ライフサイエンスコーパス: castration

1 ion was an effective alternative to surgical castration.

2 anced post-pubertally, and was eliminated by castration.

3 reduction of circulating androgen levels by castration.

4 nts no longer respond to medical or surgical castration.

5 androgen-intact mice and in tumors surviving castration.

6 and m3 under androgen deprivation mimicking castration and androgen receptor inhibition.

7 es their survival and regeneration following castration and subsequent androgen restoration.

8 PKM2 and as such, it is a potent inducer of castration and therapy resistance.

9 ive androgen-deprivation therapy by surgical castration and those who receive gonadotropin-releasing

10 ld, 157 (73%) were retired, 87 (41%) were on castration-based treatment, 19 (9%) had received chemoth

11 population of cancer cells that can tolerate castration de novo, enabling the tumour to evade androge

12 e pigs, one of the alternatives for surgical castration, entails the possible occurrence of boar tain

13 lls was sufficient to restore sensitivity to castration in a mouse xenograft model system.

14 n in the prostate, and confers resistance to castration-induced involution.

15 n resistant and are more inclined to develop castration-induced neuroendocrine differentiation.

16 While castration of dystrophin and utrophin double mutant (mdx

17 While castration of mdx-dm mice resulted in weaker muscle and

18 Because of the need to abolish the castration of piglets without anaesthesia/analgesia, the

19 During the evolution into castration or therapy resistance, prostate cancer cells

20 Castration prior to activating stabilized beta-catenin s

21 renal EGFR levels in female Dsk5 mice, while castration protected against the kidney injury in male D

22 ion is synergistic in androgen sensitive and castration recurrent CaP models in vitro and in vivo.

23 herapy (ADT) prevents effective treatment of castration-recurrent (CR) prostate cancer (CaP).

24 for neuroendocrine neoplasms and metastatic castration-refractory prostate cancer.

25 Prostate cancer (PC) progressed to castration resistance (CRPC) is a fatal disease.

26 ght into the bona fide mechanisms underlying castration resistance and provide the foundation for the

27 onally impair HR prior to the development of castration resistance and that, this potentially could b

28 ibition prevented the development of NED and castration resistance in vivo.

29 Castration resistance involves reactivation of androgen

30 In prostate cancer, the development of castration resistance is pivotal in progression to aggre

31 Tumors in which castration resistance was conferred by NEK6 were predomi

32 associated fibroblast-secreted NRG1 mediates castration resistance, recommending novel applications o

33 to the identification of known mediators of castration resistance, which served to validate the scre

34 , chromatin landscape, and leads to relative castration resistance.

35 (PCa) development and progression, including castration resistance.

36 rapeutic target for metabolic adaptation and castration-resistance of prostate cancer cells.

37 Castration-resistance prostate cancer (CRPC), also known

38 germline DDR (gDDR) mutations on metastatic castration-resistance prostate cancer (mCRPC) outcomes.

39 otein kinase A under conditions that promote castration-resistance, eliciting its binding to the spli

40 n of BMI1 is critical for the development of castration-resistance.

41 e tumors derived from the Sca-1(+) cells are castration resistant and are more inclined to develop ca

42 antiandrogen enzalutamide (Enz) extends the castration resistant prostate cancer (CRPC) patients' su

43 enzalutamide (Enz) has improved survival in castration resistant prostate cancer (CRPC) patients.

44 er almost always recurs as a more aggressive castration resistant prostate cancer (CRPC).

45 docetaxel cycles in patients with metastatic castration resistant prostate cancer (mCPRC) has not bee

46 ogens is a standard treatment for metastatic castration resistant prostate cancer (mCRPC), but it ine

47 widely used drug in patients with metastatic castration resistant prostate cancer (mCRPC).

48 is study, we generated two anti-androgen and castration resistant prostate cancer cell models that do

49 d matched transcriptome data from metastatic castration resistant prostate cancer patients and redisc

50 en receptor (AR) may play a critical role in castration resistant prostate cancer.

51 A subset of castration resistant prostate cancers become androgen re

52 for the progression of prostate cancer to a castration-resistant (CRPC) state.

53 tions in patients with CRPC-NE compared with castration-resistant adenocarcinoma, supporting greater

54 spliced long noncoding RNA downregulated in castration-resistant advanced prostate cancer.

