prognosis and resistance to endocrine therapy.

16 rapy should receive ovarian suppression with endocrine therapy.

17 predictive and early-response biomarkers for endocrine therapy.

18 cer or in patients with tumors refractory to endocrine therapy.

19 es with worse clinical outcome regardless of endocrine therapy.

20 uality of life, and monitor for adherence to endocrine therapy.

21 ients with progression after receiving prior endocrine therapy.

22 reast cancer that has progressed on previous endocrine therapy.

23 efine a subset of patients who received only endocrine therapy.

24 ive breast cancer is frequently sensitive to endocrine therapy.

25 ssessing in vivo pharmacodynamic response to endocrine therapy.

26 n demonstrated alone and in combination with endocrine therapy.

27 ausal patients who had not received previous endocrine therapy.

28 y benefit from lapatinib in combination with endocrine therapy.

29 may also be offered ovarian suppression with endocrine therapy.

30 tive breast cancer patients as responders to endocrine therapy.

31 -free survival time in patients treated with endocrine therapy.

32 els were suppressed in patients treated with endocrine therapy.

33 atively poor outcome in patients who undergo endocrine therapy.

34 used to predict prognosis and sensitivity to endocrine therapy.

35 luable to select ovarian cancer patients for endocrine therapy.

36 stemic treatment for advanced disease except endocrine therapy.

37 chemotherapy, it appears to respond well to endocrine therapy.

38 ffect residual risk following treatment with endocrine therapy.

39 st cancer patients resistant to conventional endocrine therapy.

40 er cell lines and xenografts, alone and with endocrine therapy.

41 and ER ChIP-Seq, and to examine response to endocrine therapy.

42 atic ER-positive breast cancer refractory to endocrine therapy.

43 ients with breast cancer who did not receive endocrine therapy.

44 matase inhibitor for 10 years total adjuvant endocrine therapy.

45 could be a predictive marker of response to endocrine therapy.

46 ignaling, cell proliferation and response to endocrine therapy.

47 n the 40% patient subset with prior adjuvant endocrine therapy.

48 chromatin openness, underlies resistance to endocrine therapy.

49 in patients with breast cancer treated with endocrine therapy.

50 for patients with breast cancer treated with endocrine therapy.

51 ancers are tolerant or acquire resistance to endocrine therapy.

52 o exemestane to complete 5 years of adjuvant endocrine therapy.

53 val by a number of months when combined with endocrine therapy.

54 of distant recurrence for patients receiving endocrine therapy.

55 stem/pluripotent genes, which was lost with endocrine therapy.

56 breast cancer that progressed after previous endocrine therapy.

57 athway is a known mechanism of resistance to endocrine therapy.

58 tatic breast cancer (BC) in combination with endocrine therapy.

59 tients without previous exposure to adjuvant endocrine therapy.

60 alpha gene expression is a critical topic of endocrine therapy.

61 plasticity under the control of hormones and endocrine therapy.

62 re found in >20% of tumours that progress on endocrine therapies.

63 get ERalpha (ESR1) raised hopes for improved endocrine therapies.

64 risk was lowest on average-did well with all endocrine therapies.

65 prognosis and is necessary for a response to endocrine therapies.

66 , have been linked to acquired resistance to endocrine therapies.

67 ived xenograft samples that are resistant to endocrine therapies.

68 iated with a decreased response of tumors to endocrine therapies.

69 14-3-3zeta and enhance the effectiveness of endocrine therapies.

70 e with metastatic disease following adjuvant endocrine therapies.

71 r another, six (1%) considered not receiving endocrine therapy, 19 (3%) decided not to receive endocr

72 noma, had completed treatment (not including endocrine therapy) 2 months to 5 years previously, were

73 int was delayed local efficacy at the end of endocrine therapy (5 years) on the basis of DCE MR imagi

74 on-resistant PCa (CRPC) with next-generation endocrine therapies abiraterone and enzalutamide.

