ライフサイエンスコーパス: androgen deprivation

1 survival under metabolic stresses, including androgen deprivation.

2 prostate cancer cells were more resistant to androgen deprivation.

3 sed migration, including under conditions of androgen deprivation.

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

5 deprivation and 770 assigned to intermittent androgen deprivation.

6 ty remains critical for tumor growth despite androgen deprivation.

7 increased stem cell-like features following androgen deprivation.

8 ate cancer may indicate the need for earlier androgen deprivation.

9 h localized prostate cancer not treated with androgen deprivation.

10 No randomized trials evaluated primary androgen deprivation.

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

12 metastases but did not confer resistance to androgen deprivation.

13 state cancer are metastatic and resistant to androgen deprivation.

14 tors in malignancies no longer responsive to androgen deprivation.

15 R nuclear localization that was inhibited by androgen deprivation.

16 enograft progression to CRPC after prolonged androgen deprivation.

17 killing by cytotoxic chemotherapy following androgen deprivation.

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

19 y (35%) than with radiation therapy (12%) or androgen deprivation (11%).

20 prostatectomy, 58%; radiation therapy, 43%; androgen deprivation, 86%).

21 Androgen deprivation (AD) therapy failure leads to termi

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

23 Androgen deprivation added to definitive radiation or su

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

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 eneration can occur after repeated cycles of androgen deprivation and replacement in rodents.

28 ostate persists unabated under conditions of androgen deprivation and throughout the course of diseas

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

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

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

32 ormone-refractory disease is unresponsive to androgen-deprivation, androgen receptor (AR)-regulated s

33 ainly with combinations of antiandrogens and androgen deprivation, are the mainstay treatment for adv

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

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

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

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

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

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

40 Intermittent androgen deprivation can be considered as an alternative

41 Although androgen deprivation can initially lead to remission, th

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

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

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

45 Androgen deprivation constitutes the principal therapy f

46 tion-independent cells compared with that in androgen deprivation-dependent cells.

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

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

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

50 en percent of patients subsequently required androgen deprivation for recurrence after conventional d

51 Intermittent androgen deprivation has been studied as an alternative.

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

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 loratory analysis of a trial of intermittent androgen deprivation (IAD) in men with biochemical relap

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

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

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

59 It is also used for androgen deprivation in hormone-dependent prostate carci

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 Long-term use of androgen deprivation in prostate cancer patients continu

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

64 sociated death domain (TRADD) was reduced in androgen deprivation-independent cells compared with tha

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

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

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

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

69 Androgen deprivation influenced the differentiated pheno

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

71 Androgen deprivation is the mainstay of therapy for prog

72 Androgen deprivation is the standard therapy for patient

73 Furthermore, androgen deprivation led to castration-resistant prostat

74 Correspondingly, androgen deprivation markedly attenuates the frequency a

75 rtion of this variation ranging from 13% for androgen deprivation monotherapy to 74% for cryoablation

76 brachytherapy, 4.0% cryoablation, and 14.4% androgen deprivation monotherapy.

77 trata; older men were more likely to receive androgen deprivation monotherapy.

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

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

80 Androgen deprivation or AR blockage with inhibitor MDV31

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

82 Androgen deprivation or AR inhibition significantly incr

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

84 Androgen deprivation or treatment with androgen receptor

85 Continue androgen deprivation (pharmaceutical or surgical) indefi

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 Finally, we found that androgen deprivation reduces TRADD expression in vitro a

89 F-kappaB demonstrated anti-tumor activity in androgen deprivation-resistant prostate cancer xenograft

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

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

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

93 tion therapy (RT) with or without short-term androgen deprivation (STAD).

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

95 f rat prostate epithelial cells subjected to androgen deprivation (that resulted in loss of nuclear C

96 Androgen deprivation therapies (ADT) directed against th

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

98 Prostate cancers (PCa) that relapse after androgen deprivation therapies [castration-resistant PCa

99 Resistance to androgen deprivation therapies and increased androgen re

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

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

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

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

104 When added to androgen deprivation, therapies demonstrating improved s

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

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

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

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

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

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

111 TMPRSS2:ERG is down-regulated in response to androgen deprivation therapy (ADT) and whether AR reacti

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

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

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

115 Whether androgen deprivation therapy (ADT) causes excess cardiov

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

117 ess likely than African Americans to receive androgen deprivation therapy (ADT) compared with surgery

118 omy (RP) or radiation (RT) were treated with androgen deprivation therapy (ADT) comprised of leuproli

119 Androgen deprivation therapy (ADT) for advanced prostate

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

121 III randomized trial to evaluate neoadjuvant androgen deprivation therapy (ADT) in combination with e

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

123 Androgen deprivation therapy (ADT) increases the risk fo

124 Androgen deprivation therapy (ADT) is a standard adjunct

125 Androgen deprivation therapy (ADT) is first-line therapy

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

127 Androgen deprivation therapy (ADT) is the mainstay treat

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

129 Androgen deprivation therapy (ADT) may contribute to dep

130 Androgen deprivation therapy (ADT) remains a common trea

131 drogens/androgen receptor (AR) functions via androgen deprivation therapy (ADT) remains the standard

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

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

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

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

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

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

138 Androgen deprivation therapy (ADT), an important treatme

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

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

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

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

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

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

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

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

147 ate prostate-specific antigen increase after androgen deprivation therapy (ADT).

