ライフサイエンスコーパス: antiandrogen

1 ollowing treatment with castration and/or an antiandrogen.

2 ing hormone-releasing hormone agonist and an antiandrogen.

3 h less than as compared with 6 months of the antiandrogen.

4 iently to necessitate discontinuation of the antiandrogen.

5 owth and decreased sensitivity (>3.5x) to an antiandrogen.

6 ro-2,2-bis(p-chlorophenyl)ethylene (DDE), an antiandrogen.

7 ncreasing on castration therapy including an antiandrogen.

8 rone metabolites and derivatives as a potent antiandrogen.

9 ailure with hormone therapy that included an antiandrogen.

10 ts, and the suppression was attenuated by an antiandrogen.

11 ostate cancer exposed to clinically relevant antiandrogens.

12 n for urothelial bladder cancer therapy with antiandrogens.

13 hrough structural modifications of hydantoin antiandrogens.

14 al activity is not regulated by androgens or antiandrogens.

15 here is a need to find novel and more potent antiandrogens.

16 ction with AR are regulated by androgens and antiandrogens.

17 where it can be stabilized by androgens and antiandrogens.

18 nes or growth factors or by cotreatment with antiandrogens.

19 independent of the presence of androgens or antiandrogens.

20 ngs provide insight toward the design of new antiandrogens.

21 activity and reduces the agonist activity of antiandrogens.

22 tribute to this acquired agonist activity of antiandrogens.

23 , because the transactivation was blocked by antiandrogens.

24 including prostate cancer in the presence of antiandrogens.

25 eptor (AR) and are potentially responsive to antiandrogens.

26 peutic resistance to taxane chemotherapy and antiandrogens.

27 sm-based environmental screening of pro- and antiandrogens.

28 ction, validating the model for detection of antiandrogens.

29 utilized for structure-based design of novel antiandrogens.

30 and restored responsiveness to androgens and antiandrogens.

31 ere then treated with placebo, flutamide (an antiandrogen; 33 mg/kg/day), or toremifene (10 mg/kg/day

32 e identified and confirmed the highly potent antiandrogen 4-methyl-7-diethylaminocoumarin (C47) and t

33 H agonists (0% to 4%) than with nonsteroidal antiandrogens (4% to 10%).

34 From 2006 to 2012, 10,656 men were on antiandrogens (AA), 26,959 were on gonadotropin-releasin

35 The mechanisms of how antiandrogens acquire this agonist activity during hormo

36 Despite the development of second-generation antiandrogens, acquired resistance to hormone therapy re

37 Next-generation antiandrogens act through inhibiting androgen synthesis

38 ed, progesterone generally is regarded as an antiandrogen, acting centrally to inhibit sexual behavio

39 related to the estrogen, glucocorticoid, and antiandrogen activities), reactive modes of action (geno

40 as an androgen-dependent tumor, agents with antiandrogen activity have become the focus for chemopre

41 rogen synthesis and, in some cases, to exert antiandrogen activity, did in fact translate to an inhib

42 ng hormone-releasing hormone analogue and an antiandrogen agent for 7 months.

43 ients receiving a standard, first-generation antiandrogen agent with a falling PSA level at the time

44 Among these drugs, a second-generation antiandrogen agent, enzalutamide, was proposed because i

45 o the progression of glioblastoma (GBM), and antiandrogen agents have the potential to be used for th

46 nd 39 have been identified as a new class of antiandrogen agents, and these compounds or their new sy

47 Current therapies include the use of antiandrogens aimed at inhibiting the transcriptional ac

48 riazole core in the scaffold of nonsteroidal antiandrogens allowed the development of small molecules

49 The novel antiandrogen and AR activities of decursin and decursin-

50 ort the discovery of strong and long-lasting antiandrogen and AR activities of the ethanol extract of

51 , we identified decursin from AGN as a novel antiandrogen and AR compound with an IC50 of approximate

52 drogen, ligand-occupied GR acts as a partial antiandrogen and attenuates the AR-dependent transcripti

53 Conversely, 4 months of antiandrogen and estrogen treatment in male-to-female tr

54 maging techniques to track tumor response to antiandrogen and rapamycin treatment in a prostate-speci

55 esistant prostate carcinoma progressing with antiandrogen and taxane therapy was treated with lutetiu

56 Preoperative treatment with oral antiandrogens and 5-reductase inhibitors appears to redu

57 monal therapies, mainly with combinations of antiandrogens and androgen deprivation, are the mainstay

58 cancer cells and that a combined therapy of antiandrogens and anti-PI3K/Akt inhibitors may be worth

59 s in the understanding of the optimal use of antiandrogens and managing treatment-induced erectile dy

60 ntribute to the acquired agonist activity of antiandrogens and plays an important role in making pros

61 ferase assay further demonstrates that these antiandrogens and related compounds significantly enhanc

62 lecular rationale for the development of new antiandrogens and selective AR modulators.

