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1 ) in obese male Zucker rats, both intact and castrated.
2 testosterone-induced restoration paradigm in castrates.
3 aP tumors with or without NE allografts were castrated 2 weeks after NE tumor inoculation, and change
4 ales, and saporin-treated males who had been castrated 6 weeks previously and given testosterone repl
5                                              Castrated adult male hamsters were subjected to right sp
6 Androgen target tissue uptake was evident in castrated adult male rats; however, in DES-treated, AR-p
7                    To address this issue, we castrated adult male white-crowned sparrows and rapidly
8 n(-/-) mice and rescued effector function in castrated and immunized wild-type mice.
9  season in adult male green anoles that were castrated and implanted with either testosterone (T) or
10  of apoE4 on cognitive function in males, we castrated and sham-castrated apoE4, apoE3, and Apoe-/- m
11 e mice that were gonad-intact, castrated, or castrated and treated with estradiol implants.
12 d males were both demasculinized (chemically castrated) and completely feminized as adults.
13 PCa, but patients invariably relapse despite castrate androgen levels (castration-resistant PCa, CRPC
14                              Consistent with castrate androgen levels, androgen-regulated genes were
15                                         When castrated animals are maintained, the emergence of andro
16                                     Thus, in castrated animals bearing MDA-PCa-2b cancers, the admini
17 e tmeff2 transcription, androgen delivery to castrated animals carrying CWR22 xenografts increases TM
18 ell as the corticosterone response to LPS in castrated animals that had had their testes intact over
19               In the gastrocnemius muscle of castrated animals, HB treatment significantly increased
20 d promote prostate xenograft tumor growth in castrated animals.
21                                              Castrated ApoE(-/-):Ins2(+/Akita) mice showed a reductio
22 ive function in males, we castrated and sham-castrated apoE4, apoE3, and Apoe-/- male mice and behavi
23     On the contrary, castrated, but not sham-castrated, apoE4 mice showed improved acquisition over t
24             Accordingly, these cells grew in castrated as well as intact male mice.
25 grin is required for tumor growth in vivo of castrated as well as of noncastrated mice.
26 weeks of age; in the second group, mice were castrated at 10 weeks of age, allowed to recover for 10
27     Performance in adult males that had been castrated at birth was still enhanced by exposure to an
28 ondrial DNA-deficient cells formed tumors in castrated athymic mice, whereas LNCaP did not.
29 r the administration of 17-beta-estradiol to castrated B6 male mice as compared with nonoperated male
30 unized BALB/c, BALB/cBy, IL-6-deficient, and castrated BALB/c mice with trifluoroacetyl chloride-hapt
31 elease over the 24 h period in adult animals castrated before puberty in contrast to animals castrate
32                             On the contrary, castrated, but not sham-castrated, apoE4 mice showed imp
33 ment partially reduced OS in VP epithelia of castrates, but the level remained higher than in intact
34  of estradiol benzoate (OVX+E), OVX females, castrated (CAST) males, and intact males.
35                                  Sixty-eight castrate, chemotherapy-naive men with HRPC were enrolled
36 ntratumoral androgen levels when passaged in castrate compared with eugonadal animals.
37 evious second-line hormonal therapies, and a castrate concentration of testosterone.
38 astration-resistant prostate cancer, who had castrate concentrations of testosterone and an Eastern C
39  SVs that provide a survival advantage under castrate conditions, enabling resistance to hormone ther
40  regulators was shown to promote survival in castrate conditions-mimicking first line treatment resis
41 gression to CRPC by sensitising PC cells to 'castrate' conditions-that is, low levels of testicular a
42 on vs. intact control, P < 0.01; and 68% vs. castrated control, P < 0.05).
43 on vs. intact control, P < 0.01; and 75% vs. castrated control, P < 0.05).
44   F18-fluorodihydrotestosterone is active in castrate disease and is emerging as a valuable pharmacod
45 ication of time to hormone refractoriness in castrate disease and overall survival.
46 l. show that germ-free mice, when chemically castrated, do not lose bone - a finding that unequivocal
47  epithelial proliferation in both intact and castrated EAF2-/-Pten+/- mice.
48                                 Animals were castrated either prepubertally (28 days) or in adulthood
49 n sources may sustain tumor growth despite a castrate environment.
