ライフサイエンスコーパス: androgen deprivation

1 nner, while de-repressing AR expression upon androgen deprivation.

2 metastases but did not confer resistance to androgen deprivation.

3 state cancer are metastatic and resistant to androgen deprivation.

4 tors in malignancies no longer responsive to androgen deprivation.

5 R nuclear localization that was inhibited by androgen deprivation.

6 enograft progression to CRPC after prolonged androgen deprivation.

7 killing by cytotoxic chemotherapy following androgen deprivation.

8 survival under metabolic stresses, including androgen deprivation.

9 prostate cancer cells were more resistant to androgen deprivation.

10 sed migration, including under conditions of androgen deprivation.

11 ancer who achieve a good initial response to androgen deprivation.

12 deprivation and 770 assigned to intermittent androgen deprivation.

13 ty remains critical for tumor growth despite androgen deprivation.

14 increased stem cell-like features following androgen deprivation.

15 of the gene and expression was restored upon androgen deprivation.

16 esistance and NEPC evolution upon subsequent androgen deprivation.

17 cal and molecular properties that respond to androgen-deprivation.

18 cal information; sRT; timing and duration of androgen deprivation; 3-y PSA results; and clinical even

19 Androgen deprivation (AD) therapy failure leads to termi

20 ndomly assigned within 30 days of initiating androgen deprivation (AD) to cixutumumab added to a lute

21 n the context of radiotherapy and short-term androgen deprivation (AD), potential surrogates under lo

22 Androgen deprivation added to definitive radiation or su

23 survival (OS) of men with mPCa treated with androgen deprivation (ADT) with and without prostate RT.

24 cal information, sRT, timing and duration of androgen deprivation (ADT), 3 year PSA results and clini

25 igh-risk disease is often under-treated with androgen deprivation alone, particularly among older men

26 nalysis: 765 randomly assigned to continuous androgen deprivation and 770 assigned to intermittent an

27 an prostate cancer, including sensitivity to androgen deprivation and induced response to hypoxia and

28 However, androgen-deprivation and/or AR targeting-based therapies

29 scence contributes to PC cell survival under androgen deprivation, and C/EBPbeta-deficient cells were

30 sion also occur in the normal prostate after androgen deprivation, and CXCL13 is expressed by myofibr

31 we show that RUNX1(+) PLCs are unaffected by androgen deprivation, and do not contribute to the regen

32 Curcumin cooperated in vivo with androgen deprivation as indicated by a reduction in tumo

33 is a hallmark of prostate cancer (PCa) with androgen deprivation being standard therapy.

34 Prostate cancer is initially responsive to androgen deprivation, but the effectiveness of androgen

35 iptional regulation of PCGEM1 in response to androgen deprivation by p54/nrb.

36 n deprivation (IAD) compared with continuous androgen deprivation (CAD) for treatment of prostate can

37 uggested that patients undergoing continuous androgen deprivation (CAD) have superior survival and ti

38 However, phase III trials testing continuous androgen deprivation (CAD) versus IAD have reached incon

39 Intermittent androgen deprivation can be considered as an alternative

40 Although androgen deprivation can initially lead to remission, th

41 n and invasion of LNCaP-C4-2 cells and under androgen deprivation conditions largely blocked cell div

42 quired for prostate cancer cell growth under androgen-deprivation conditions in vitro and in vivo, an

43 ing miR-135a can restore AR expression under androgen-deprivation conditions, thus contributing to th

44 Androgen deprivation constitutes the principal therapy f

45 e apoptotic and fibrotic pathways, including androgen deprivation, downregulation of the androgen rec

46 ells of hormonally intact prostate but, upon androgen deprivation, exclusively labels a type of lumin

47 iescent and refractory to stresses including androgen deprivation, exhibit high clonogenic potential,

48 olide) are the standard agents for achieving androgen deprivation for prostate cancer despite the ini

49 Intermittent androgen deprivation for prostate-specific antigen (PSA)

50 Intermittent androgen deprivation has been studied as an alternative.

51 erstanding of the long-term complications of androgen deprivation has changed the initial approach to

52 en by androgen receptor (AR) is treated with androgen deprivation; however, therapy failure results i

53 ty exists regarding benefits of intermittent androgen deprivation (IAD) compared with continuous andr

54 Intermittent androgen deprivation (IAD) has been widely tested in pro

55 or progressive prostate cancer, intermittent androgen deprivation (IAD) is one of the most common and

56 survival with intermittent versus continuous androgen deprivation in a noninferiority randomized tria

57 NTS was acutely induced by androgen deprivation in animal models of prostate cancer

58 androgens suppress CDCP1 expression and that androgen deprivation in combination with loss of PTEN pr

59 ccupies a distinct set of genomic loci after androgen deprivation in CRPC.