63 fect was observed when LX1 was combined with antiandrogens and taxanes, indicating the potential for

64 Aromatase inhibitors together with an antiandrogen appear to be a very promising treatment for

65 ion aromatase inhibitors in combination with antiandrogens appear effective in preventing bone age ad

66 as observed when AR signaling was blocked by antiandrogens, AR RNA interference, or targeted disrupti

67 Molecular dynamics simulations performed on antiandrogen-AR complexes suggested a mechanism by which

68 Traditional models for in vivo evaluation of antiandrogens are cumbersome because they rely on physio

69 Antiandrogens are initially effective in controlling pro

70 ding certain estrogens, progestins, and even antiandrogens as androgens.

71 Using the antiandrogen Bicalutamide (Casodex((R))), which slows do

72 comparable to that produced by the synthetic antiandrogen bicalutamide (Casodex) at the same concentr

73 K1 IC(50)=26 microM), in comparison with the antiandrogen bicalutamide (Casodex) in AIPC cells.

74 The use of the antiandrogen bicalutamide (Casodex) rescued LNCaP cells

75 The antiandrogen bicalutamide is widely used in the treatmen

76 whereas suppression of AR activity with the antiandrogen bicalutamide sensitized androgen-dependent,

77 r relative affinity than the clinically used antiandrogen bicalutamide, reduce the efficiency of its

78 27 loss was also examined in response to the antiandrogen bicalutamide.

79 ed the AR, an effect that was blocked by the antiandrogen bicalutamide.

80 d radiolabeled several analogs of the potent antiandrogen bicalutamide: [18F]bicalutamide, 4-[76Br]br

81 ependent prostate cancer is the nonsteroidal antiandrogen, bicalutamide, either as monotherapy or wit

82 (>1 log) potency compared with the standard antiandrogen, bicalutamide, in both binding affinity to

83 DI PCa cells was completely resistant to the antiandrogen, bicalutamide.

84 drogen receptor (AR) by androgen ablation or antiandrogens, but unfortunately, it is not curative.

85 ls of androgen receptor confer resistance to antiandrogens by amplifying signal output from low level

86 Mixtures of antiandrogens can suppress testosterone synthesis in hum

87 argeted therapy, including GnRH agonists and antiandrogens, cannot completely shut down AR signaling.

88 ivity to the growth-inhibitory action of the antiandrogen Casodex and inhibits anchorage-independent

89 The antiandrogen Casodex blocked the effect of androgen, imp

90 androgen receptor (AR) in these cells by the antiandrogen casodex or by the anti-AR small interfering

91 ty compared with untreated controls, and the antiandrogen, casodex, inhibited the mibolerone-stimulat

92 n kinase (Erk/MAPK) kinase (MEK); or (c) the antiandrogen, Casodex; or when the cells were cultured u

93 Unlike the clinically important antiandrogens, casodex and hydroxyflutamide, both D36 an

94 m responding to cabazitaxel chemotherapy and antiandrogen combination therapy.

95 onadotropin-releasing hormone agonists, oral antiandrogens, combined androgen blockade, bilateral orc

96 cally involves administration of "classical" antiandrogens, competitive inhibitors of androgen recept

97 A subset of antiandrogen compounds, the N-aryl-3,3,3-trifluoro-2-hyd

98 Widespread environmental antiandrogen contamination has been associated with nega

99 In contrast, hydroxyflutamide (HF), an antiandrogen currently used to treat prostate cancer pat

100 ehyde conjugate tethered to the nonsteroidal antiandrogen, cyanonilutamide (RU 56279), for the treatm

101 Second-line hormonal therapy (eg, antiandrogens, CYP17 inhibitors) may be considered in pa

102 The agonist activity of the antiandrogen cyproterone acetate was abolished in ebp1 t

103 antimineralocorticoid spironolactone and the antiandrogen cyproterone acetate.