50 s conferred by the selective pressure of the castrate environment.
51       We discovered that small arteries from castrated Ephb6 gene KO males showed increased contracti
52                Consistent with this finding, castrated Ephb6 KO mice presented heightened BP compared
53 econd experiment, male whiptail lizards were castrated for 1 week or for 6 weeks.
54 Male Japanese macaques (Macaca fuscata) were castrated for 5-7 months and then treated for 3 months w
55 differences in sexual behavior in intact and castrated geckos.
56  development and resist androgen ablation in castrated hosts, and they harbor highly tumorigenic cast
57 nsferred quantified precursors into congenic castrated hosts.
58 trated before puberty in contrast to animals castrated in adulthood in which testosterone significant
59 ompared between long and short days, between castrated, intact, and castrated with testosterone repla
60 re effective in restoring sexual activity in castrated KN males than IL males.
61 ty is generally restored in CRPC despite the castrate level of androgens, it is unclear whether AR si
62 evels of testosterone on day 4, and profound castrate levels (<20 ng per deciliter) on day 15.
63 nt was sustained testosterone suppression to castrate levels (<50 ng per deciliter) through 48 weeks.
64  that reduce circulating androgen ligands to castrate levels and/or block ligand binding.
65 ors; however, tumors that can proliferate in castrate levels of androgen eventually arise.
66 ndrogen receptor activation persists despite castrate levels of circulating androgens.
67 on complex facilitates reactivation by AR at castrate levels of ligand.
68 1 month prior to 3 of 4 trial days to induce castrate levels of T.
69 or survival and time to progression if lower castrate levels of testosterone (< 0.7 nmol/L) are achie
70         Prostate cancers progressing despite castrate levels of testosterone are considered castratio
71              The percentage of patients with castrate levels of testosterone on day 4 was 56.0% with
72 ority with respect to the primary end point, castrate levels of testosterone on day 4, and profound c
73                                         When castrated long day-housed mice were provided with long d
74 ion of 10b suppressed luteinizing hormone in castrated macaques.
75 eks' gestation, n = 6) were xenografted into castrate male nude mice which were then treated for 35 d
76                                              Castrate male rats were subjected to behavioral tests af
77  sex behaviors toward an estrous female or a castrated male (presented in separate tests), again, whe
78 BM of all the sham shock groups and with the castrated male and both female rat groups subjected to T
79                                           In castrated male and female GPR-4 rats, the LH pulse frequ
80                                              Castrated male B6 mice showed higher lipopolysaccharide-
81  MBP-primed T cells isolated from female and castrated male but not from male mice induced the expres
82    However, MBP-primed T cells of female and castrated male but not male mice induced microglial acti
83  MBP-primed T cells isolated from female and castrated male but not male mice were capable of inducin
84 ants in the medial preoptic nucleus (POM) of castrated male canaries (Serinus canaria) increase song
85    Moreover, oral administration of R-13b to castrated male cynomolgus monkeys resulted in a signific
86 ine the response of the SNB in prepubertally castrated male gerbils receiving delayed hormone replace
87                                        Eight castrated male Holstein calves received a single oral do
88                      In contrast, female and castrated male MBP-primed T cells expressed both alpha4
89  maze arms and arms that contained intact or castrated male mice and partially prevented loss of this
90  (CFW) female resident mice were housed with castrated male mice and tested for aggression toward fem
91     Reversal of nigrostriatal pathologies in castrated male mice by subcutaneous implantation of 5alp
92                                  Analysis of castrated male mice from other strains (A/J, DBA/2J, AKR
93 ed renal CYP2J5 expression, and treatment of castrated male mice or female mice with 5alpha-dihydrote
94 ation-recurrent CWR22R tumor-bearing athymic castrated male mice produced a 28-fold increase in intra
95  and alpha-synuclein were higher in nigra of castrated male mice than normal male mice.
96 gly, MBP-primed T cells of male, female, and castrated male mice were able to induce microglial activ
97 , treatment of ovariectomized female mice or castrated male mice with 17beta-estradiol causes a furth
98 ed splenic IL-6 and serum estrogen levels in castrated male mice, and IL-6 induction by 17beta-estrad
99 protein (MBP)-primed T cells from female and castrated male mice, but not from male mice, produced pr
100                        Here, we show that in castrated male mice, neutrophil maturation and function
101 e effectively normalized the tumor burden in castrated male mice.