75 HC-defined luminal A tumors independently of endocrine therapy administration.

76 s studies suggest that adherence to adjuvant endocrine therapy (AET) for patients with breast cancer

77 monstrated the clinical benefits of adjuvant endocrine therapy (AET) in preventing recurrence and dea

78 sly demonstrated that a switch from adjuvant endocrine therapy after 2 to 3 years of tamoxifen to exe

79 suitable for the addition of palbociclib to endocrine therapy after tumour recurrence is crucial for

80 n intermediate recurrence score who received endocrine therapy alone (12.3+/-2.4%) and among those wi

81 gned to chemoendocrine therapy (CT+E) versus endocrine therapy alone (E), allowing us to quantify the

82 Clinicians may offer endocrine therapy alone for these patients.

83 Clinicians may recommend endocrine therapy alone for women older than age 50 year

84 and node-negative breast cancer who received endocrine therapy alone in the B-14 (n = 577) and TAILOR

85 eeded to identify patient subgroups for whom endocrine therapy alone might be appropriate for first-l

86 tment (TAILORx) evaluating noninferiority of endocrine therapy alone versus chemoendocrine therapy fo

87 n identify which patients would do well with endocrine therapy alone versus those who require adjuvan

88 free survival in patients with RS </= 11 and endocrine therapy alone was 98% versus 92% and 98% in RS

89 50 years of age or younger who had received endocrine therapy alone, the estimated (+/-SE) rate of d

90 ocrine therapy plus HER2-targeted therapy or endocrine therapy alone.

91 ed at least one dose of CDKI or placebo with endocrine therapy (an aromatase inhibitor [letrozole or

92 hormone receptors renders TNBC resistant to endocrine therapies and lends to its critical absence of

93 s associated with resistance to AR-targeting endocrine therapies and poor outcomes.

94 s in delineating mechanisms of resistance to endocrine therapies and potential strategies to overcome

95 the potential negative interactions between endocrine therapy and chemotherapy.

96 s as novel biomarkers of patient response to endocrine therapy and corroborates the importance of tra

97 These findings suggest that a combination of endocrine therapy and DAXX-stabilizing agents may inhibi

98 stemness, suggesting that the combination of endocrine therapy and DAXX-stabilizing agents may inhibi

99 ain viability and were sensitive to combined endocrine therapy and FGFR1 inhibition.

100 aware of the benefits and risks of adjuvant endocrine therapy and has been referred to discuss the r

101 in clinical specimens following neoadjuvant endocrine therapy and in HT refractory metastatic diseas

102 However, the development of resistance to endocrine therapy and metastatic progression are leading

103 breast cancer, who had relapsed on or after endocrine therapy and mTOR inhibitors, were recruited fr

104 anced breast cancer who were pretreated with endocrine therapy and mTOR inhibitors.

105 lationships between initiation of CLM during endocrine therapy and outcome.

106 receptor-positive (ER positive) BC receiving endocrine therapy and possessing PIK3CA mutations.

107 ay serve as a novel predictor of response to endocrine therapy and potential therapeutic target.

108 nografts from primary ER(+) breast tumors to endocrine therapy and reduces tamoxifen-induced endometr

109 pecific adverse events (AEs) associated with endocrine therapy and related to depletion or blocking o

110 e associated with irreversible-resistance to endocrine therapy and subsequent secondary resistance to

111 as bone marrow that remain quiescent during endocrine therapy and subsequently proliferate to produc

112 Predicting response to endocrine therapy and survival in oestrogen receptor pos

113 After long-standing use of endocrine therapy and targeted biological therapy, impro

114 TAT3 signaling in CSC-mediated resistance to endocrine therapy and the potential of SFX-01 for improv

115 rine therapy, 19 (3%) decided not to receive endocrine therapy, and 71 (11%) considered receiving end

116 ith hormone receptor-positive tumors receive endocrine therapy, and a minority receive chemotherapy a

117 r predicting which patients may benefit from endocrine therapy, and no other assays are recommended f

118 events that are otherwise suppressed during endocrine therapy, and provides pre-clinical rationale f

119 ive breast cancers following radiotherapy or endocrine therapy, and this drives tumorigenesis and the

120 ation factors were age at diagnosis, planned endocrine therapy, and treating centre.