60 Notably, RG7112 was highly synergistic with androgen deprivation in LNCaP xenograft tumors.

61 ith improved CSS and duration of response to androgen deprivation in men being treated for biochemica

62 e tumors and tissue cultured with androgens, androgen deprivation in the medium led to decreased expr

63 We found that murine androgen deprivation in vivo elicited RNA expression pat

64 beta is critical for complete maintenance of androgen deprivation-induced senescence and that targeti

65 In summary, we show for the first time that androgen deprivation induces EMT in both normal prostate

66 Taken together, our findings indicate that androgen deprivation induces NCoA2, which in turn mediat

67 Upon androgen deprivation, induction of C/EBPbeta is facilita

68 Androgen deprivation influenced the differentiated pheno

69 Androgen deprivation is currently a standard-of-care, fi

70 Androgen deprivation is the cornerstone of prostate canc

71 Androgen deprivation is the standard therapy for patient

72 Furthermore, androgen deprivation led to castration-resistant prostat

73 Correspondingly, androgen deprivation markedly attenuates the frequency a

74 berrantly high expression of m1 and m3 under androgen deprivation mimicking castration and androgen r

75 ement, prostatectomy, radiotherapy (RT), and androgen deprivation monotherapy, respectively.

76 ho received treatment combinations including androgen deprivation (n = 207) reported significantly po

77 expression prevents growth arrest following androgen deprivation or anti-androgen challenge.

78 ostate cancers, including those resistant to androgen deprivation or antiandrogen therapies.

79 Androgen deprivation or AR blockage with inhibitor MDV31

80 l role in prostate cancer (PCa) growth, with androgen deprivation or AR down-regulation causing cell-

81 Androgen deprivation or AR inhibition significantly incr

82 ore </=4 + 3, stage </=T2), with no previous androgen deprivation or treatment for prostate cancer, a

83 Androgen deprivation or treatment with androgen receptor

84 Continue androgen deprivation (pharmaceutical or surgical) indefi

85 assigned to RP alone or neoadjuvant CHT with androgen deprivation plus docetaxel (75 mg/m(2) body sur

86 Prostate cancer risk grouping, androgen deprivation, race, age-adjusted CCI, L5HU, and

87 rentiation, was ascertained as we found that androgen deprivation reduced expression of Ptpn1 in CD4

88 In vivo, androgen deprivation resulted in reduced growth and CD24

89 substantial decrease with IAD in exposure to androgen deprivation, resulting in less cost, inconvenie

90 redicted course of the disease under various androgen-deprivation schedules.

91 ls acutely or chronically exposed to ENZA or androgen deprivation, suggesting that autophagy is an im

92 ancer patients will initially respond to the androgen deprivation, the disease often progresses to ca

93 Androgen deprivation therapies (ADT) directed against th

94 rostate cancer (PCa) is usually treated with androgen deprivation therapies (ADTs).

95 Resistance to androgen deprivation therapies and increased androgen re

96 tate cancer cells respond heterogeneously to androgen deprivation therapies and reveals characteristi

97 ding domain (AR-LBD), the intended target of androgen deprivation therapies including CRPC therapies

98 lapse, also after administration of adjuvant androgen deprivation therapies.

99 arising from a range of etiologies including androgen-deprivation therapies (ADTs), has been reported

100 cer (PCa) and its activity can be blocked by androgen-deprivation therapies (ADTs).

