ライフサイエンスコーパス: metastatic prostate cancer

1 survival (OS) in men with castrate-resistant metastatic prostate cancer.

2 patients diagnosed with locally advanced and metastatic prostate cancer.

3 engineered mouse model of highly penetrant, metastatic prostate cancer.

4 ntial target of therapeutic intervention for metastatic prostate cancer.

5 CAD to treat relapsing, locally advanced, or metastatic prostate cancer.

6 ve extended survival in castration-resistant metastatic prostate cancer.

7 andard care for metastatic or high-risk, non-metastatic prostate cancer.

8 o change the way we treat patients with bone-metastatic prostate cancer.

9 There is currently no imaging biomarker for metastatic prostate cancer.

10 ne scan response to sunitinib among men with metastatic prostate cancer.

11 has now entered phase 3 testing in men with metastatic prostate cancer.

12 ecreased expression of SPARCL1 in high-grade/metastatic prostate cancer.

13 is a standard chemotherapy for patients with metastatic prostate cancer.

14 long survival in men with castrate-resistant metastatic prostate cancer.

15 ling circuit with functional significance in metastatic prostate cancer.

16 ave utility specifically for advanced and/or metastatic prostate cancer.

17 cancer, especially for androgen-independent metastatic prostate cancer.

18 pendent quantification of bone metastasis in metastatic prostate cancer.

19 e as a surrogate measure of AR expression in metastatic prostate cancer.

20 ould be useful for the treatment of HRPC and metastatic prostate cancer.

21 ular endothelial growth factor-C (VEGF-C) in metastatic prostate cancer.

22 uding precocious puberty, endometriosis, and metastatic prostate cancer.

23 is no evidence of an effect in men with non-metastatic prostate cancer.

24 hylation is significantly more pronounced in metastatic prostate cancer.

25 MCM7 is both amplified and overexpressed in metastatic prostate cancer.

26 pin-driven therapeutic targeting in advanced metastatic prostate cancer.

27 f these rearrangements in hormone-refractory metastatic prostate cancer.

28 ings of novel agents in castration-resistant metastatic prostate cancer.

29 1 are correlated with hormone-refractory and metastatic prostate cancer.

30 most commonly used drug for the treatment of metastatic prostate cancer.

31 treatment response in a preclinical model of metastatic prostate cancer.

32 astration-resistant (ie, hormone-refractory) metastatic prostate cancer.

33 ing expression array data from localized and metastatic prostate cancer.

34 n shown to improve survival in patients with metastatic prostate cancer.

35 that PCBP2 RNA was consistently elevated in metastatic prostate cancer.

36 oint for improving survival in patients with metastatic prostate cancer.

37 tion (AD) has been the mainstay for treating metastatic prostate cancer.

38 the form of dietary soy, with lower rates of metastatic prostate cancer.

39 antitumor activity in patients with castrate metastatic prostate cancer.

40 ssess PSMA-targeted T cells in patients with metastatic prostate cancer.

41 s (DC) were administered to 20 patients with metastatic prostate cancer.

42 ane antigen) is a novel targeted therapy for metastatic prostate cancer.

43 treatment for men with de novo or recurrent metastatic prostate cancer.

44 ational clinical trials against advanced and metastatic prostate cancer.

45 and (131)I-MIP-1095 for endoradiotherapy of metastatic prostate cancer.

46 n epithelial cells representing invasive and metastatic prostate cancer.

47 peptide sequences was observed in samples of metastatic prostate cancer.

48 ive tumor sites in patients with progressive metastatic prostate cancer.

49 ZH2) is overexpressed in hormone-refractory, metastatic prostate cancer.

50 us regarding IGF1R expression in primary and metastatic prostate cancer.

51 gainst the self-protein PSA in patients with metastatic prostate cancer.

52 nti-PSCA mAbs for the treatment of local and metastatic prostate cancer.

53 e presence of a homozygous deletion found in metastatic prostate cancer.

54 e changes in the bone scans of patients with metastatic prostate cancer.

55 sensitivity and specificity for detection of metastatic prostate cancer.