104 t these tumors can develop resistance to the antiandrogen drug enzalutamide by a phenotypic shift fro

105 o the antiprogestin, antiglucocorticoid, and antiandrogen drug mifepristone (RU486).

106 of metastatic prostate cancer consists of an antiandrogen drug plus castration.

107 eride, as SRD5A2 inhibitors, are widely used antiandrogen drugs for benign prostate hyperplasia.

108 nts are not inhibited by currently available antiandrogen drugs, development of new drugs targeting t

109 antiandrogen resistance in prostate cancer, antiandrogens effective for both the androgen receptor (

110 Ketoconazole or antiandrogens (eg, bicalutamide, flutamide, nilutamide)

111 In prostate cancer, resistance to the antiandrogen enzalutamide (Enz) can occur through bypass

112 While the antiandrogen enzalutamide (Enz) extends the castration r

113 The antiandrogen enzalutamide (Enz) has improved survival in

114 ried to find new treatment strategy based on antiandrogen enzalutamide (Enz).

115 tumors develop resistance to new-generation antiandrogen enzalutamide through lineage plasticity, ch

116 X' prostate cancer model is resistant to the antiandrogen enzalutamide via activation of an alternati

117 The second-generation antiandrogen enzalutamide was recently approved for pati

118 n a previous trial, we found that adding the antiandrogen flutamide to leuprolide acetate (a syntheti

119 iestrogen tamoxifen or with the nonsteroidal antiandrogen flutamide to probe for additional evidence

120 ine whether the cellular accumulation of the antiandrogen flutamide, a drug commonly used in the trea

121 The antiandrogen flutamide, however, had no discernible impa

122 sactivation by AR and further suppresses the antiandrogen flutamide-mediated inhibition of AR activit

123 erone (Schering AG) is clinically used as an antiandrogen for inoperable prostate cancer, virilizing

124 might facilitate the development of a better antiandrogen for the treatment of prostate cancer.

125 yflutamide, which is the currently available antiandrogen for the treatment of prostate cancer.

126 Development of resistance to antiandrogens for treating advanced prostate cancer is a

127 ndrogen receptor (AR) activity modulation by antiandrogens from fluid biopsies.

128 he common A-ring-linkage-B-ring nonsteroidal antiandrogens' general pharmacophore allowed the develop

129 Antiandrogens given to antagonize androgen receptor (AR)

130 Although enhanced UGT2B17 expression by antiandrogens has been reported in androgen-dependent pr

131 Although hormone therapy with antiandrogens has been widely used for the treatment of

132 The majority of available antiandrogens have been reported to possess agonist acti

133 Antiandrogens have been used in the treatment of HS, and

134 Because ARA70 can promote the antiandrogen hydroxyflutamide (HF)-enhanced AR transacti

135 with androgenic activity and that two potent antiandrogens, hydroxyflutamide (Eulexin) and bicalutami

136 Because two potent antiandrogens, hydroxyflutamide (Eulexin), and bicalutam

137 g mammalian two-hybrid assay, we report that antiandrogens, hydroxyflutamide, bicalutamide (casodex),

138 t in survival should be offered nonsteroidal antiandrogen in addition to castrate therapy.

139 tudies have reported that linuron acts as an antiandrogen in vitro and in vivo and disrupts mammalian

140 activity and rescues the normal function of antiandrogens in prostate cancer cells.

141 rtaken to test the efficacy of flutamide (an antiandrogen) in the transgenic adenocarcinoma of the mo

142 ion that W-7 was as effective as Casodex, an antiandrogen, in blocking AR-regulated expression of pro

143 hRNA or G(alphai)-shRNA, and not the classic antiandrogens including enzalutamide, bicalutamide, or h

144 tients and can be observed with a variety of antiandrogens, including flutamide, bicalutamide, and me

145 In 3D monocultures, antiestrogens and antiandrogens induced anoikis by abrogating anchorage-in

146 Antiandrogen-induced autophagy is mediated through the a

147 s and dose responsive reduction of classical antiandrogen-induced prostate specific antigen expressio

148 signaling pathway, including more effective antiandrogens, inhibitors of CYP17, an enzyme required f

149 mutations in androgen receptor (AR) convert antiandrogens into AR agonists, promoting prostate tumor

150 ates may be somewhat lower if a nonsteroidal antiandrogen is used as monotherapy.