101 When added to androgen deprivation, therapies demonstrating improved s

102 Concordance was greatest for androgen deprivation therapy (ADT) (86.0%, n = 308) alon

103 We recently found an association between androgen deprivation therapy (ADT) and Alzheimer's disea

104 The potential association between androgen deprivation therapy (ADT) and cardiovascular mo

105 ing body of evidence supports a link between androgen deprivation therapy (ADT) and cognitive dysfunc

106 isk disease were all prescribed 24 months of androgen deprivation therapy (ADT) and had lymph node ir

107 Furthermore, the influences of androgen deprivation therapy (ADT) and its duration on (

108 ity regarding the influence of sequencing of androgen deprivation therapy (ADT) and radiotherapy (RT)

109 ) in patients is the resistance of tumors to androgen deprivation therapy (ADT) and their subsequent

110 f of these men are subsequently treated with androgen deprivation therapy (ADT) at some point.

111 Prostate tumors develop resistance to androgen deprivation therapy (ADT) by multiple mechanism

112 Despite the fact that androgen deprivation therapy (ADT) can effectively reduc

113 Whether androgen deprivation therapy (ADT) causes excess cardiov

114 nical trials have established the benefit of androgen deprivation therapy (ADT) combined with radioth

115 ged with the combination of radiotherapy and androgen deprivation therapy (ADT) compared with ADT alo

116 Androgen deprivation therapy (ADT) for advanced prostate

117 Bicalutamide (Bic) is frequently used in androgen deprivation therapy (ADT) for treating prostate

118 Androgen deprivation therapy (ADT) has become a standard

119 ly associated with postoperative response to androgen deprivation therapy (ADT) in a subset analysis

120 The use of androgen deprivation therapy (ADT) in the treatment of a

121 We previously showed androgen deprivation therapy (ADT) induces nMET in castr

122 Androgen deprivation therapy (ADT) is a standard adjunct

123 Radiotherapy in combination with androgen deprivation therapy (ADT) is a standard treatme

124 Androgen deprivation therapy (ADT) is still a mainstay o

125 e upon androgen receptor (AR) signaling, and androgen deprivation therapy (ADT) is the accepted treat

126 Androgen deprivation therapy (ADT) is the mainstay treat

127 Androgen deprivation therapy (ADT) is the standard care

128 make up a heterogeneous population for whom androgen deprivation therapy (ADT) is the usual treatmen

129 on of abiraterone acetate plus prednisone to androgen deprivation therapy (ADT) led to a significant

130 Androgen deprivation therapy (ADT) may contribute to dep

131 Patients who had received second-line androgen deprivation therapy (ADT) or chemotherapy were

132 receptor (AR) after failure of AR-targeting androgen deprivation therapy (ADT) prevents effective tr

133 Androgen deprivation therapy (ADT) remains a common trea

134 TITAN study, the addition of apalutamide to androgen deprivation therapy (ADT) significantly improve

135 get for adjuvant therapy in combination with androgen deprivation therapy (ADT) to prevent androgen-i

136 ons partially explain the failure of current androgen deprivation therapy (ADT) to reduce/prevent and

137 c stroke were 1.19 (95% CI, 1.05-1.34) after androgen deprivation therapy (ADT) vs no ADT and 1.21 (9

138 of treatment with leuprolide and flutamide, androgen deprivation therapy (ADT) was stopped until pro

139 rvational studies have associated the use of androgen deprivation therapy (ADT) with an increased ris

140 g patients with prostate cancer who received androgen deprivation therapy (ADT), after adjustment for

141 Androgen deprivation therapy (ADT), an important treatme

142 GG) from transrectal US-guided biopsy, prior androgen deprivation therapy (ADT), and any prior CT res

143 d phenotypic change of prostate cancer after androgen deprivation therapy (ADT), and it ultimately de

144 High-risk patients received long-term androgen deprivation therapy (ADT), and some intermediat

145 minated prostate cancer initially respond to androgen deprivation therapy (ADT), but virtually all pa

146 isting therapies for prostate cancer such as androgen deprivation therapy (ADT), destroy the bulk of

147 In spite of an initial clinical response to androgen deprivation therapy (ADT), the majority of pros

148 The primary end point was androgen deprivation therapy (ADT)-free survival.

149 cancer before and 4 wk after treatment with androgen deprivation therapy (ADT).

150 ressor gene whose expression is inhibited by androgen deprivation therapy (ADT).