55 quired for neuroendocrine prostate cancer, a castration-resistant aggressive form of the disease, and

56 -positive PCa cells and organoids, including castration-resistant and enzalutamide-resistant cells.

57 ts reveal that RUNX1(+) PLCs is an intrinsic castration-resistant and self-sustained lineage that eme

58 n with advanced PC (proven metastatic and/or castration-resistant biochemical progression) were rando

59 Silencing NEK6 in castration-resistant cancer cells was sufficient to rest

60 the previously identified NKX3.1(+) luminal castration-resistant cells.

61 However, almost all patients relapse with castration-resistant disease (CRPC) when treated with an

62 ostate cancers, but effective treatments for castration-resistant disease remain elusive.

63 However, it eventually leads to a castration-resistant disease that is highly metastatic.

64 cancer growth, progression, and emergence of castration-resistant disease.

65 plice variants (AR-SV)-driven advanced stage castration-resistant disease.

66 and m3 signaling is sufficient to induce the castration-resistant growth of PCa cells.

67 knockdown of YAP abolished m1 and m3-induced castration-resistant growth of PCa cells.

68 rom a prostate adenocarcinoma histology to a castration-resistant neuroendocrine prostate cancer (CRP

69 ly labels a type of luminal stem cells named castration-resistant Nkx3.1-expressing cells (CARNs).

70 he maintenance of daughter cells produced by castration-resistant Nkx3.1-expressing luminal stem cell

71 as well as a dramatic response of metastatic castration-resistant PC after PSMA radioligand therapy.

72 e potential to expand options for metastatic castration-resistant PC.

73 protein levels increase with progression to castration-resistant PCa (CRPC) and high levels of Bag-1

74 m3 gene gain or amplification is frequent in castration-resistant PCa (CRPC) compared with hormone-se

75 reverses cancer aggressiveness and inhibits castration-resistant PCa (CRPC) in xenograft and autocht

76 r (PCa) in many countries, but its effect on castration-resistant PCa (CRPC) is limited.

77 T well, most of them will eventually develop castration-resistant PCa (CRPC).

78 LRIG1 also inhibits castration-resistant PCa and exhibits therapeutic effica

79 docetaxel or cabazitaxel in 2 patients with castration-resistant PCa with clinical responses.

80 iochemical recurrence, and 23 for metastatic castration-resistant PCa.

81 apies have gained attention as adjuvants for castration-resistant PCa.

82 1 inhibition via shRNA or PX-12 reverses the castration-resistant phenotype of CRPC cells, significan

83 of these AR circRNAs was upregulated during castration-resistant progression of PDXs.

84 rine differentiation but does not impact the castration-resistant property.

85 oncogenic MUC1-C protein is overexpressed in castration-resistant prostate cancer (CRPC) and NEPC, bu

86 ent castration-sensitive phenotype to lethal castration-resistant prostate cancer (CRPC) are poorly u

87 inistered intravenously for the treatment of castration-resistant prostate cancer (CRPC) as the oral

88 rapies have significantly improved survival, castration-resistant prostate cancer (CRPC) cells are ev

89 d PET is potentially useful for screening of castration-resistant prostate cancer (CRPC) clinical tri

90 evels of BMI1 and that BMI1 was increased in castration-resistant prostate cancer (CRPC) from both hu

91 tor antagonist approved for the treatment of castration-resistant prostate cancer (CRPC) in chemother

92 Finally, ZBTB7A suppressed the growth of castration-resistant prostate cancer (CRPC) in vitro and

93 The development of castration-resistant prostate cancer (CRPC) is associate

94 Castration-resistant prostate cancer (CRPC) is defined b

95 nce of prostate cancer either in the form of castration-resistant prostate cancer (CRPC) or transdiff

96 tably progress on AR-targeted therapies to a castration-resistant prostate cancer (CRPC) phenotype th

97 of AR signalling remains the main driver of castration-resistant prostate cancer (CRPC) progression.

98 Castration-resistant prostate cancer (CRPC) remains a ma

99 en deprivation therapy (ADT) induces nMET in castration-resistant prostate cancer (CRPC) specimens.

100 s reactivated, signaling onset of the lethal castration-resistant prostate cancer (CRPC) stage.

101 Castration-resistant prostate cancer (CRPC) that has dev

102 benign prostate tissues, and even more so in castration-resistant prostate cancer (CRPC) tumors.