56 Notch as a potential therapeutic target for metastatic prostate cancer.

57 cacy of potential targeted therapies on bone metastatic prostate cancer.

58 SI) as an imaging biomarker in patients with metastatic prostate cancer.

59 nthesis inhibitor, in the early treatment of metastatic prostate cancer.

60 membrane antigen minibody, in patients with metastatic prostate cancer.

61 e biodistribution and kinetics for targeting metastatic prostate cancer.

62 sis and therapy in patients with relapsed or metastatic prostate cancer.

63 thylcholine PET/CT study on 12 patients with metastatic prostate cancer.

64 OC insecticides and PCBs in the etiology of metastatic prostate cancer.

65 ic tools that act combinatorially to inhibit metastatic prostate cancer.

66 tastases in the context of androgen-deprived metastatic prostate cancer.

67 pes that becomes dysregulated in primary and metastatic prostate cancer.

68 e inhibitors for evaluation in patients with metastatic prostate cancer.

69 rnative option in patients with recurrent or metastatic prostate cancer.

70 oma is a common characteristic of aggressive metastatic prostate cancer.

71 oved targeted therapies are needed to combat metastatic prostate cancer.

72 enriched in various phenotypes of late-stage metastatic prostate cancer.

73 al avenue for the treatment of recurrent and metastatic prostate cancer.

74 d the initiation of chemotherapy in men with metastatic prostate cancer.

75 dronic acid in men with castration-sensitive metastatic prostate cancer.

76 s chaperone as a therapeutic target to treat metastatic prostate cancer.

77 y effective in preventing the development of metastatic prostate cancers.

78 av3 and EphA2 was elevated in late-stage and metastatic prostate cancers.

79 tutes the principal therapy for advanced and metastatic prostate cancers.

80 in primary prostate cancers, but more so in metastatic prostate cancers.

81 s (AR) are overexpressed in most primary and metastatic prostate cancers.

82 on of this pathway in hormone-refractory and metastatic prostate cancers.

83 en nonrecurrent primary prostate cancers and metastatic prostate cancers.

84 Met is also expressed in localized and metastatic prostate cancers.

85 vanced, anaplastic, castration-resistant and metastatic prostate cancers.

86 say was positive in 71% of our patients with metastatic prostate cancer, 14% of healthy control men a

87 Among men with locally advanced or metastatic prostate cancer, ADT plus abiraterone and pre

88 ing/focal adhesion interactions in targeting metastatic prostate cancer and (b) a potential value for

89 ); 16 had CIM evidence of new or progressive metastatic prostate cancer and 1 had high clinical suspi

90 Eligible patients had metastatic prostate cancer and a PSA level higher than 4

91 monly found on the surface of late-stage and metastatic prostate cancer and a well-known imaging biom

92 titutively increased in androgen-independent metastatic prostate cancer and correlates with poor prog

93 erm overall survival and lower incidences of metastatic prostate cancer and death from prostate cance

94 pathways can be simultaneously activated in metastatic prostate cancer and establish EZH2 as a drive

95 We examined primary and metastatic prostate cancer and found that miR-31 express

96 It is often downregulated in metastatic prostate cancer and has been reported as a po

97 unique apoptosis mode in the development of metastatic prostate cancer and identification of molecul

98 ously reported that EZH2 is overexpressed in metastatic prostate cancer and is a marker of aggressive

99 s consistently and strongly overexpressed in metastatic prostate cancer and is secreted in a biologic

100 planning (223)RaCl2 therapy of patients with metastatic prostate cancer and its impact on the therape

101 d normal controls, and between patients with metastatic prostate cancer and local-regional disease (P

102 In patients, PMEPA1 expression decreased in metastatic prostate cancer and low Pmepa1 correlated wit

103 ites in patients with progressive clinically metastatic prostate cancer and may be a promising agent

104 tive changes in PET imaging of patients with metastatic prostate cancer and of facilitating therapy m

105 on or point mutation is reasonably common in metastatic prostate cancer and the resulting activation

106 rmation on OS in men with castrate-resistant metastatic prostate cancer, and this information may be

