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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
6 Androgen target tissue uptake was evident in castrated adult male rats; however, in DES-treated, AR-p
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
13 PCa, but patients invariably relapse despite castrate androgen levels (castration-resistant PCa, CRPC
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
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
26 weeks of age; in the second group, mice were castrated at 10 weeks of age, allowed to recover for 10
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
33 ment partially reduced OS in VP epithelia of castrates, but the level remained higher than in intact
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
44 F18-fluorodihydrotestosterone is active in castrate disease and is emerging as a valuable pharmacod
46 l. show that germ-free mice, when chemically castrated, do not lose bone - a finding that unequivocal
54 Male Japanese macaques (Macaca fuscata) were castrated for 5-7 months and then treated for 3 months w
56 development and resist androgen ablation in castrated hosts, and they harbor highly tumorigenic cast
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
61 ty is generally restored in CRPC despite the castrate level of androgens, it is unclear whether AR si
63 nt was sustained testosterone suppression to castrate levels (<50 ng per deciliter) through 48 weeks.
69 or survival and time to progression if lower castrate levels of testosterone (< 0.7 nmol/L) are achie
72 ority with respect to the primary end point, castrate levels of testosterone on day 4, and profound c
75 eks' gestation, n = 6) were xenografted into castrate male nude mice which were then treated for 35 d
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
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
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
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
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
104 neurons appeared in the SNB of prepubertally castrated male Mongolian gerbils within 2 days of the st
106 rotein and mRNA in the female and neonatally castrated male MPN on PN 4, indicating that the neonatal
111 uration of action was also determined in the castrated male rat assay to measure the extent (efficacy
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
123 n stimulation reward in gonadally intact and castrated males and in females at estrous cycle stages a
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
130 early- or late-postnatally transected males, castrated males left untreated or treated with estradiol
132 ricularly (ICV) or systemically to intact or castrated males with or without concomitant androgen rep
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
147 rance was increased by approximately 100% in castrated men and was associated with a two-fold reducti
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
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
157 tore neutrophil counts via stabilizing AR in castrated mice, but not in ARKO and testicular feminizat
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
165 ings related to persistent AR signaling in a castrate milieu can be harnessed to produce significant
167 support the importance of autophagy for both castrate-naive and castrate-resistant growth in a newly
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
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
184 High levels of AR predicted shorter time to castrate prostate-specific antigen increase after androg
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
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
193 ming unit colonies compared with plasma from castrated rats subjected to either sham shock with lapar
196 FLIP protein expression is downregulated in castrated rats, while in LNCaP cells, androgens regulate
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
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
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
216 A with concomitant development of metastatic castrate-resistant disease in a large cohort of prostate
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
226 ent prognostic information on OS in men with castrate-resistant metastatic prostate cancer, and this
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
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.
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
248 to monitor CTCs in patients with metastatic castrate-resistant prostate cancer (mCRPC) undergoing tr
251 te cancer tumours promote the progression of castrate-resistant prostate cancer by producing lymphoto
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
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
267 d for prostate cancer progression, including castrate-resistant prostate cancer; mechanistically, by
269 state stromal TGF-beta signaling potentiated castrate-resistant prostate tumors, in a Wnt-dependent m
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
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
288 man prostate cancer xenografts in nude mice, castrated the mice, and blocked IL-6 activity using a ne
290 ecialized on diverse Caryophyllaceae plants, castrating their hosts through manipulation of the hosts
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