151 in prostate cancer (PCa) patients receiving androgen deprivation therapy (ADT).

152 ar processes underlying CRPC survival during androgen deprivation therapy (ADT).

153 by androgen steroid hormones, and delayed by androgen deprivation therapy (ADT).

154 ate cancer who were initiating or continuing androgen deprivation therapy (ADT).

155 Androgen deprivation therapy (ADT, surgical or medical c

156 Androgen deprivation therapy (ADTh) remains a mainstay o

157 llular and molecular changes in tumors after androgen deprivation therapy (castration).

158 Intermittent androgen deprivation therapy (IADT) is an attractive tre

159 nt with prostatectomy (n = 402) or EBRT with androgen deprivation therapy (n = 217) for men with unfa

160 now appears to extend survival compared with androgen deprivation therapy alone.

161 l, primary Gleason score, and prior therapy (androgen deprivation therapy and external-beam radiation

162 eater than 0.5 ng/mL following radiation and androgen deprivation therapy appears to identify men pri

163 tation and measures to reduce the effects of androgen deprivation therapy are required.

164 vanced prostate cancer responds initially to androgen deprivation therapy by depletion of gonadal tes

165 s with advanced prostate cancer treated with androgen deprivation therapy experience relapse with rel

166 All patients received neoadjuvant androgen deprivation therapy for 3-6 months before the s

167 stics increasing stroke risk include medical androgen deprivation therapy for ischemic and any stroke

168 Androgen deprivation therapy for prostate cancer (PCa) b

169 In patients undergoing androgen deprivation therapy for prostate cancer, AR dri

170 Ptpn1 in CD4 cells from patients undergoing androgen deprivation therapy for prostate cancer.

171 Androgen deprivation therapy has been the standard of ca

172 cross-resistance to taxane chemotherapy and androgen deprivation therapy in advanced prostate cancer

173 pects of treatment is the role of short-term androgen deprivation therapy in combination with definit

174 te cancer, discuss the limits of traditional androgen deprivation therapy in the form of gonadotropin

175 Androgen deprivation therapy in the treatment of prostat

176 of prostate cancer metastases to bone after androgen deprivation therapy is a major clinical challen

177 Androgen deprivation therapy is the most effective treat

178 advanced metastatic disease (n = 103), after androgen deprivation therapy only (n = 16), after surger

179 my, external beam radiation therapy, primary androgen deprivation therapy or brachytherapy.

180 we aimed to test the safety and efficacy of androgen deprivation therapy plus ipilimumab.

181 astatic tumors that have become resistant to androgen deprivation therapy represent the major challen

182 dose conformal radiotherapy with neoadjuvant androgen deprivation therapy showed an advantage in bioc

183 e radiotherapy and lower rates of additional androgen deprivation therapy than those with extrafossa

184 verall survival was reported when short-term androgen deprivation therapy was added to radiotherapy.

185 Androgen deprivation therapy was continued in both arms.

186 Patients on androgen deprivation therapy were excluded.

187 As the current androgen deprivation therapy with anti-androgens may pro

188 l evidence for and against use of short-term androgen deprivation therapy with dose-escalated radioth

189 Androgen deprivation therapy with leuprolide acetate was

190 evaluating the impact on survival of salvage androgen deprivation therapy with or without agents show

191 diation therapy (79.1% vs. 82.1%, P = 0.55), androgen deprivation therapy within the 6 mo preceding i

192 nists, chemotherapy-induced ovarian failure, androgen deprivation therapy, and aromatase inhibitors c

193 or radiation therapy followed by 6 months of androgen deprivation therapy, and followed for a median

194 radical prostatectomy, radical radiotherapy, androgen deprivation therapy, and watchful waiting).

195 Even with stringent androgen deprivation therapy, androgen receptor signalin

196 served in prostate cancer patients receiving androgen deprivation therapy, highlighting the evolution

197 n a considerable proportion of men receiving androgen deprivation therapy, however, PCa progresses to

198 Compared with men who did not receive androgen deprivation therapy, more men who received the

199 Despite resistance to initial androgen deprivation therapy, most men respond to second

200 Resistance to androgen deprivation therapy, or castration-resistant pr

201 ion-resistant prostate cancer (CR-PCa) after androgen deprivation therapy, the mainstay systemic trea

202 frequently detected (75% of cases) following androgen deprivation therapy, with further significant (

203 oised for selection as dominant clones after androgen deprivation therapy.