103 ity due to prostate cancer happen because of castration-resistant prostate cancer (CRPC) which invari

104 3 ((223)Ra) can prolong survival in men with castration-resistant prostate cancer (CRPC) who have sym

105 Castration-resistant prostate cancer (CRPC) with neuroen

106 new insights into the molecular landscape of castration-resistant prostate cancer (CRPC), identifying

107 r (NEPC), an extremely aggressive variant of castration-resistant prostate cancer (CRPC), is increasi

108 sistance to androgen deprivation therapy, or castration-resistant prostate cancer (CRPC), is often ac

109 articularly virulent form of this disease is castration-resistant prostate cancer (CRPC), where patie

110 ecific antigen can hamper early diagnosis of castration-resistant prostate cancer (CRPC).

111 dministration in 2012 to treat patients with castration-resistant prostate cancer (CRPC).

112 V7 plays an important role in progression of castration-resistant prostate cancer (CRPC).

113 prostate cancer patients eventually develop castration-resistant prostate cancer (CRPC).

114 overall survival from endocrine therapies in castration-resistant prostate cancer (CRPC).

115 e variants (AR-Vs) drives the progression of castration-resistant prostate cancer (CRPC).

116 P/FKBP51/IKKalpha complex and progression of castration-resistant prostate cancer (CRPC).

117 inevitably relapses and progresses to lethal castration-resistant prostate cancer (CRPC).

118 biraterone and enzalutamide in patients with castration-resistant prostate cancer (CRPC).

119 approval of abiraterone for the treatment of castration-resistant prostate cancer (CRPC).

120 genic pathways that contribute to metastatic castration-resistant prostate cancer (CRPC).

121 s receiving ADT eventually develop incurable castration-resistant prostate cancer (CRPC).

122 t al. expose new possibilities for targeting castration-resistant prostate cancer (CRPC).

123 ion inevitably drives disease progression to castration-resistant prostate cancer (CRPC).

124 one of the principal treatments for men with castration-resistant prostate cancer (CRPC).

125 are effective initially for the treatment of castration-resistant prostate cancer (CRPC).

126 ; however, therapy failure results in lethal castration-resistant prostate cancer (CRPC).

127 lind, phase 3 trial, men with nonmetastatic, castration-resistant prostate cancer (defined on the bas

128 I]) in patients who have advanced metastatic castration-resistant prostate cancer (mCRPC) and are rec

129 lterations are common in men with metastatic castration-resistant prostate cancer (mCRPC) and may con

130 linical data indicate activity in metastatic castration-resistant prostate cancer (mCRPC) and synergi

131 o androgen receptor inhibition in metastatic castration-resistant prostate cancer (mCRPC) and whether

132 ults in a subset of patients with metastatic castration-resistant prostate cancer (mCRPC) but still e

133 sma DNA has been characterized in metastatic castration-resistant prostate cancer (mCRPC) but the pla

134 Metastatic castration-resistant prostate cancer (mCRPC) develops re

135 Metastatic castration-resistant prostate cancer (mCRPC) has a highl

136 Metastatic castration-resistant prostate cancer (mCRPC) is a hetero

137 Metastatic castration-resistant prostate cancer (mCRPC) is immunolo

138 mic analysis of 429 patients with metastatic castration-resistant prostate cancer (mCRPC) linked with

139 tumor cells (CTC) from 179 unique metastatic castration-resistant prostate cancer (mCRPC) patients to

140 he OS in black and white men with metastatic castration-resistant prostate cancer (mCRPC) who were tr

141 Purpose In patients with metastatic castration-resistant prostate cancer (mCRPC), overall su

142 ptake in skeletal metastases from metastatic castration-resistant prostate cancer (mCRPC).

143 PRLT) is an emerging treatment in metastatic castration-resistant prostate cancer (mCRPC).

144 eptor expression in patients with metastatic castration-resistant prostate cancer (mCRPC).

145 o detect lesions in patients with metastatic castration-resistant prostate cancer (mCRPC).

146 state cancer differ from those of metastatic castration-resistant prostate cancer (mCRPC).

147 there are no curative options for metastatic castration-resistant prostate cancer (mCRPC).

148 ses to treatment in patients with metastatic castration-resistant prostate cancer (mCRPC).

149 g resistance mechanism to anti-AR therapy in castration-resistant prostate cancer (mCRPC).

150 lly significant co-occurrences in metastatic castration-resistant prostate cancer (mCRPC).