121 ade, number of excisions, radiotherapy (RT), endocrine therapy, and year of surgery, margin width was

122 dy Group, was stratified by type of previous endocrine therapy (aromatase inhibitors only vs selectiv

123 se 4/6 inhibitors (CDKIs) are indicated with endocrine therapy as first-line or second-line treatment

124 nced or metastatic disease should be offered endocrine therapy as first-line therapy, except in cases

125 e findings support future trials of extended endocrine therapy as primary nonoperative treatment of s

126 his guideline puts forth recommendations for endocrine therapy as treatment for women with HR-positiv

127 se; the 2 vs 4 arm randomization option; and endocrine therapy assignment with and without adjustment

128 to identify responders and nonresponders to endocrine therapy at an early stage.

129 Endocrine therapy-based neoadjuvant treatment for lumina

130 acknowledges that there are limited data on endocrine therapy benefit for cancers with 1% to 10% of

131 zing ER-targeted drug dosage, and predicting endocrine therapy benefit.

132 After 5 years of adjuvant endocrine therapy, breast-cancer recurrences continued t

133 east cancer with prior clinical benefit from endocrine therapy but later progression on aromatase inh

134 atients developed resistance to this type of endocrine therapy but the molecular mechanisms governing

135 nes whether a breast cancer patient receives endocrine therapy, but does not guarantee patient respon

136 scular disease incidence was compared across endocrine therapy categories.

137 Furthermore, a triple combination of endocrine therapy, CDK4/6, and PI3K inhibition was more

138 Additional combinations of palbociclib with endocrine therapy, chemotherapy, and targeted therapy ha

139 breast cancer who have not received previous endocrine therapy compared with a third-generation aroma

140 Adjuvant endocrine therapy compromises bone health in patients wi

141 ontinuum of recurrence risk to individualize endocrine therapy decision making for premenopausal wome

142 Endocrine therapy did not have to be the most recent the

143 Age, education, time since treatment, and endocrine therapy did not moderate observed cognitive de

144 than 35 years stopped all protocol-assigned endocrine therapy early.

145 sitive patients who have progressed on prior endocrine therapy; early reports show no benefit for add

146 ad relapsed or progressed after at least one endocrine therapy (either in advanced or metastatic or a

147 However, resistance to endocrine therapies, especially in the setting of advanc

148 -stage breast cancer after the initiation of endocrine therapy (ET) to determine whether this therapy

149 own about the efficacy of the combination of endocrine therapy (ET) with trastuzumab or with the pote

150 terising luminal breast cancers treated with endocrine therapy (ET), suggesting a more complex interp

151 Conclusions and Relevance: Neoadjuvant endocrine therapy, even as monotherapy, is associated wi

152 od or who underwent radical prostatectomy or endocrine therapy exhibited slightly lower HRs for prost

153 is elevated in breast cancer patients after endocrine therapy failure.

154 ermine prognosis and to predict benefit from endocrine therapies for breast cancer patients.

155 Function Trial) trials investigated adjuvant endocrine therapies for premenopausal women with hormone

156 e therapy, and 71 (11%) considered receiving endocrine therapy for < 5 years; 65 (10%) used fertility

157 e (ER(+)) breast cancer who receive standard endocrine therapy for 5 years remain at risk of distant

158 The administration of endocrine therapy for 5 years substantially reduces recu

159 isease relapse or progression after previous endocrine therapy for advanced disease during treatment

160 Primary endocrine therapy for ductal carcinoma in situ (DCIS) as

161 well-informed decisions on whether to extend endocrine therapy for each individual patient.