204 diation therapy or radiation and 6 months of androgen deprivation therapy.

205 on-resistant mesenchymal-like tumor cells to androgen deprivation therapy.

206 with prostate cancer undergoing intermittent androgen deprivation therapy.

207 l vesicle invasion, lymph node invasion, and androgen deprivation therapy.

208 androgen situations such as those imposed by androgen deprivation therapy.

209 cancer (CRPC) survival and growth even after androgen deprivation therapy.

210 hibit prostate cancers that are resistant to androgen deprivation therapy.

211 nt of prostate cancers that are resistant to androgen deprivation therapy.

212 n resistant prostate cancer (CRPC) after the androgen deprivation therapy.

213 r (PCa), and PCa growth can be suppressed by androgen deprivation therapy.

214 from a clinical trial of neoadjuvant intense androgen deprivation therapy.

215 they become hormone refractory after initial androgen deprivation therapy.

216 ivity, cell proliferation, and resistance to androgen deprivation therapy.

217 on to castration resistance during and after androgen deprivation therapy.

218 ognostic factor for PCM following RT without androgen deprivation therapy.

219 ular imaging in CRPC, even in the context of androgen deprivation therapy.

220 an evaluation of intermittent vs. continuous androgen deprivation therapy.

221 and fatigue are reported in men treated with androgen deprivation therapy.

222 adiotherapy who otherwise receive palliative androgen deprivation therapy.

223 ration de novo, enabling the tumour to evade androgen deprivation therapy.

224 as a reduction in PSA levels of >50% without androgen deprivation therapy.

225 motherapy can improve survival compared with androgen deprivation therapy.

226 PCs that had survived hormone (androgen)-deprivation therapy (n = 21) had a significant

227 (56.5% v 71.3%), were less likely to receive androgen-deprivation therapy (79.5% v 87.8%), and slight

228 MRC PR07 randomized phase III trial compared androgen-deprivation therapy (ADT) alone versus ADT with

229 Twenty-four patients received androgen-deprivation therapy (ADT) and were excluded for

230 ion of prostate cancer development regarding androgen-deprivation therapy (ADT) and/or immunotherapy

231 ith RP, whereas 148 of 605 patients received androgen-deprivation therapy (ADT) at the time of PET/CT

232 Men receiving androgen-deprivation therapy (ADT) for prostate cancer m

233 atic men with prostate cancer progression on androgen-deprivation therapy (ADT) from academic, commun

234 Androgen-deprivation therapy (ADT) has been the backbone

235 Although intermittent androgen-deprivation therapy (ADT) has not been associat

236 sly reported that radiotherapy (RT) added to androgen-deprivation therapy (ADT) improves survival in

237 r disease (CVD) and the duration and type of androgen-deprivation therapy (ADT) in men with prostate

238 Dose-escalated radiotherapy (RT) with androgen-deprivation therapy (ADT) is a standard definit

239 ling is a key driver of prostate cancer, and androgen-deprivation therapy (ADT) is a standard treatme

240 neuroendocrine prostate cancer (NEPC) after androgen-deprivation therapy (ADT) is well-known.

241 h localized prostate cancer, the addition of androgen-deprivation therapy (ADT) or a brachytherapy bo

242 ectively randomized clinical trial comparing androgen-deprivation therapy (ADT) plus docetaxel with A

243 tical pathway for prostate cancer cells, and androgen-deprivation therapy (ADT) remains the principal

244 vival pathway for prostate cancer cells, and androgen-deprivation therapy (ADT) remains the principal

245 Androgen-deprivation therapy (ADT) through surgical cast

246 treated with SRT with or without concurrent androgen-deprivation therapy (ADT) were obtained from 10

247 Outcomes are improved by concomitant androgen-deprivation therapy (ADT) with radiation therap

248 Of the 118 patients, 45 were receiving androgen-deprivation therapy (ADT) within at least 6 mo

249 gulated by androgens, and this suggests that androgen-deprivation therapy (ADT) would lead to hyperac

250 e cancer who have a poor response to initial androgen-deprivation therapy (ADT), as reflected by a pr

251 f this combination in men starting long-term androgen-deprivation therapy (ADT), using a multigroup,

252 are upregulated in prostate cancer following androgen-deprivation therapy (ADT).

