ライフサイエンスコーパス: antiandrogen

1 ing hormone-releasing hormone agonist and an antiandrogen.

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

3 iently to necessitate discontinuation of the antiandrogen.

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

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

6 ncreasing on castration therapy including an antiandrogen.

7 rone metabolites and derivatives as a potent antiandrogen.

8 ailure with hormone therapy that included an antiandrogen.

9 ollowing treatment with castration and/or an antiandrogen.

10 al activity is not regulated by androgens or antiandrogens.

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

12 ction with AR are regulated by androgens and antiandrogens.

13 where it can be stabilized by androgens and antiandrogens.

14 nes or growth factors or by cotreatment with antiandrogens.

15 independent of the presence of androgens or antiandrogens.

16 ngs provide insight toward the design of new antiandrogens.

17 activity and reduces the agonist activity of antiandrogens.

18 tribute to this acquired agonist activity of antiandrogens.

19 , because the transactivation was blocked by antiandrogens.

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

21 peutic resistance to taxane chemotherapy and antiandrogens.

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

23 ction, validating the model for detection of antiandrogens.

24 utilized for structure-based design of novel antiandrogens.

25 and restored responsiveness to androgens and antiandrogens.

26 ostate cancer exposed to clinically relevant antiandrogens.

27 n for urothelial bladder cancer therapy with antiandrogens.

28 hrough structural modifications of hydantoin antiandrogens.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 Antiandrogens are initially effective in controlling pro

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

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

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

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

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

67 The antiandrogen bicalutamide is widely used in the treatmen

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

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

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

71 27 loss was also examined in response to the antiandrogen bicalutamide.

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

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

74 (>1 log) potency compared with the standard antiandrogen, bicalutamide, in both binding affinity to

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

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

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

78 Mixtures of antiandrogens can suppress testosterone synthesis in hum

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

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

81 The antiandrogen Casodex blocked the effect of androgen, imp

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

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

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

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

86 m responding to cabazitaxel chemotherapy and antiandrogen combination therapy.

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

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

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

90 Widespread environmental antiandrogen contamination has been associated with nega

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

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

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

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

95 antimineralocorticoid spironolactone and the antiandrogen cyproterone acetate.

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

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

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

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

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

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

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

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

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

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

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

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

108 The antiandrogen flutamide, however, had no discernible impa

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

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

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

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

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

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

115 Antiandrogens given to antagonize androgen receptor (AR)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Antiandrogen-induced autophagy is mediated through the a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 Nonsteroidal antiandrogen monotherapy merits discussion as an alterna

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

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

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

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

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

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

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

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

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

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

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

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

161 4E (eIF4E) phosphorylation, while the use of antiandrogens relieved this suppression, thereby trigger

162 To circumvent antiandrogen resistance in prostate cancer, antiandrogen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 Antiandrogens target ligand-binding domain of androgen r

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

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

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

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

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

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

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

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

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

189 pment of resistance to androgen ablation and antiandrogen therapies.

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

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

192 Immediate antiandrogen therapy after radical prostatectomy and pel

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

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

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

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

197 Resistance to antiandrogen therapy in patients with metastatic prostat

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

199 Antiandrogen therapy is only palliative, and chemotherap

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

201 Nonsteroidal antiandrogen therapy may be discussed as an alternative,

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

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

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

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

206 Whether antiandrogen therapy with radiation therapy will further

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

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

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

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

211 rogen receptor expression and sensitivity to antiandrogen therapy.

212 approach for extending clinical responses to antiandrogen therapy.

213 Survivin via AKT could mediate resistance to antiandrogen therapy.

214 upporting a novel mechanism of resistance to antiandrogen therapy.

215 ciated with the development of resistance to antiandrogen therapy.

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

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

218 dditional loss of Trp53 causes resistance to antiandrogen therapy.

219 om a patient with disease progression during antiandrogen therapy.

220 eficiency was apparent in patients receiving antiandrogen therapy.

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

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

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

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

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

226 Antiandrogen treatment also altered the expression of mu

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

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

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

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

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

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

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

234 way of assessing prostatic tumor response to antiandrogen treatment.

235 Conversely, antiandrogens up-regulate PSMA expression.

236 .92; P = .001) with each additional month of antiandrogen use after analysis was adjusted for these k

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

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

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

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

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

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

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

244 Flutamide is a novel antiandrogen with fewer side effects.

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

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

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

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

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

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

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

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

253 The utility of antiandrogen withdrawal in patients with progressive dis

254 Antiandrogen withdrawal is efficacious in approximately

255 Antiandrogen withdrawal is now a mandatory maneuver befo

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

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

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

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

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

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

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

263 to respond to hormonal maneuvers even after antiandrogen withdrawal.

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

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