ライフサイエンスコーパス: endocrine therapy

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

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

3 n demonstrated alone and in combination with endocrine therapy.

4 ausal patients who had not received previous endocrine therapy.

5 y benefit from lapatinib in combination with endocrine therapy.

6 may also be offered ovarian suppression with endocrine therapy.

7 tive breast cancer patients as responders to endocrine therapy.

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

9 els were suppressed in patients treated with endocrine therapy.

10 atively poor outcome in patients who undergo endocrine therapy.

11 used to predict prognosis and sensitivity to endocrine therapy.

12 luable to select ovarian cancer patients for endocrine therapy.

13 stemic treatment for advanced disease except endocrine therapy.

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

15 ffect residual risk following treatment with endocrine therapy.

16 st cancer patients resistant to conventional endocrine therapy.

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

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

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

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

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

22 matase inhibitor for 10 years total adjuvant endocrine therapy.

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

24 ignaling, cell proliferation and response to endocrine therapy.

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

26 chromatin openness, underlies resistance to endocrine therapy.

27 in patients with breast cancer treated with endocrine therapy.

28 for patients with breast cancer treated with endocrine therapy.

29 ancers are tolerant or acquire resistance to endocrine therapy.

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

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

32 e patients are or soon develop resistance to endocrine therapy.

33 of lesions in patients scheduled to receive endocrine therapy.

34 (ERalpha) and consequently do not respond to endocrine therapy.

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

36 ted with disease progression and response to endocrine therapy.

37 diseases, with the highest risk for those on endocrine therapy.

38 ts intrinsic tumoral sensitivity to adjuvant endocrine therapy.

39 ve breast cancers undergoing radiotherapy or endocrine therapy.

40 hormone receptor positive received adjuvant endocrine therapy.

41 ession in patients receiving chemotherapy or endocrine therapy.

42 erapy, postmastectomy radiation therapy, and endocrine therapy.

43 odel of acquired breast cancer resistance to endocrine therapy.

44 provide a potential alternative approach to endocrine therapy.

45 ignaling and their importance in response to endocrine therapy.

46 receptor expression on efficacy of adjuvant endocrine therapy.

47 y to complete a total of 5 years of adjuvant endocrine therapy.

48 are unclear despite being a major problem in endocrine therapy.

49 can occur despite appropriate treatment with endocrine therapy.

50 receptor-positive breast cancer who received endocrine therapy.

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

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

53 plasticity under the control of hormones and endocrine therapy.

54 therapy, postsurgical radiation therapy, and endocrine therapy.

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

56 conferring poor prognosis and resistance to endocrine therapy.

57 rapy should receive ovarian suppression with endocrine therapy.

58 predictive and early-response biomarkers for endocrine therapy.

59 es with worse clinical outcome regardless of endocrine therapy.

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

61 ients with progression after receiving prior endocrine therapy.

62 reast cancer that has progressed on previous endocrine therapy.

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

64 ssessing in vivo pharmacodynamic response to endocrine therapy.

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

66 14-3-3zeta and enhance the effectiveness of endocrine therapies.

67 breast cancer physiology and is targeted by endocrine therapies.

68 d overall survival and predicted response to endocrine therapies.

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

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

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

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

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

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

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

76 ination of signatures for (1) sensitivity to endocrine therapy, (2) chemoresistance, and (3) chemosen

77 nd Dec 31, 2007, 30 642 men received primary endocrine therapy, 26 432 curative treatment, and 19 526

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

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

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

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

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

83 y important benefits from switching adjuvant endocrine therapy after 2 to 3 years of tamoxifen to exe

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

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

86 of IBTR in the model included adjuvant RT or endocrine therapy, age, margin status, number of excisio

87 d patients with ER-positive breast cancer to endocrine therapy alone or endocrine therapy plus chemot

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

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

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

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

92 linical approach may be to use both adjuvant endocrine therapy and chemotherapy in this rare subset o

93 the potential negative interactions between endocrine therapy and chemotherapy.

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

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

96 Targeted therapies such as endocrine therapy and growth factor receptor inhibitors

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

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

99 eptor (ER)-positive cancers are sensitive to endocrine therapy and may not derive much further benefi

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

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

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

103 ctor receptor HER2/neu predict resistance to endocrine therapy and poor outcome.

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

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

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

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

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

109 ancer remain at high risk of relapse despite endocrine therapy and, in addition, might benefit from a

110 er cells is crucial for the effectiveness of endocrine therapies, and its loss is a hallmark of endoc

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

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

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

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

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

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

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

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

119 presentation, final margins, and receipt of endocrine therapy between the two cohorts.

120 ter 2-3 years of tamoxifen, and (3) extended endocrine therapy beyond 5 years.

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

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

123 ive breast cancers respond well initially to endocrine therapies, but often develop resistance during

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

125 nthracycline and paclitaxel chemotherapy and endocrine therapy, but there was no significant interact

126 a levels and sensitivity of LTLT-Ca cells to endocrine therapy by down-regulation of Her-2/MAPK pathw

127 scular disease incidence was compared across endocrine therapy categories.

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

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

130 tients receiving LET, representing the first endocrine therapy comparable to LET in ABC.