102 of 17beta-estradiol on acute wound repair in castrated male mice.
103 in (MBP)-primed T cells of male, female, and castrated male mice.
104 neurons appeared in the SNB of prepubertally castrated male Mongolian gerbils within 2 days of the st
105                                Housed with a castrated male mouse, most intact resident CFW females r
106 rotein and mRNA in the female and neonatally castrated male MPN on PN 4, indicating that the neonatal
107                                              Castrated male piglets born to sows fed a vitamin A-depl
108                                              Castrated male pigs (n = 34) were treated with physiolog
109       The population consisted of female and castrated male pigs that were sired by boars represented
110  healthy, anesthetized juvenile (2-3 months) castrated male pigs.
111 uration of action was also determined in the castrated male rat assay to measure the extent (efficacy
112                                In a standard castrated male rat model, several compounds showed good
113 ormone release over time was measured in the castrated male rat.
114 y intact male rats, LES was seen reliably in castrated male rats and in female rats, although it fluc
115 uring clonogenic growth of BM progenitors in castrated male rats and in ovariectomized and proestrus
116 80%) release for >72 h after sc injection to castrated male rats at a standard dose of 50 mug/rat in
117 ay), or vehicle were administered acutely to castrated male rats that bore subcutaneous (sc) dihydrot
118 sent in male rats after T/HS is also lost in castrated male rats.
119 is not observed in proestrus female rats and castrated male rats.
120 rmacologic activity of selected compounds in castrated male rats.
121        We housed photostimulated, intact and castrated male starlings with a female or alone.
122 rred to mount an estrous female instead of a castrated male.
123 n stimulation reward in gonadally intact and castrated males and in females at estrous cycle stages a
124                                              Castrated males and those receiving the competitive andr
125 ay hyperresponsiveness was also decreased in castrated males and was increased in females administere
126  effect was transient in females paired with castrated males but more persistent in those with vasect
127                                              Castrated males developed more severe hepatitis than did
128                                              Castrated males had significantly greater numbers of GnR
129                                   T-replaced castrated males injected centrally with mixed arginine v
130 early- or late-postnatally transected males, castrated males left untreated or treated with estradiol
131                                    Untreated castrated males served as an additional control group.
132 ricularly (ICV) or systemically to intact or castrated males with or without concomitant androgen rep
133                                  Thirty-five castrated males with physiologic T replacement (n=7/grou
134 (approximately 45%) reversed by exogenous T (castrated males with T replacement).
135 obtained from intact males, castrated males, castrated males with T replacement, and intact females.
136 sequently, we found that treating neonatally castrated males with testosterone propionate (TP) in adu
137  showed a higher frequency of mortality than castrated males without hormone replacement or nonoperat
138 s of delayed TP replacement in prepubertally castrated males, and 16 days of treatment did not furthe
139 ffects, RCA were obtained from intact males, castrated males, castrated males with T replacement, and
140  in CBT during the light phase in neonatally castrated males.
141 rostrocaudal extent is not, compared to sham-castrated males.
142 EAE than ovariectomized females or intact or castrated males.
143 zed females and from gonadally intact versus castrated males.
144 les had lower corticosterone than those with castrated males.
145                        While vehicle-treated castrated mdx mice exhibited cardiopulmonary impairment
146 sponse and outcomes with enzalutamide in non-castrate men with prostate cancer.
147 rance was increased by approximately 100% in castrated men and was associated with a two-fold reducti
148            A total of 10 noncastrated and 20 castrated men with prostate cancer were studied to achie
149  and has antitumor activity in patients with castrate metastatic prostate cancer.
150  is upregulated in LAPC-4 AI tumors grown in castrated mice and describe a molecular mechanism by whi
151 androgen-independent CWR22 PCa xenografts in castrated mice and generated a cell line from one of the
152                              In contrast, in castrated mice bearing both LNCaP and NE-10 tumors, LNCa
153 dent state to an androgen-independent state, castrated mice carrying 104-S tumors were given the synt
154 5alpha-dihydrotestosterone (DHT) implants in castrated mice increased Kcne4 expression >3-fold (P = 0
155  In addition, 17-beta-estradiol-supplemented castrated mice showed a higher frequency of mortality th
156 natal prostates and re-growth of prostate in castrated mice triggered by hormone replacement.