107 A high percentage of TRAMP mice develop metastatic prostate cancer, and thus the TRAMP model is

108 of whole-body tumor burden in patients with metastatic prostate cancer, and to standardize the evalu

109 romal cells, 73 primary prostate cancers, 91 metastatic prostate cancers, and 25 noncancerous prostat

110 androgen deprivation therapy for advanced or metastatic prostate cancer are at risk for both hypogona

111 Therapeutic options for men with metastatic prostate cancer are expanding.

112 reatment options for patients with high-risk metastatic prostate cancer are now available, which desc

113 erized a transgenic mouse model (CR2-TAg) of metastatic prostate cancer arising in the neuroendocrine

114 d, is significantly more highly expressed in metastatic prostate cancer as compared with localized pr

115 immunotherapy should still be efficacious in metastatic prostate cancer as radioisotopes are brought

116 otein, is highly expressed in both local and metastatic prostate cancers as well as in a large propor

117 The cumulative incidence of metastatic prostate cancer at 12 years was 14.5% in the

118 ent, suggesting new strategies for targeting metastatic prostate cancer based on integrin expression.

119 ere are currently no effective therapies for metastatic prostate cancer because the molecular mechani

120 ncology trials are not always applicable for metastatic prostate cancer, better ways of following res

121 The whole body, bone, and brain metastatic prostate cancer burden was reduced by oral CC

122 s 3 through 5 prostatic adenocarcinomas, and metastatic prostate cancer, but largely undetectable in

123 associated with greater risk of aggressive, metastatic prostate cancers, but in vivo functional data

124 d by demonstrating overexpression of MTA1 in metastatic prostate cancer by immunoblot analysis.

125 man cell line and a mouse model suggest that metastatic prostate cancer cell detachment may be favore

126 l as actin-based motility and migration in a metastatic prostate cancer cell line (i.e., PC-3) withou

127 SU-PR1, DU145, and PC-3), but not in one non-metastatic prostate cancer cell line (LNCaP.FGC).

128 n this study, we found that migration of the metastatic prostate cancer cell line Du145 was substanti

129 physiological intensity, while the strongly metastatic prostate cancer cell line PC-3-M migrates ano

130 th the mRNA and protein levels in the highly metastatic prostate cancer cell line PC3.

131 A) technology to down-regulate ADAM15 in the metastatic prostate cancer cell line, PC-3.

132 UC18 mRNA and protein was expressed in three metastatic prostate cancer cell lines (TSU-PR1, DU145, a

133 Metastatic prostate cancer cell lines and bone metastasi

134 ration of highly metastatic relative to less metastatic prostate cancer cell lines to bone.

135 In addition, pathway blockade in three metastatic prostate cancer cell lines with cyclopamine o

136 mund-Thomson syndrome, is highly elevated in metastatic prostate cancer cell lines.

137 at Snail repressed the expression of RKIP in metastatic prostate cancer cell lines.

138 v was incubated at 37 degrees C for 1 h with metastatic prostate cancer cells (DU145) to assess the t

139 phingolipid metabolism in hormone-refractory metastatic prostate cancer cells and evaluated its poten

140 CD82 was palmitoylated when expressed in PC3 metastatic prostate cancer cells and that palmitoylation

141 It has been suggested that bone metastatic prostate cancer cells are osteomimetic and ca

142 Here, we describe how metastatic prostate cancer cells breach BMEC monolayers

143 sion molecule (ALCAM), is actively shed from metastatic prostate cancer cells by the sheddase ADAM17

144 tion of the Akt/PKB survival pathway in bone-metastatic prostate cancer cells compared to nonmetastat

145 Most notably, RecQL4 knockdown in metastatic prostate cancer cells drastically reduced the

146 Consistently, PLK1 downregulation in metastatic prostate cancer cells enhances epithelial cha

147 We previously showed that bone-metastatic prostate cancer cells exposed to human bone m

148 mens that p45-sErbB3 was highly expressed in metastatic prostate cancer cells in bone.