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

132 er tissues that are known to be resistant to endocrine therapy compared with HER2/neu-negative tissue

133 Adjuvant endocrine therapy compromises bone health in patients wi

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

135 breast cancer cells respond to the stress of endocrine therapies determines whether they will acquire

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

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

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

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

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

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

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

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

144 tor (ER)-positive breast tumors treated with endocrine therapy fail to respond, and the remainder is

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

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

147 Therefore, trials assessing endocrine therapies for this patient population need ext

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

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

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

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

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

153 er wild-type or mutant, and be combined with endocrine therapy for maximal efficacy when treating ER(

154 ession in patients receiving chemotherapy or endocrine therapy for MBC.

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

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

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

158 The absence of benefit from endocrine therapy for women with ER-negative invasive br

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

160 Endocrine therapy has successfully been used to treat es

161 Although second generation endocrine therapies have significantly improved survival

162 n breast cancer is predictive of response to endocrine therapy; however, resistance is common in ERal

163 axane and anthracycline-based regimens (then endocrine therapy if estrogen receptor [ER]-positive).

164 if node-negative and high SET or after chemo-endocrine therapy if intermediate or high SET.

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

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

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

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

169 Resistance to endocrine therapy in breast cancer is associated with ac

170 Resistance to endocrine therapy in breast cancer is common.

171 dings also imply that acquired resistance to endocrine therapy in breast cancer may be abrogated by c

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

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

174 ing IGF-IR alone in abrogating resistance to endocrine therapy in breast cancer.

175 g chemoprevention in breast cancer, adjuvant endocrine therapy in early-stage breast cancer, and salv

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

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

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

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

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

181 n that predicted poor outcome after adjuvant endocrine therapy in patients.

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

183 tase inhibitors (AI) are employed widely for endocrine therapy in postmenopausal women with breast ca

184 restoring ERalpha and the responsiveness to endocrine therapy in some endocrine-insensitive ERalpha-

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

186 d toxicity data from the available trials of endocrine therapy in the postmenopausal setting.

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

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

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

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

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

192 Resistance to chemotherapy and endocrine therapy is a major cause of breast cancer trea

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

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

195 If adjuvant endocrine therapy is indicated for breast cancer treatme

196 Endocrine therapy is preferable to chemotherapy as first

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

198 Endocrine therapy is the main therapeutic option for pat

199 Although endocrine therapy is the mainstay of adjuvant treatment

200 unced in tumor tissue remaining after either endocrine therapy (letrozole) or chemotherapy (docetaxel

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

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

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

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

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

206 eived 5 years of tamoxifen alone as adjuvant endocrine therapy (n = 225 and 298, respectively), a coh

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

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

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

210 ion predicted survival benefit from adjuvant endocrine therapy, not inherent prognosis.

211 Resistance to endocrine therapy occurs in virtually all patients with

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

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

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

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

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

217 Phase III proof-of-efficacy trials of endocrine therapy plus bevacizumab are in progress (Canc

218 breast cancer to endocrine therapy alone or endocrine therapy plus chemotherapy.

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

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

221 Thus, in response to various endocrine therapy regimens, these xenograft breast tumor

222 y seemed to enhance the efficacy of adjuvant endocrine therapy related to SET index.

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

224 Resistance to endocrine therapies remains a major problem in the manag

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

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

227 the development of estrogen independence and endocrine therapy resistance in breast cancer patients m

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

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

230 uggest the importance of clonal selection in endocrine therapy resistance of breast cancer.

231 es a potential molecular explanation for the endocrine therapy resistance seen in ERalpha-positive br

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

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

234 To obtain insight into the genomic basis of endocrine therapy resistance, we characterized MCF-7 mon

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

236 ving anchorage-independent proliferation and endocrine therapy resistance.

237 sociated with both experimental and clinical endocrine therapy resistance.

238 ting that FGFR1 overexpression also promotes endocrine therapy resistance.

239 gens may prevent or delay the development of 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 This is the first complete panel of endocrine therapy-resistant cell lines, which were gener

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

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

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

248 -positive breast cancers to a metastatic and endocrine therapy-resistant phenotype via increased MAPK

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

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

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

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

253 This annotation reveals endocrine therapy-response specific regulatory networks

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

255 For men on endocrine therapy, risks for DVT (SIR 2.48, 95% CI 2.25-

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

257 aromatase inhibitor (AI) as primary (initial endocrine therapy), sequential (using both tamoxifen and

258 A genomic index for sensitivity to endocrine therapy (SET) index was defined from genes coe

259 As adjuvant endocrine therapy, she began monthly goserelin administr

260 dies, the mTOR inhibitor everolimus added to endocrine therapy showed antitumor activity.

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

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

263 Endocrine therapies target the activation of the oestrog

264 tumors can be used to predict the success of endocrine therapies targeting the estrogen receptor (ER)

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

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

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

268 Luminal breast cancers are treated with endocrine therapies that target ER.

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 e PI3K pathway associated with resistance to endocrine therapy, the state of clinical development of

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

274 Endocrine therapy to block the ER pathway is highly effe

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

276 Endocrine therapy trials were excluded.

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

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

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

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

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

282 outcome of patients developing resistance to endocrine therapy warrants additional studies.

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

284 Endocrine therapy was given to patients with hormone rec

285 Endocrine therapy was prescribed for women with hormone

286 Endocrine therapy was recommended after chemotherapy in

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

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

289 with acquired or de novo resistance to these endocrine therapies were profiled for gene expression an

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

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

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

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

294 irable outcome can be prevented by combining endocrine therapies with Notch inhibition.

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

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

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

298 Endocrine therapy with tamoxifen (TAM) significantly imp

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

300 ast carcinoma, who had undergone neoadjuvant endocrine therapy within the past 6 months, underwent US