157 tore neutrophil counts via stabilizing AR in castrated mice, but not in ARKO and testicular feminizat
158                  We previously observed that castrated mice, compared to sham-operated mice, perform
159                               In DES-treated castrated mice, DHT implants restored SV weights to norm
160  the androgen-dependent LNCaP cell line into castrated mice, has a greatly reduced amount of normal m
161  growth in androgen-depleted agar but not in castrated mice, showing a clear distinction between the
162 ation and prostate xenograft tumor growth in castrated mice.
163 ptor antagonists induce tumour regression in castrated mice.
164 e-growth triggered by hormone replacement in castrated mice.
165 ings related to persistent AR signaling in a castrate milieu can be harnessed to produce significant
166 deficient prostate tumor progression in both castrate-naive and castrate-resistant cancers.
167 support the importance of autophagy for both castrate-naive and castrate-resistant growth in a newly
168                               Interestingly, castrated normoglycemic ApoE(-/-) mice developed larger
169                                         Male castrated nude mice received eight s.c. grafts of juveni
170  different mouse models, including intact or castrated nude mice xenografted with androgen-sensitive
171  cells or androgen-insensitive C81 cells and castrated nude mice xenografted with castration-resistan
172             When orthotopically implanted in castrated nude mice, LNCaP-GRP produced aggressive tumor
173 tation (p53(R273H)) facilitates AI growth in castrated nude mice.
174             Thus, adult male rats neonatally castrated on the first day after birth displayed reducti
175 uction, we paired females with vasectomised, castrated or intact males, or other females.
176 tand these differences, subsets of mice were castrated or ovariectomized at 5 weeks of age.
177                          To explore this, we castrated or sham-operated male rats on the day of birth
178 lices from male mice that were gonad-intact, castrated, or castrated and treated with estradiol impla
179 hort day photoperiod and either left intact, castrated, or castrated with testosterone replacement.
180 ubcutaneous (SC) adipose tissue from normal, castrated, or steroid-implanted animals were isolated an
181 ng treatment with single-agent pertuzumab in castrate patients with hormone-refractory prostate cance
182 nically significant single-agent activity in castrate patients with HRPC at either of the tested dose
183 alamic or adrenal stress response in animals castrated prepubertally.
184  High levels of AR predicted shorter time to castrate prostate-specific antigen increase after androg
185 obust PET imaging capacity of PSES-TSTA in a castrated prostate xenograft model.
186                  In support of this finding, castrated Pten3CKO mice also exhibited decreased levels
187 afted under the back skin or scrotal skin of castrated pubertal rhesus macaques and matured to produc
188 we measured the FE related phenotypes of 236 castrated purebred Yorkshire boars, and selected 10 extr
189 e a dose-dependent suppression of LH in male castrate rats via both i.v. and p.o. dosing.
190 post-MCAO accelerated functional recovery in castrate rats, suggesting a potential therapeutic role f
191 yze the trends observed for LH inhibition in castrated rats and monkeys that served as preliminary in
192                  Testosterone replacement in castrated rats partially reduced expression of Noxs but
193 ming unit colonies compared with plasma from castrated rats subjected to either sham shock with lapar
194                                          The castrated rats were given testosterone replacement.
195          In a 2 week Hershberger model using castrated rats, the compound showed dose-dependent effec
196  FLIP protein expression is downregulated in castrated rats, while in LNCaP cells, androgens regulate
197 l anabolic effect via oral administration in castrated rats.
198 ce expression of fear-potentiated startle in castrated rats.
199 th either E2 or DHT alone, attenuated LES in castrated rats.
200 ates were significantly larger than those of castrates receiving blank capsules (p < 0.0001).
201                              Bony metastatic castrate-refractory prostate cancer (CRPC) has a poor pr
202 mechanisms that underlie the pathogenesis of castrate resistance is therefore needed to develop novel
203 respond to ADT, most will eventually develop castrate resistance, defined as disease progression desp
204 during disease progression and contribute to castrate resistance.