149 form of ErbB3 was present and upregulated in metastatic prostate cancer cells in lymph nodes and bone

150 Overexpression of EWI2/PGRL in Du145 metastatic prostate cancer cells inhibits cell migration

151 Ectopic reexpression of PKD1 in metastatic prostate cancer cells reversibly suppressed e

152 ereas overexpression of recombinant HDAC1 in metastatic prostate cancer cells suppressed P-Rex1 expre

153 ed that P-Rex1 expression was much higher in metastatic prostate cancer cells than in prostate epithe

154 refore, there is a dominant factor(s) in the metastatic prostate cancer cells that confers specific p

155 letely inhibited lung colonization of highly metastatic prostate cancer cells without affecting the g

156 tatic prostate cancer PC-3 cells than in non-metastatic prostate cancer cells, and HDAC inhibitors on

157 ation of phosphorylated cofilin is higher in metastatic prostate cancer cells, and that a partial red

158 astically reduced the growth and survival of metastatic prostate cancer cells, indicating that RecQL4

159 -Rex1, but not its 'GEF-dead' mutant, in non-metastatic prostate cancer cells, such as CWR22Rv1, incr

160 arkedly elevated P-Rex1 transcription in non-metastatic prostate cancer cells, whereas overexpression

161 lls treated with conditioned media from bone metastatic prostate cancer cells.

162 ls than in prostate epithelial cells and non-metastatic prostate cancer cells.

163 regulator, is abnormally expressed in highly metastatic prostate cancer cells.

164 associated with increased bFGF production in metastatic prostate cancer cells.

165 ell shape, and abolished the invasiveness of metastatic prostate cancer cells.

166 ound MTA1 to be selectively overexpressed in metastatic prostate cancer compared with clinically loca

167 or differentially expressed in localized and metastatic prostate cancer compared with normal prostate

168 tate cancer, and to an even higher degree in metastatic prostate cancer compared with normal prostate

169 r (miR-23b/-27b), are downregulated in human metastatic prostate cancer compared with primary tumors

170 -1) is reported in the sera of patients with metastatic prostate cancer compared with that of benign

171 y therapy for advanced (locally extensive or metastatic) prostate cancer consists of androgen depriva

172 Metastatic prostate cancer continues to pose a difficult

173 tudies of patients with castration-resistant metastatic prostate cancer (CRMPC) suggest that chemothe

174 se of the trial, one each from laryngeal and metastatic prostate cancer, deemed probably unrelated to

175 Metastatic prostate cancer demonstrated significantly hi

176 lyses of human expression data revealed that metastatic prostate cancer deposits had lower PPM1A expr

177 Metastatic prostate cancer detected by (18)F-fluorocholi

178 Purpose Systemic Therapy for Advanced or Metastatic Prostate Cancer: Evaluation of Drug Efficacy

179 of PCSM at diagnosis in men with primary non-metastatic prostate cancer, even when accounting for com

180 The emergence of recurrent, metastatic prostate cancer following the failure of andr

181 ges in early NaF PET/CT response measures in metastatic prostate cancer for correlation to clinical o

182 100 kinases potentially implicated in human metastatic prostate cancer for functional evaluation.

183 rst reported transgenic model of spontaneous metastatic prostate cancer for studies of this advanced

184 Metastatic prostate cancers from anorchid men express tr

185 All 12 patients with progressive metastatic prostate cancer had at least 1 lesion site of

186 ivity, which itself has been associated with metastatic prostate cancer, had a differential effect on

187 ically localized prostate cancers and 27% of metastatic prostate cancers harboring the TMPRSS2-ERG ge

188 frequency of such mutations in patients with metastatic prostate cancer has not been established.

189 primary treatment modality for patients with metastatic prostate cancer; however, the role of androge

190 timate associations between OC exposures and metastatic prostate cancer in a population-based cohort

191 ivating protein (RasGAP) gene DAB2IP induces metastatic prostate cancer in an orthotopic mouse tumor

192 that has considerable promise for therapy of metastatic prostate cancer in androgen-unresponsive pati

193 important implications for the treatment of metastatic prostate cancer in bone.