253 1 (1245C) allele would exhibit resistance to androgen-deprivation therapy (ADT).

254 tumors to once again respond to conventional androgen-deprivation therapy (ADT).

255 ormone-sensitive prostate cancer responds to androgen-deprivation therapy (ADT); however, therapeutic

256 th metastatic prostate cancer progressing on androgen-deprivation therapy (castration-resistant prost

257 Primary androgen-deprivation therapy (PADT) is often used to tre

258 er median overall survival than placebo plus androgen-deprivation therapy among men with nonmetastati

259 is characterized by abbreviated response to androgen-deprivation therapy and in approximately 30% of

260 uld contribute to induction of the EMT after androgen-deprivation therapy and metastasis.

261 ncer (PCa) differs between those who receive androgen-deprivation therapy by surgical castration and

262 (ie, < 0.7 mmol/L) within the first year of androgen-deprivation therapy correlates with improved CS

263 ent-related adverse effects in men receiving androgen-deprivation therapy for prostate cancer.

264 Androgen-deprivation therapy has been identified to indu

265 l radiation therapy in 19.3% of patients and androgen-deprivation therapy in 7.4%.

266 standing of the development of resistance to androgen-deprivation therapy in prostate cancer.

267 Androgen-deprivation therapy is a commonly used treatmen

268 While androgen-deprivation therapy is transiently effective in

269 esized that chemohormonal therapy (CHT) with androgen-deprivation therapy plus docetaxel before RP wo

270 tic prostate cancer following the failure of androgen-deprivation therapy represents the lethal pheno

271 Enzalutamide plus androgen-deprivation therapy resulted in longer median o

272 ly using PARP inhibitors in combination with androgen-deprivation therapy upfront in advanced or high

273 ve prostate cancer and bone metastases whose androgen-deprivation therapy was initiated within 6 mont

274 Androgen-deprivation therapy was used in fewer patients

275 <=10 months) who were continuing to receive androgen-deprivation therapy were randomly assigned (in

276 e examined whether the survival advantage of androgen-deprivation therapy with radiotherapy (ADT plus

277 g patients with prostate cancer treated with androgen-deprivation therapy, appropriately prescribed e

278 rostate cancer choosing EBRT with or without androgen-deprivation therapy, brachytherapy boost (LDR o

279 high-risk prostate cancer receiving EBRT and androgen-deprivation therapy, brachytherapy boost (LDR o

280 ials are evaluating the role of intermittent androgen-deprivation therapy, early chemotherapy, and no

281 ctomy who develop biochemical failure during androgen-deprivation therapy.

282 , in whom the disease has progressed despite androgen-deprivation therapy.

283 rostate-specific antigen > 0.2 mg/mL) during androgen-deprivation therapy.

284 ondary end points included the initiation of androgen-deprivation therapy.

285 -sensitive prostate cancer who are receiving androgen-deprivation therapy.

286 n prostate tumors from patients treated with androgen-deprivation therapy.

287 ity fractures are potential complications of androgen-deprivation therapy.

288 teoporotic fracture risk among men receiving androgen-deprivation therapy.

289 e-specific antigen (PSA) levels while taking androgen-deprivation therapy.

290 herapy regimens in combination with standard androgen-deprivation therapy.

291 54 patients) while they continued to receive androgen-deprivation therapy.

292 ts] twice daily) or placebo while continuing androgen-deprivation therapy.

293 s that are poised for clonal selection after androgen-deprivation therapy.

294 comorbidities within 1.5 years of initiating androgen-deprivation therapy.

295 t TXNDC5 is up-regulated following long-term androgen-deprivation treatment (ADT) and is highly overe

296 Intermittent androgen deprivation was noninferior to continuous thera

297 Intermittent androgen deprivation was not inferior to continuous ther

298 Androgen deprivation was not permitted with therapy.

299 Androgen deprivation was not permitted.

300 liter or lower to continuous or intermittent androgen deprivation, with patients stratified according