162 ha mutations Y537S and D538G is common after endocrine therapy for estrogen receptor alpha (ERalpha)

163 Systemic therapies include endocrine therapy for hormone receptor-positive disease,

164 mprove the risk-benefit of extended adjuvant endocrine therapy for late recurrence in patients with o

165 rgeted therapy, and three others reported on endocrine therapy for patients with HER-positive advance

166 Aromatase inhibitors (AIs) are the standard endocrine therapy for postmenopausal breast cancer; howe

167 inhibitors has therefore become a first-line endocrine therapy for postmenopausal women with ER(+) br

168 Endocrine therapy given for 5-10 y after surgery improve

169 uced Ki67(2W) do well with adjuvant standard endocrine therapy (giving consideration to clinical-path

170 While endocrine therapy has considerably reduced recurrence an

171 receptor-positive (ER(+) breast cancer), and endocrine therapy has improved survival for patients wit

172 Endocrine therapy has successfully been used to treat es

173 Although second generation endocrine therapies have significantly improved survival

174 chemotherapy) who were randomly assigned to endocrine therapy (hazard ratio for the comparison of hi

175 eral targeted therapies, collectively termed endocrine therapy, impinge on estrogen-induced ERalpha a

176 Combination of CDK4/6 inhibitors and endocrine therapy improves clinical outcome in advanced

177 Addition of palbociclib to endocrine therapy improves progression-free survival in

178 h reduced response and overall survival from endocrine therapies in castration-resistant prostate can

179 describe benefits and toxicities of adjuvant endocrine therapies in women younger than 35 years with

180 e response from the addition of taselisib to endocrine therapy in a neoadjuvant setting is consistent

181 potentially overcome or delay resistance to endocrine therapy in advanced breast cancer that is posi

182 Resistance to endocrine therapy in breast cancer is common.

183 The estrogen receptor (ER) is a target for endocrine therapy in breast cancer patients.

184 promising approach to overcome resistance to endocrine therapy in breast cancer.

185 the predictive value of (18)F-FES PET/CT for endocrine therapy in epithelial ovarian cancer patients

186 ificant additional information on DRFS after endocrine therapy in estrogen receptor (ER) -positive no

187 o investigate the benefit of adding CDKIs to endocrine therapy in patients whose tumours might have d

188 Phase III trials of buparlisib and endocrine therapy in patients with ER-positive breast ca

189 and has been used for predicting response to endocrine therapy in patients with ER-positive metastati

190 ationale for the use of PI3K inhibitors plus endocrine therapy in patients with PIK3CA mutations.

191 xemestane are reasonable options as adjuvant endocrine therapy in postmenopausal patients with hormon

192 treatment for ER+ breast cancer, the role of endocrine therapy in the neoadjuvant setting is unclear.

193 Administration approval in combination with endocrine therapy in the treatment of hormone receptor p

194 benefit for addition of IGF1R inhibitors to endocrine therapy in this setting.

195 tive breast cancer are treated with adjuvant endocrine therapy, including selective estrogen receptor

196 geted therapies that enhance the efficacy of endocrine therapy; inhibitors of mTOR and inhibitors of

197 simultaneously at the time of initiation of endocrine therapy (instead of the current approach of se

198 treatment of this breast cancer subtype with endocrine therapies is effective in the adjuvant and rec

199 Resistance to endocrine therapy is a major impediment to successful tr

200 tudy show that PI3K inhibition combined with endocrine therapy is effective in postmenopausal women w

201 If adjuvant endocrine therapy is indicated for breast cancer treatme

202 Endocrine therapy is preferable to chemotherapy as first

203 s an increased risk of VTE immediately after endocrine therapy is restricted to tamoxifen.

204 Although endocrine therapy is the mainstay of adjuvant treatment

205 Endocrine therapy is usually effective in these hormone-

206 receptor-positive disease without receipt of endocrine therapy, lymphovascular invasion, multifocal d

207 lesterol-lowering medication during adjuvant endocrine therapy may have a role in preventing breast c

208 st that patients with ILC receiving adjuvant endocrine therapy may not benefit as much as patients wi

209 suggest that combining PI3K inhibitors with endocrine therapy may overcome resistance.