151 relentless progression to lethal metastatic castration-resistant prostate cancer (mCRPC).

152 nd therapy (RLT) of patients with metastatic castration-resistant prostate cancer (mCRPC).

153 s), and subsequent progression to metastatic castration-resistant prostate cancer (mCRPC).

154 graphic response in patients with metastatic castration-resistant prostate cancer (mCRPC).

155 te cancer (NEPC), the most lethal subtype of castration-resistant prostate cancer (PCa), for which th

156 Treatment of advanced metastatic castration-resistant prostate cancer after failure of ap

157 se 3 trial involving men with nonmetastatic, castration-resistant prostate cancer and a prostate-spec

158 aged 18 years or older with non-metastatic, castration-resistant prostate cancer and a prostate-spec

159 vation therapy among men with nonmetastatic, castration-resistant prostate cancer and a rapidly risin

160 labeled PSMA-617 in patients with metastatic castration-resistant prostate cancer and a single functi

161 py-naive, asymptomatic or mildly symptomatic castration-resistant prostate cancer and bone metastases

162 symptomatic skeletal events in patients with castration-resistant prostate cancer and bone metastases

163 keletal event-free survival in patients with castration-resistant prostate cancer and bone metastases

164 le for participation if they had: metastatic castration-resistant prostate cancer and had received no

165 ional program in both androgen-sensitive and castration-resistant prostate cancer and inhibited tumou

166 ety and survival of patients with metastatic castration-resistant prostate cancer and liver metastase

167 ee survival among men who had nonmetastatic, castration-resistant prostate cancer and rapidly increas

168 en receptor-regulated miRNA overexpressed in castration-resistant prostate cancer and that miR-32 can

169 role for BAT in the management of metastatic castration-resistant prostate cancer and the optimal str

170 It occurred in both androgen-dependent and castration-resistant prostate cancer and was associated

171 tion of survival in patients with metastatic castration-resistant prostate cancer but also engage a c

172 zole that was developed for the treatment of castration-resistant prostate cancer but was dropped in

173 ificant gains in the treatment of metastatic castration-resistant prostate cancer by radioligands tar

174 dex, clinicians and patients with metastatic castration-resistant prostate cancer can be reassured th

175 lidated using a DNAJA1 inhibitor (116-9e) in castration-resistant prostate cancer cell (CRPC) and sph

176 xpression of miR-1205 were increased in both castration-resistant prostate cancer cell lines and in p

177 occur early are an unmet need in metastatic castration-resistant prostate cancer clinical research a

178 sponse end points for early-phase metastatic castration-resistant prostate cancer clinical trials.

179 relates with prostate cancer progression and castration-resistant prostate cancer development.

180 rovements to prognostic models in metastatic castration-resistant prostate cancer have the potential

181 ) by 8.5 months versus placebo in metastatic castration-resistant prostate cancer in a phase II study

182 tion of genomic stratification of metastatic castration-resistant prostate cancer in clinical practic

183 Metastatic castration-resistant prostate cancer is enriched in DNA

184 metastatic disease to management of men with castration-resistant prostate cancer metastatic to bone.

185 te cancer cell lines and cfDNA obtained from castration-resistant prostate cancer patients.

186 u-PSMA) radionuclide treatment in metastatic castration-resistant prostate cancer patients.

187 overall survival in patients with metastatic castration-resistant prostate cancer previously treated

188 or enzalutamide in patients with metastatic castration-resistant prostate cancer previously treated

189 8 years or older with progressing metastatic castration-resistant prostate cancer previously treated

190 tandard of care for patients with metastatic castration-resistant prostate cancer progressing after d

191 ing markers for AR/AR-variant expression and castration-resistant prostate cancer progression.