194 minating a novel candidate driver underlying metastatic prostate cancer in current smokers.

195 ed clinically to treat localized and osseous metastatic prostate cancer in men.

196 o treat spontaneously developing primary and metastatic prostate cancer in the transgenic TRAMP mouse

197 senger RNA and EZH2 protein are increased in metastatic prostate cancer; in addition, clinically loca

198 diagnostic accuracy for lesion detection in metastatic prostate cancer, including bone metastases.

199 w age-median are at very low 20-year risk of metastatic prostate cancer, individualized screening int

200 of therapeutic strategies for incurable bone metastatic prostate cancer is an urgent need.

201 Metastatic prostate cancer is differentiated by expressi

202 Metastatic prostate cancer is treated with drugs that an

203 ate cancer is an androgen-dependent disease; metastatic prostate cancer is typically treated by andro

204 FACS-sorted single luminal and basal cells), metastatic prostate cancer lesions and circulating tumor

205 activity to prevent or halt the formation of metastatic prostate cancer lesions in bone.

206 MKK4 protein is the result of allelic loss, metastatic prostate cancer lesions were examined for los

207 nd further elevation in castration-resistant metastatic prostate cancer lesions.

208 Metastatic prostate cancer may respond initially to horm

209 d minimally symptomatic castration-resistant metastatic prostate cancer (mCRPC).

210 promises to diagnose and stage patients with metastatic prostate cancer more accurately than current

211 Smokers develop metastatic prostate cancer more frequently than nonsmoke

212 DeltaPten mice) develop androgen-independent metastatic prostate cancer more rapidly than control (De

213 ts the major therapeutic target for treating metastatic prostate cancer (mPC).

214 xternal beam radiotherapy (RT), for men with metastatic prostate cancer (mPCa).

215 numerous oncogenic alterations implicated in metastatic prostate cancer, mutations of kinases are rar

216 5), localized prostate cancer (n = 116), and metastatic prostate cancer (n = 17) demonstrated mean AM

217 Men with metastatic prostate cancer often have bone-only disease

218 al log-transformed lipid-adjusted PCB 44 and metastatic prostate cancer (OR = 0.74; 95% CI: 0.56, 0.9

219 ts (n = 1822) with metastatic breast cancer, metastatic prostate cancer, or multiple myeloma who had

220 n 5 had a 15-fold higher risk for developing metastatic prostate cancer (P = 0.001; 95% confidence in

221 s were validated in vivo with models of bone metastatic prostate cancer (PAIII and C4-2B).

222 ting, 2 repeat bone scans were obtained from metastatic prostate cancer patients after a single 600-M

223 radical prostatectomy patients as well as 7 metastatic prostate cancer patients and 14 healthy men w

224 etected in circulating EV from the plasma of metastatic prostate cancer patients and was LO specific.

225 The survival of hormone-refractory metastatic prostate cancer patients has improved with th

226 trols, and CXCL5 serum levels were higher in metastatic prostate cancer patients relative to patients

227 p bone scan study: 2 follow-up bone scans of metastatic prostate cancer patients were analyzed to det

228 limit of detection) and (ii) crude sera from metastatic prostate cancer patients.

229 te, pamidronate disodium, on pain control in metastatic prostate cancer patients.

230 metastatic colorectal cancer patients and 30 metastatic prostate cancer patients.

231 Silencing endogenous P-Rex1 in metastatic prostate cancer PC-3 cells selectively inhibi

232 with the P-Rex1 promoter were much weaker in metastatic prostate cancer PC-3 cells than in non-metast

233 prostate-specific membrane antigen (PSMA) in metastatic prostate cancer (PC), the goal of this study

234 n urgent need for an effective treatment for metastatic prostate cancer (PC).

235 In metastatic prostate cancer (PCa) cells, imbalance betwee

236 showed that beta1 integrins are activated in metastatic prostate cancer (PCa) cells, increasing PCa m

237 Metastatic prostate cancer (PCa) is one of the leading c

238 rapy) for radioguided surgery (RGS) of small metastatic prostate cancer (PCa) soft-tissue lesions.