210 In patients who underwent endocrine therapy (n = 174), parenchymal enhancement was

211 herapy improves progression-free survival in endocrine therapy-naive and endocrine therapy-resistant

212 Eligible patients were endocrine therapy-naive, with WHO performance status 0-2

213 ctive: To evaluate the effect of neoadjuvant endocrine therapy (NET) on the response rate and the rat

214 ausal women at increased risk, the choice of endocrine therapy now includes anastrozole (1 mg/day) in

215 Resistance to endocrine therapy occurs in virtually all patients with

216 al women receiving letrozole for neoadjuvant endocrine therapy, OFS was achieved more quickly and mai

217 Patients treated with endocrine therapy often develop resistance, either de no

218 etermine the long-term influence of adjuvant endocrine therapies on CVD in a cohort of postmenopausal

219 ses of RT), and (3) what are the benefits of endocrine therapy on local recurrence, and do they justi

220 le to fulvestrant in cell lines resistant to endocrine therapy or bearing ESR1 mutations.

221 risk is not mitigated by favorable biology, endocrine therapy, or a radiation boost.

222 were not treated, who received tamoxifen as endocrine therapy, or who were treated with an aromatase

223 rvival was 8.8 months in favour of CDKI plus endocrine therapy over placebo plus endocrine therapy (r

224 lable clinical evidence for chemotherapy and endocrine therapy patterns of response.

225 irst-line therapy or, for selected patients, endocrine therapy plus HER2-targeted therapy or endocrin

226 azard ratio 0.23 [0.07-0.79], P = 0.02) from endocrine therapies (pre-chemotherapy).

227 Conversely, endocrine therapy promoted rapid protein depletion due t

228 gen-receptor-positive ILRR received adjuvant endocrine therapy, radiation therapy was mandated for pa

229 DKI plus endocrine therapy over placebo plus endocrine therapy (range across the trials 6.8-13.3 mont

230 s of ER expression in recurrent tumors after endocrine therapy remain elusive.

231 Resistance to endocrine therapy remains a major clinical problem in br

232 We also assessed endocrine therapy resistance by clinical parameters, qua

233 Endocrine therapy resistance frequently develops in estr

234 Multiple mechanisms of endocrine therapy resistance have been identified, inclu

235 rlies changes in regulatory networks driving endocrine therapy resistance in breast cancer.

236 nduced cancer stem-like cells and leading to endocrine therapy resistance in OXPHOS-dependent breast

237 HIF-1alpha was able to confer endocrine therapy resistance to ERalpha(+) breast cancer

238 rigenesis in vitro and in vivo and conferred endocrine therapy resistance to previously sensitive bre

239 naling is affected by genetic alterations in endocrine therapy resistance.

240 ween IL-6 and STAT3 driving tumor growth and endocrine therapy resistance.

241 t ligand-binding domain dysfunction leads to endocrine therapy resistance.

242 sm for altering cell signaling and acquiring endocrine therapy resistance.

243 tes progression to an ER(-), mesenchymal and endocrine therapy resistant phenotype.

244 efficacious in treating both ER-positive and endocrine therapy-resistant disease.

245 t KDM3A is required for growth in a model of endocrine therapy-resistant disease.

246 free survival in endocrine therapy-naive and endocrine therapy-resistant metastatic settings.

247 of having a toolkit of AEs for treatment of endocrine therapy-resistant tumors driven by different c

248 e (PI3K) pathway activation is a hallmark of endocrine therapy-resistant, hormone receptor-positive b

249 and FOXM1 enables greater discrimination of endocrine therapy responders and non-responders in patie

250 of HIF-1alpha and the role of HIF-1alpha in endocrine therapy response are unknown.

251 l ((18)F-FES) uptake and early assessment of endocrine therapy response using (18)F-FDG and (18)F-flu

252 ctive values of molecular imaging agents for endocrine therapy response.