192 Patients with non-metastatic, castration-resistant prostate cancer receiving enzalutam

193 e-capture RNA-seq dataset from 47 metastatic castration-resistant prostate cancer samples and ribodep

194 ndred consecutive patients with metastasized castration-resistant prostate cancer scheduled for PSMA

195 In castration-resistant prostate cancer specimens, the copy

196 rom 294 patients with progressing metastatic castration-resistant prostate cancer taken prior to star

197 with radiographically documented metastatic castration-resistant prostate cancer that had progressed

198 to evaluate BAT in patients with metastatic castration-resistant prostate cancer that progressed aft

199 t randomised clinical trials with metastatic castration-resistant prostate cancer to estimate the gro

200 gen and antiandrogen therapies in metastatic castration-resistant prostate cancer to maximise therape

201 ficantly longer for patients with metastatic castration-resistant prostate cancer treated with this c

202 EGFR associated with the LIFR and SUCLG2 in castration-resistant prostate cancer tumors.

203 iation dosimetry, 4 patients with metastatic castration-resistant prostate cancer underwent serially

204 rmance status <=2) with confirmed metastatic castration-resistant prostate cancer were randomly assig

205 Data from 13 patients with metastatic castration-resistant prostate cancer were retrospectivel

206 USE M1-in which 266 patients with metastatic castration-resistant prostate cancer were treated with p

207 r enzalutamide), in patients with metastatic castration-resistant prostate cancer who had been previo

208 patients (mean age, 72.9 y) with metastatic castration-resistant prostate cancer who had been referr

209 RP inhibitor olaparib in men with metastatic castration-resistant prostate cancer who had disease pro

210 In men with metastatic castration-resistant prostate cancer who had disease pro

211 ds: Fifty patients with PSMA-avid metastatic castration-resistant prostate cancer who had progressed

212 ide or abiraterone among men with metastatic castration-resistant prostate cancer who had qualifying

213 Among men with metastatic castration-resistant prostate cancer who had tumors with

214 r enzalutamide), in patients with metastatic castration-resistant prostate cancer who were previously

215 fit of treating STEAP1-expressing metastatic castration-resistant prostate cancer with an STEAP1-targ

216 b has antitumour activity against metastatic castration-resistant prostate cancer with DDR gene aberr

217 Furthermore, patients with castration-resistant prostate cancer with increased tumo

218 ve seen the start of treatment of metastatic castration-resistant prostate cancer with prostate-speci

219 d no survival benefit in men with metastatic castration-resistant prostate cancer with the addition o

220 patients with chemotherapy-naive metastatic castration-resistant prostate cancer without visceral me

221 th metastatic breast and six with metastatic castration-resistant prostate cancer, isolated via CellS

222 Among men with nonmetastatic, castration-resistant prostate cancer, metastasis-free su

223 d characterization of circRNAs in metastatic castration-resistant prostate cancer, the major cause of

224 Among men with nonmetastatic, castration-resistant prostate cancer, the percentage of

225 ee survival in patients with non-metastatic, castration-resistant prostate cancer.

226 presenting with high-risk, non- metastatic, castration-resistant prostate cancer.

227 th cabazitaxel alone for men with metastatic castration-resistant prostate cancer.

228 it had no effect on OS or AWE in metastatic castration-resistant prostate cancer.

229 RT) for the treatment of liver metastases of castration-resistant prostate cancer.

230 improve the outcomes of men with metastatic castration-resistant prostate cancer.

231 o centres in men with progressive metastatic castration-resistant prostate cancer.

232 for clinical translation to treat metastatic castration-resistant prostate cancer.

233 ity of DSTP3086S in patients with metastatic castration-resistant prostate cancer.

234 ectomy, and cohort B patients had metastatic castration-resistant prostate cancer.

235 proach to treat metastatic hormone-naive and castration-resistant prostate cancer.

236 overall survival in patients with metastatic castration-resistant prostate cancer.

237 nd consequent cell proliferation, leading to castration-resistant prostate cancer.

238 le and may contribute to the genetic risk of castration-resistant prostate cancer.

239 astasis and death in men with nonmetastatic, castration-resistant prostate cancer.

240 ay ultimately lead to a new therapy for AR+, castration-resistant prostate cancer.

241 d with improved overall survival in men with castration-resistant prostate cancer.

242 om initial diagnosis to advanced, metastatic castration-resistant prostate cancer.

243 lpha-therapy for the treatment of metastatic castration-resistant prostate cancer.

244 rivation therapy and in approximately 30% of castration-resistant prostate cancer.

245 CBP/p300 bromodomain as a strategy to treat castration-resistant prostate cancer.

246 in men with chemotherapy-naive, metastatic, castration-resistant prostate cancer.

247 d not improve OS in patients with metastatic castration-resistant prostate cancer.

248 the RLT and care of patients with metastatic castration-resistant prostate cancer.

249 P/p300 is required to maintain the growth of castration-resistant prostate cancer.

250 ith mitoxantrone in patients with metastatic castration-resistant prostate cancer.