151 Although the therapeutic potential of these antiandrogens is apparent, it is the demonstration that

152 l androgen suppression and discontinuance of antiandrogens is recommended for men receiving chemother

153 Functionalization of API nilutamide (antiandrogen) is also reported.

154 Bicalutamide, a nonsteroidal antiandrogen, is widely used to treat men with nonmetast

155 and 4-pyridylsulfonyl moieties, yielded non-antiandrogen, KATP potassium channel openers (39, 41, an

156 After the initial response, antiandrogens lose their efficacy and eventually act as

157 d for the treatment of prostate cancer, some antiandrogens may act as androgen receptor (AR) agonists

158 expression in response to treatment with the antiandrogen MDV3100, can be quantitatively measured in

159 oral androgens is a novel mechanism by which antiandrogens mediate their effects in CRPC.

160 resistance to cabazitaxel can be overcome by antiandrogen-mediated EMT-MET cycling in androgen-sensit

161 es were measured in mice, in patients taking antiandrogen medications, and in age-matched human contr

162 results suggest that the agonist activity of antiandrogens might occur with the proper interaction of

163 the data indicate that, besides blocking AR, antiandrogens modify androgen signaling in CR-VCaP xenog

164 Nonsteroidal antiandrogen monotherapy merits discussion as an alterna

165 rits discussion as an alternative; steroidal antiandrogen monotherapy should not be offered.

166 for prostate cancer, including non-steroidal antiandrogen monotherapy.

167 ogen receptor (AR) that enable activation by antiandrogens occur in hormone-refractory prostate cance

168 ry limited space for a tether connecting the antiandrogen on the inside to the cytotoxin on the outsi

169 For previous antiandrogens, one mechanism of resistance is mutation o

170 ased on these results, but NAs act as potent antiandrogen or antiestrogens.

171 otropin-releasing hormone agonists with oral antiandrogens (OR, 4.50 [95% CI, 2.61-7.78]), estrogens

172 tested the cancer-inducing potential of the antiandrogen, p,p -DDE [1,1-dichloro-2,2-bis(p-chlorophe

173 of nonsteroidal compounds derived from known antiandrogen pharmacophores and to investigate the struc

174 veloped BF3 ligands demonstrated significant antiandrogen potency against LNCaP and Enzalutamide-resi

175 ws cellular proliferation in the presence of antiandrogens, prostate-specific antigen assay and trans

176 flow cytometry and microscopy of cells after antiandrogen-, radio-, and chemotherapy in LNCaP and PC3

177 4E (eIF4E) phosphorylation, while the use of antiandrogens relieved this suppression, thereby trigger

178 We identified CHD1 loss as a cause of antiandrogen resistance in an in vivo small hairpin RNA

179 er-associated fibroblasts (CAFs) can promote antiandrogen resistance in mouse models and in prostate

180 This work reveals a paracrine mechanism of antiandrogen resistance in prostate cancer amenable to c

181 To circumvent antiandrogen resistance in prostate cancer, antiandrogen

182 receptor (AR) is an established mechanism of antiandrogen resistance in prostate cancer.

183 c alterations, here we show that GR-mediated antiandrogen resistance is adaptive and reversible due t

184 nal plasticity that enables the emergence of antiandrogen resistance through heterogeneous mechanisms

185 ion or expression level, also contributes to antiandrogen resistance, through upregulation of the coa

186 POU3F2, NR2F1, and TBX2) that contribute to antiandrogen resistance, with associated activation of n

187 ics potential of autophagy inhibitors in the antiandrogen-resistance setting.

188 ather than clonal expansion of castration or antiandrogen-resistant cells expressing gain of function

189 ein levels in prostate cancer may facilitate antiandrogen-resistant disease.

190 ation of both androgen-dependent (LNCaP) and antiandrogen-resistant prostate cancer cells (LNCaP-B),

191 hat reduced CSE/H2S signaling contributes to antiandrogen-resistant status, and sufficient level of H

192 sed chemical screen which, based on existing antiandrogen scaffolds, identified three novel compounds

193 Thus, treatment with antiandrogens selects for gain-of-function AR mutations

194 e discussed as an alternative, but steroidal antiandrogens should not be offered as monotherapy.