253 This annotation reveals endocrine therapy-response specific regulatory networks

254 y identification of reduced effectiveness of endocrine therapy resulting from activating ESR1 mutatio

255 e development of breast cancer resistance to endocrine therapy results from an increase in cellular p

256 Exclusion criteria were ever use of adjuvant endocrine therapy, secondary malignancy, recurrence, and

257 binations, especially with immunotherapy and endocrine therapy, seem most promising in the clinical e

258 Since the addition of CDKI to endocrine therapy seemed to benefit all clinicopathologi

259 As adjuvant endocrine therapy, she began monthly goserelin administr

260 reast cancer who are candidates for adjuvant endocrine therapy should be offered tamoxifen for an ini

261 The decision regarding choice of endocrine therapy should take into consideration age, ba

262 Exposures: Women were grouped by endocrine therapy status (tamoxifen citrate only, AI onl

263 andomised breast cancer trials of CDKIs plus endocrine therapy submitted to the US Food and Drug Admi

264 Breast cancer resistance to endocrine therapies such as tamoxifen and aromatase inhi

265 Endocrine therapies target the activation of the oestrog

266 ncers express estrogen receptor-alpha (ER+), endocrine therapies targeting these receptors often fail

267 s for estrogen has led to the development of endocrine therapies that block the action of these hormo

268 Thus, endocrine therapies that inhibit the AR ligand-binding d

269 Endocrine therapies that target the dependence of this s

270 d at least partly explained by the advent of endocrine therapy that is less effective in African Amer

271 Of 789 patients who initiated CLM during endocrine therapy, the majority came from the letrozole

272 ecause of de novo and acquired resistance to endocrine therapy, there remains a need to identify whic

273 TICs are enriched by endocrine therapy through NOTCH signaling.

274 t ER(+) breast cancers develop resistance to endocrine therapy; thus, novel targets are needed to tre

275 ecommended to determine potential benefit of endocrine therapies to reduce risk of future breast canc

276 The extension of the duration of adjuvant endocrine therapy to 10 years has been shown to reduce t

277 y of molecular changes in ILC in response to endocrine therapy to date.

278 gnosis associated with neurofibromin loss in endocrine therapy-treated ER(+) breast cancer.

279 Endocrine therapy trials were excluded.

280 on of this disease to androgen independence, endocrine therapy ultimately fails to control prostate c

281 by surgical treatment choice, post-treatment endocrine therapy use, and age at diagnosis.

282 The potential benefit of escalating endocrine therapy versus tamoxifen alone is minimal for

283 ositive breast cancers develop resistance to endocrine therapy via mutation of ERs whose constitutive

284 ast cancer cells often develop resistance to endocrine therapy via restoration of the ERalpha activit

285 ined as imaging surveillance with or without endocrine therapy, vs standard surgical care.

286 Endocrine therapy was continued for a total of 5 years,

287 Endocrine therapy was given to patients with hormone rec

288 Initiation of CLM during endocrine therapy was related to improved disease-free-s

289 The initial endocrine therapy was tamoxifen alone in the majority of

290 were disease-free after 5 years of scheduled endocrine therapy, we used Kaplan-Meier and Cox regressi

291 reast cancer that had progressed on previous endocrine therapy were stratified by sensitivity to prev

292 ovarian suppression in addition to adjuvant endocrine therapy, whereas lower-risk patients should no

293 ndent predictor of outcome in the context of endocrine therapy, whereas RAS/RAF mutations are rare in

294 mine whether patients should be treated with endocrine therapy, which is designed to block ERalpha si

295 e, and open novel perspectives for combining endocrine therapies with PRMT1 inhibitors in ERalpha-pos

296 erformed before and 7-9 d after the start of endocrine therapy with fulvestrant.

297 An alternative schedule of extended adjuvant endocrine therapy with letrozole, including intermittent

298 ogists made a preliminary recommendation for endocrine therapy with or without chemotherapy on the ba

299 RT alone may represent a better option than endocrine therapy with respect to compliance, toxic effe

300 nhibitors (AIs) are the preferred first-line endocrine therapy, with or without the cyclin-dependent