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

149 Androgen deprivation therapy (ADT, surgical or medical c

150 Androgen deprivation therapy (ADTh) remains a mainstay o

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

152 ilure (FFBF; P < .001), freedom from salvage androgen deprivation therapy (FFADT; P = .0011), and rel

153 Primary androgen deprivation therapy (PADT) is frequently offere

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

155 d prostate cancer that had progressed during androgen deprivation therapy and did not receive prior t

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

157 Although androgen deprivation therapy appears to increase overall

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

159 on the cardiovascular risks associated with androgen deprivation therapy even when administered for

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

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

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

163 eview the current data on adverse effects of androgen deprivation therapy for prostate cancer and to

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

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

166 Androgen deprivation therapy has been the standard of ca

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

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

169 pite the existing data supporting the use of androgen deprivation therapy in prostate cancer patients

170 androgen receptor that led to the advent of androgen deprivation therapy in the 1940s, there has lon

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

172 Androgen deprivation therapy in the treatment of prostat

173 Treatment of advanced prostate cancer with androgen deprivation therapy inevitably renders the tumo

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

175 numbers are small, the response to adjuvant androgen deprivation therapy is associated with ERG stat

176 Primary androgen deprivation therapy is not associated with impr

177 Androgen deprivation therapy is the major treatment for

178 Androgen deprivation therapy is the most common treatmen

179 Androgen deprivation therapy is the most effective treat

180 In addition, androgen deprivation therapy may be associated with earl

181 ession in vitro and in vivo, suggesting that androgen deprivation therapy may promote the development

182 ant prostate cancer (CRPC) that occurs after androgen deprivation therapy of primary prostate cancer

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

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

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

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

187 Primary androgen deprivation therapy was associated with lower 1

188 Androgen deprivation therapy was continued in both arms.

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

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

191 Androgen deprivation therapy with leuprolide acetate was

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

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

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

195 Almost all prostate cancers recur during androgen deprivation therapy, and new evidence suggests

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

197 Even with stringent androgen deprivation therapy, androgen receptor signalin

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

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

200 vanced prostate cancer patients treated with androgen deprivation therapy, progression of the disease

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

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

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

204 motherapy can improve survival compared with androgen deprivation therapy.

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

206 they become hormone refractory after initial androgen deprivation therapy.

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

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

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

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

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

212 nism of recurrence of prostate cancer during androgen deprivation therapy.

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

214 d are more likely to be managed with primary androgen deprivation therapy.

215 national Japanese registry of men receiving androgen deprivation therapy.

216 oid use, previous osteoporotic fracture, and androgen deprivation therapy.

217 r progression after remission in response to androgen deprivation therapy.

218 tion-independent prostate cancer (PCa) after androgen deprivation therapy.

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

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

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

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

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

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

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

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

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

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

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

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

231 It is not known whether short-term androgen-deprivation therapy (ADT) before and during rad

232 Androgen-deprivation therapy (ADT) for prostate cancer i

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

234 to moderate reductions in reimbursement for androgen-deprivation therapy (ADT) for prostate cancer,

235 Androgen-deprivation therapy (ADT) for the suppression o

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

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

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

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

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

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

242 Androgen-deprivation therapy (ADT) is associated with gr

243 Androgen-deprivation therapy (ADT) is the most common an

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

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

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

247 Androgen-deprivation therapy (ADT) through surgical cast

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

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

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

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

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

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

254 1 (1245C) allele would exhibit resistance to androgen-deprivation therapy (ADT).

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

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

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

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

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 atients treated with salvage radiotherapy or androgen-deprivation therapy for biochemical failure.

264 new vertebral fractures among men receiving androgen-deprivation therapy for nonmetastatic prostate

265 neral density and fractures in men receiving androgen-deprivation therapy for nonmetastatic prostate

266 re us to reevaluate the target and timing of androgen-deprivation therapy for prostate cancer patient

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

268 Androgen-deprivation therapy has been identified to indu

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

270 Androgen-deprivation therapy is a commonly used treatmen

271 While androgen-deprivation therapy is transiently effective in

272 Androgen-deprivation therapy is well-established for tre

273 Prostate cancers that progress during androgen-deprivation therapy often overexpress the andro

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

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

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

277 Androgen-deprivation therapy was used in fewer patients

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

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

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

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

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

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

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

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

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

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

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

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

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

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

292 te cancer (PC) progression and resistance to androgen-deprivation therapy.

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

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

295 Androgen deprivation used adjuvant to radical prostatect

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

300 estramustine, given in addition to standard androgen deprivation, would delay the appearance of cast