195 t of the commercially available nonsteroidal antiandrogens show a common scaffold consisting of two a

196 This novel antiandrogen showed an increased (>1 log) potency compar

197 Antiandrogen strategies remain the prostate cancer treat

198 Next generation antiandrogens such as enzalutamide (Enz) are effective i

199 nist effects, as compared with commonly used antiandrogens such as hydroxyflutamide and bicalutamide,

200 All current antiandrogens, such as Bicalutamide, Flutamide, Nilutami

201 is blocked by ligand binding domain-targeted antiandrogens, such as MDV3100, or by selective siRNA si

202 m that is distinct from clinically available antiandrogens, such that it might inform novel methods t

203 signaling by means of androgen withdrawal or antiandrogen suppressed the growth of LAPC-4 cells to a

204 Antiandrogens target ligand-binding domain of androgen r

205 es in the dose-response curves of individual antiandrogens that became more pronounced as the number

206 valuated mixtures composed of four and eight antiandrogens that contained the pharmaceuticals ketocon

207 nds optimized from a screen for nonsteroidal antiandrogens that retain activity in the setting of inc

208 itor of androgen synthesis (CYP17 inhibitor)/antiandrogen) that is significantly more effective than

209 that Survivin can mediate resistance to such antiandrogen therapies based on our assays.

210 Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology wit

211 strategy for sequencing between androgen and antiandrogen therapies in metastatic castration-resistan

212 -free survival rate for the CRPC patients on antiandrogen therapies is only 8-19 months.

213 rostate cancer has been transformed by novel antiandrogen therapies such as enzalutamide.

214 Resistance invariably develops to antiandrogen therapies used to treat newly diagnosed pro

215 aling and will respond to potent second-line antiandrogen therapies, including bicalutamide (CASODEX(

216 gh there has been substantial advancement in antiandrogen therapies, resistance to these treatments r

217 pment of resistance to androgen ablation and antiandrogen therapies.

218 g those resistant to androgen deprivation or antiandrogen therapies.

219 and potentially extend clinical response to antiandrogen therapies.

220 undergo radiation therapy and receive either antiandrogen therapy (24 months of bicalutamide at a dos

221 in detection efficacy was present regarding antiandrogen therapy (P = 0.0783).

222 abel enzalutamide or a standard nonsteroidal antiandrogen therapy (standard-care group).

223 Immediate antiandrogen therapy after radical prostatectomy and pel

224 mly assigned patients who had never received antiandrogen therapy and who had distant metastases from

225 Although initially successful, antiandrogen therapy eventually fails and androgen deple

226 use the optimal timing of the institution of antiandrogen therapy for prostate cancer is controversia

227 It is hypothesized that administration of antiandrogen therapy in an intermittent, as opposed to c

228 Resistance to antiandrogen therapy in patients with metastatic prostat

229 eting of Survivin may enhance sensitivity to antiandrogen therapy in prostate cancer.

230 Antiandrogen therapy is only palliative, and chemotherap

231 on therapy, brachytherapy, and cryosurgery), antiandrogen therapy management of erectile dysfunction,

232 Nonsteroidal antiandrogen therapy may be discussed as an alternative,

233 growth and survival and that treatment with antiandrogen therapy provides selective pressure and alt

234 et for developing therapeutic agents for the antiandrogen therapy that almost always fails in the tre

235 iochemically motivated mathematical model of antiandrogen therapy that can be tested prospectively as

236 The addition of 24 months of antiandrogen therapy with daily bicalutamide to salvage

237 Whether antiandrogen therapy with radiation therapy will further

238 de treatment is poorly responsive to further antiandrogen therapy, and paradoxically, rapid cycling b

239 mechanism of resistance to second-generation antiandrogen therapy, highlighting the therapeutic poten

240 llular plasticity that, when challenged with antiandrogen therapy, promotes resistance through lineag

241 which tends to be accelerated by the current antiandrogen therapy, we identify Peruvoside, a cardiac

242 were randomly assigned to receive immediate antiandrogen therapy, with either goserelin, a synthetic

243 ve an inferior response to second-generation antiandrogen therapy.

244 Survivin via AKT could mediate resistance to antiandrogen therapy.

245 upporting a novel mechanism of resistance to antiandrogen therapy.

246 ciated with the development of resistance to antiandrogen therapy.

247 cells resistant to androgen ablation and/or antiandrogen therapy.

248 tients treated with androgen ablation and/or antiandrogen therapy.

249 om a patient with disease progression during antiandrogen therapy.

250 eficiency was apparent in patients receiving antiandrogen therapy.

251 rogen receptor expression and sensitivity to antiandrogen therapy.