251 overall survival in patients with metastatic castration-resistant prostate cancer.

252 erapeutic option in patients with metastatic castration-resistant prostate cancer.

253 rials that enrolled patients with metastatic castration-resistant prostate cancer.

254 6 signaling as a central mechanism mediating castration-resistant prostate cancer.

255 sing antitumor effect in advanced metastatic castration-resistant prostate cancer.

256 approved for the treatment of nonmetastatic, castration-resistant prostate cancer.

257 tment failure and poor outcome in metastatic castration-resistant prostate cancer.

258 regulatory role of methylation in metastatic castration-resistant prostate cancer.

259 rated with Pten loss to drive AR-independent castration-resistant prostate cancer.

260 t a new therapeutic target in the metastatic castration-resistant prostate cancer.

261 se II trial involving 30 men with metastatic castration-resistant prostate cancer.

262 eatment response in patients with metastatic castration-resistant prostate cancer.

263 tions and response to olaparib in metastatic castration-resistant prostate cancer.

264 n emerging treatment modality for metastatic castration-resistant prostate cancer.

265 ll as in androgen-dependent tumours, such as castration-resistant prostate cancer.

266 ific membrane antigen (PSMA) in metastasized castration-resistant prostate cancer.

267 BET bromodomain inhibition in AR-independent castration-resistant prostate cancers (CRPC), whose freq

268 report that approximately 20% of metastatic castration-resistant prostate cancers express neither AR

269 have shown promising activity in metastatic castration-resistant prostate cancers in single-group cl

270 in human NEPC tumors compared to primary and castration-resistant prostate cancers, and its expressio

271 ate homologous recombination (HR) defects in castration-resistant prostate cancers, rendering these t

272 llows functional substitution for AR in some castration-resistant prostate cancers.

273 administered to patients who had metastatic castration-resistant prostate carcinoma and who had exha

274 report on our experience with a series of 73 castration-resistant prostate carcinoma patients treated

275 n age, 69 y; range, 45-85 y) with metastatic castration-resistant prostate carcinoma were treated wit

276 e-genome and transcriptome sequencing of 100 castration-resistant prostate metastases, we discovered

277 lt mouse prostate luminal cells contain both castration-resistant Sox2-expressing Sca-1(+) cells and

278 t becomes ineffective as PCa progresses to a castration-resistant state (CRPC).

279 y to the clinical CRPC, orthotopically grown castration-resistant VCaP (CR-VCaP) xenografts express h

280 tate cancer and inhibited tumour growth in a castration-resistant xenograft model.

281 reatment of a wide spectrum of PCs including castration-resistant, Enz-R, and/or AR SV-dependent adva

282 tion along passaging and are relatively more castration-resistant.

283 resistant Sox2-expressing Sca-1(+) cells and castration-responsive Sca-1(-) cells.

284 hich prostate cancer shifts from an indolent castration-sensitive phenotype to lethal castration-resi

285 ind, phase 3 study, patients with metastatic castration-sensitive prostate cancer (defined as not rec

286 en with newly diagnosed high-risk metastatic castration-sensitive prostate cancer (mCSPC).

287 Ninety-nine patients with castration-sensitive prostate cancer and prostate-specif

288 Additionally, we imaged one patient with castration-sensitive prostate cancer before and 4 wk aft

289 Methods: 76 men with metastatic castration-sensitive prostate cancer recruited from 2005

290 eatment or previous docetaxel for metastatic castration-sensitive prostate cancer were allowed.

291 rall increase in 2-year MFS in patients with castration-sensitive prostate cancer, with the possible

292 and effective option for men with metastatic castration-sensitive prostate cancer.

293 atment failure (THTF) in men with metastatic castration-sensitive prostate cancer.

294 c information on THTF in men with metastatic castration-sensitive prostate cancer.

295 on-free survival in patients with metastatic castration-sensitive prostate cancer.

296 mouse xenograft model and in a patient with castration-sensitive prostate cancer.

297 gs can help clinicians decide on the optimal castration strategy for individual patients.

298 ndergo painful surgical procedures (surgical castration, tail docking, teeth clipping), which farmers

299 ence interval [CI], 94.9 to 97.9) maintained castration through 48 weeks, as compared with 88.8% (95%

300 Replacing surgical castration with immunocastration, avoiding tail docking