205  to AR antagonists in hormone responsive and castrate resistant PC models.
206 sted IKBKE inhibitors could be beneficial to castrate resistant PC patients.
207 h taxanes improves survival in patients with castrate resistant prostate cancer (CRPC).
208 e enriched in clinical samples of metastatic castrate resistant prostate cancer (mCRPC).
209  variant 7 (AR-V7) is frequently detected in castrate resistant prostate cancer and associated with r
210 20 (both free and in CSLPHNPs) re-sensitizes castrate resistant prostate cancer cells and tumors to d
211 AR-V7 in improving outcomes of patients with castrate resistant prostate cancer.
212 ying progression of prostate cancer (PCa) to castrate-resistant (CR) and metastatic disease are poorl
213 the field is to identify mechanisms by which castrate-resistant AR activity and pioneer factor functi
214 R-targeted therapy and progression to lethal castrate-resistant cancer, the molecular regulators of A
215 tumor progression in both castrate-naive and castrate-resistant cancers.
216 A with concomitant development of metastatic castrate-resistant disease in a large cohort of prostate
217 growth in models of hormone-sensitive and of castrate-resistant disease was observed.
218 on in tumor growth and delay to the onset of castrate-resistant disease.
219 n deprivation, would delay the appearance of castrate-resistant disease.
220 nce of autophagy for both castrate-naive and castrate-resistant growth in a newly developed GEMM, sug
221 sing hormone [LHRH] +/- bicalutamide) and in castrate-resistant men (enzalutamide or abiraterone) wit
222                                           In castrate-resistant metastatic disease, development of no
223 l treatment with curative intent to a lethal castrate-resistant metastatic disease.
224 cer that is coincident with the emergence of castrate-resistant metastatic disease.
225                        Eighty-seven men with castrate-resistant metastatic prostate cancer underwent
226 ent prognostic information on OS in men with castrate-resistant metastatic prostate cancer, and this
227 agents shown to prolong survival in men with castrate-resistant metastatic prostate cancer.
228 ET/CT with overall survival (OS) in men with castrate-resistant metastatic prostate cancer.
229 ntain androgen dependence and in a subset of castrate-resistant PCa cells, dependent on Akt activatio
230 H +/- bicalutamide (cohort 1) and 7 men with castrate-resistant PCa commencing either enzalutamide or
231 nt on the presence of a hormone-sensitive or castrate-resistant PCa phenotype.
232 stine and estramustine before emergence of a castrate-resistant phenotype.
233            The primary end point was time to castrate-resistant progression as shown by increasing pr
234 secondary hormonal manipulations in men with castrate-resistant prostate cancer (CRPC) creates a comp
235 tially effective, acquired resistance termed castrate-resistant prostate cancer (CRPC) develops.
236                                              Castrate-resistant prostate cancer (CRPC) is a fatal, me
237  from localized prostate cancer to incurable castrate-resistant prostate cancer (CRPC) is driven by c
238 rsistent androgen signaling is implicated in castrate-resistant prostate cancer (CRPC) progression.
239 in the transition from androgen-dependent to castrate-resistant prostate cancer (CRPC) remains a clin
240 s) provide a mechanism of therapy evasion in castrate-resistant prostate cancer (CRPC), yet mechanism
241  in human prostate cancer tissues, including castrate-resistant prostate cancer (CRPC).
242 d-line hormonal therapy for the treatment of castrate-resistant prostate cancer (CRPC).
243 uated for interference with chemotherapy for castrate-resistant prostate cancer (CRPC).
244 deprivation, the disease often progresses to castrate-resistant prostate cancer (CRPC).
245  (AR) antagonist with activity in metastatic castrate-resistant prostate cancer (CRPC).
246 ease stages, including the advanced stage of castrate-resistant prostate cancer (CRPC).
247 ment shown to prolong survival in metastatic castrate-resistant prostate cancer (CRPC).
248  to monitor CTCs in patients with metastatic castrate-resistant prostate cancer (mCRPC) undergoing tr
249 se II trial involving 30 men with metastatic castrate-resistant prostate cancer (mCRPC).