252 dditional loss of Trp53 causes resistance to antiandrogen therapy.

253 approach for extending clinical responses to antiandrogen therapy.

254 as hydroxyflutamide (HF) has been used as an antiandrogen to block androgen-stimulated prostate tumor

255 The tether served to attach the antiandrogen to the doxorubicin-formaldehyde conjugate v

256 antiandrogen withdrawal syndrome that allows antiandrogens to stimulate prostate tumor growth still o

257 old, P < 0.01) were further increased in the antiandrogen-treated tumors.

258 Herein, we show that antiandrogen treatment (enzalutamide or ARN-509) signifi

259 Antiandrogen treatment also altered the expression of mu

260 e, two, and three months after initiation of antiandrogen treatment are analysed using the mono-expon

261 he first time that targeting mTOR along with antiandrogen treatment exhibited additive antitumor effe

262 Given the near universal prevalence of antiandrogen treatment failure in the absence of competi

263 ollow-up, 7 of 47 men who received immediate antiandrogen treatment had died, as compared with 18 of

264 ession is inversely modulated by androgen or antiandrogen treatment in androgen-sensitive prostate ca

265 izing hormone-releasing hormone agonist with antiandrogen treatment to add (arm 1) or not (arm 2) iso

266 Eleven of the 14 had prior second-line antiandrogen treatment with abiraterone or enzalutamide,

267 herapy and antiandrogen withdrawal (if prior antiandrogen treatment), were randomized to receive vinb

268 way of assessing prostatic tumor response to antiandrogen treatment.

269 Conversely, antiandrogens up-regulate PSMA expression.

270 .92; P = .001) with each additional month of antiandrogen use after analysis was adjusted for these k

271 include antiandrogen withdrawal, sequential antiandrogen use, adrenal androgen production inhibitors

272 was significantly associated with months of antiandrogen use; regression analysis adjusted for known

273 Cyproterone acetate (CPA) is a steroidal antiandrogen used clinically in the treatment of prostat

274 e blocked completely by hydroxyflutamide, an antiandrogen used in the treatment of prostate cancer.

275 ing 2717 patients suggests that nonsteroidal antiandrogens were associated with lower overall surviva

276 nes was synthesized, and their activities as antiandrogens were tested in the human prostate cancer c

277 en withdrawal (if previously treated with an antiandrogen) were enrolled onto this phase II trial.

278 e3) as an essential epigenetic adaptation to antiandrogens, which enabled transcriptional silencing o

279 Flutamide is a novel antiandrogen with fewer side effects.

280 led to the identification of a nonsteroidal antiandrogen with improved AR antagonism and marked redu

281 preclinical data suggest that combination of antiandrogens with mTOR inhibitors might be more effecti

282 of testosterone (77%) and progression after antiandrogen withdrawal (97%) should be documented befor

283 Antiandrogen withdrawal (AAWD) results in a prostate-spe

284 spite hormonal therapy and who had undergone antiandrogen withdrawal (if previously treated with an a

285 ncer, progressive after hormonal therapy and antiandrogen withdrawal (if prior antiandrogen treatment

286 tate tumor were obtained from men undergoing antiandrogen withdrawal for AR sequence analysis and cli

287 Eligible men enrolled on a trial of antiandrogen withdrawal had a minimum prostate-specific

288 The utility of antiandrogen withdrawal in patients with progressive dis

289 Antiandrogen withdrawal is efficacious in approximately

290 Antiandrogen withdrawal is now a mandatory maneuver befo

291 Correlation of AR mutation with antiandrogen withdrawal response or survival could not b

292 on between detectability of AR mutations and antiandrogen withdrawal response or survival.

293 drogen-stimulated prostate tumor growth, the antiandrogen withdrawal syndrome that allows antiandroge

294 tate-specific antigen, which might result in antiandrogen withdrawal syndrome.

295 en receptor (AR) agonists that may result in antiandrogen withdrawal syndrome.

296 ne or more hormonal therapies and a trial of antiandrogen withdrawal were enrolled onto this phase II

297 patients have rapidly progressed and include antiandrogen withdrawal, sequential antiandrogen use, ad

298 to respond to hormonal maneuvers even after antiandrogen withdrawal.

299 s may provide a good model to develop better antiandrogens without agonist activity.

300 in combination with GnRH analogs and potent antiandrogens, would represent a powerful future strateg