250                Abiraterone treats metastatic castrate-resistant prostate cancer by inhibiting CYP17A,
251 te cancer tumours promote the progression of castrate-resistant prostate cancer by producing lymphoto
252   A9 significantly inhibits proliferation of castrate-resistant prostate cancer cells.
253  The median survival for men with metastatic castrate-resistant prostate cancer is 1-2 years, with im
254  the median survival for men with metastatic castrate-resistant prostate cancer is 1-2 years, with im
255 icate that the increase in ARV expression in castrate-resistant prostate cancer is an acute response
256  both castrate-sensitive and more aggressive castrate-resistant prostate cancer is essential to impro
257                                      Because castrate-resistant prostate cancer is refractory to most
258  molecularly characterize CTCs isolated from castrate-resistant prostate cancer patients (CRPC) recei
259 nt a cancer treatment case study (metastatic castrate-resistant prostate cancer) as a point of depart
260 g remains an important regulatory pathway in castrate-resistant prostate cancer, and its transcriptio
261 omatic, or minimally symptomatic, metastatic castrate-resistant prostate cancer, designed to stimulat
262      Additionally, in patients with advanced castrate-resistant prostate cancer, metastatic lesions e
263 t literature on the biology and treatment of castrate-resistant prostate cancer.
264 ic modality in patients with bone metastatic castrate-resistant prostate cancer.
265  promising alternatives for the treatment of castrate-resistant prostate cancer.
266 a potential alternative treatment pathway in castrate-resistant prostate cancer.
267 d for prostate cancer progression, including castrate-resistant prostate cancer; mechanistically, by
268 candidate therapeutic and imaging target for castrate-resistant prostate cancers.
269 state stromal TGF-beta signaling potentiated castrate-resistant prostate tumors, in a Wnt-dependent m
270 ancer, this disease invariably relapses to a castrate-resistant state that is generally fatal.
271 er cells evolve via multiple mechanisms to a castrate-resistant state, allowing progression to a leth
272 se of systemic therapy alone can result in a castrate-resistant state; therefore, increasing focus is
273 t with ADT and TRC105, respectively, reduced castrate-resistant tumor progression, in a model where e
274 ely abolished outgrowth of a patient-derived castrate-resistant tumor.
275 ession of PSMA in both hormone-sensitive and castrate-resistant xenotypes.
276 ostate cancer (PC) driver, even in advanced 'castrate-resistant' disease (CRPC).
277 pies, often advance to a hormone-refractory 'castrate-resistant' PC (CRPC) stage.
278 rstanding new therapeutic paradigms for both castrate-sensitive and more aggressive castrate-resistan
279 uced restoration of nNOS-immunoreactivity in castrates should accompany the restoration of copulation
280 bserved a transient luciferase expression in castrated SPlucTg male mice after supplement of androgen
281 ly of its interaction with AR-FL in the true castrate state or "absence of ligand", providing support
282 sional Clinical Opinion For men with CRPC, a castrate state should be maintained indefinitely.
283 ains dependence on AR signaling, even in the castrate state.
284                                        After castrate testosterone concentrations were reached (1.7 n
285 92%) of 121 receiving oestrogen had achieved castrate testosterone concentrations.
286 tive increasing PSA values while on ADT with castrate testosterone levels.
287 learance in patients with noncastrate versus castrate testosterone levels.
288 man prostate cancer xenografts in nude mice, castrated the mice, and blocked IL-6 activity using a ne
289 ause of the erroneous belief that its larvae castrate their hosts.
290 ecialized on diverse Caryophyllaceae plants, castrating their hosts through manipulation of the hosts
291 red nonsteroidal antiandrogen in addition to castrate therapy.
292 after castration, but growth is supported in castrates treated with estradiol.
293 ed or treated with estradiol, and transected castrates treated with estradiol.
294 sting behavior toward an estrous female or a castrated, urine-swabbed male (presented simultaneously)
295 saline-treated rats, SNB somata of T-treated castrates were significantly larger than those of castra
296 d short days, between castrated, intact, and castrated with testosterone replacement animals, and bet
297 period and either left intact, castrated, or castrated with testosterone replacement.
298 O mice presented heightened BP compared with castrated WT controls.
299 ion of PCGEM1 and promoting apoptosis in the castrated xenograft mouse model.
300          These results are important because castrated young male mice may be used as a simple, toxin

 
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