239 Treatment of metastatic prostate cancer (PCa) with single agents has

240 been associated with hormone-refractory and metastatic prostate cancer (PCa).

241 nce to antiandrogen therapy in patients with metastatic prostate cancer poses a major challenge, whic

242 The survival of patients with metastatic prostate cancer progressing on androgen-depri

243 Fourteen patients with metastatic prostate cancer received escalating amounts (

244 Twenty-one patients with metastatic prostate cancer received two monthly injectio

245 Twenty-one patients with metastatic prostate cancer received two monthly vaccinat

246 ion of the mechanisms of hormone-independent metastatic prostate cancer remains a significant and hig

247 st for clinically localized prostate cancer, metastatic prostate cancer remains essentially incurable

248 gents have demonstrated efficacy in men with metastatic prostate cancer resistant to traditional horm

249 ther agents can improve outcomes in men with metastatic prostate cancer resistant to traditional horm

250 les of docetaxel at the beginning of ADT for metastatic prostate cancer resulted in significantly lon

251 ts with organ-confined or hormone-refractory metastatic prostate cancer revealed that metastatic smal

252 immunohistochemical analysis of primary and metastatic prostate cancer samples showed increased stag

253 al, we enrolled men with locally advanced or metastatic prostate cancer scheduled to start indefinite

254 Importantly, a p53 mutation found in metastatic prostate cancer severely disrupts the p53 neg

255 mutations in DNA-repair genes among men with metastatic prostate cancer significantly exceeded the pr

256 (ADT) has been the backbone of treatment for metastatic prostate cancer since the 1940s.

257 bserved that all of the androgen-independent metastatic prostate cancer sites harboring TMPRSS2-ERG w

258 lloproteinase (MT1-MMP) in human primary and metastatic prostate cancer specimens as compared with no

259 Analysis of human bone metastatic prostate cancer specimens reveals heterogeneo

260 We have found that metastatic prostate cancer specimens, obtained through a

261 advances in the past years, the treatment of metastatic prostate cancer still remains challenging.

262 llagen previously shown to be upregulated in metastatic prostate cancer that has been used as a tissu

263 f PcG-mediated transcriptional repression in metastatic prostate cancer that is reminiscent of stem c

264 It has been shown that in metastatic prostate cancer, the amount of citrate in pro

265 ations with locally advanced and symptomatic metastatic prostate cancer, their side-effects often lea

266 Eligible patients had metastatic prostate cancer threatening enough to justify

267 Expression analysis in human metastatic prostate cancer tissue revealed that beta1 wa

268 rs as distinguishing characteristics of bone-metastatic prostate cancer tissue.

269 tate cancer cell lines and primary tumor and metastatic prostate cancer tissues from patients express

270 show that FGF19 is expressed in primary and metastatic prostate cancer tissues, where it functions a

271 stosterone ((18)F-FDHT) PET in patients with metastatic prostate cancer to assess androgen receptor e

272 ybrid cellular automaton (HCA) model of bone metastatic prostate cancer to identify the optimal thera

273 trial in patients with previously untreated metastatic prostate cancer to test the hypothesis that t

274 cancer, assessment of treatment response in metastatic prostate cancer to the bone remains a major c

275 Seven patients with progressive clinically metastatic prostate cancer underwent (18)F-FDG and (18)F

276 Eighty-seven men with castrate-resistant metastatic prostate cancer underwent (18)F-FDG PET/CT an

277 reviously demonstrated the ability to detect metastatic prostate cancer using N-[N-[(S)-1,3-dicarboxy

278 ediating DNA-repair processes among men with metastatic prostate cancer was 11.8%, which was signific

279 Metastatic prostate cancer was two times as likely among

280 and is also expressed in 87.5% of the human metastatic prostate cancers we examined.

281 clinical trial that treated 27 patients with metastatic prostate cancer, we aimed to test the safety

282 redictive serum biomarkers for management of metastatic prostate cancer, we used phage display finger

283 copathological data from 10,139 men with non-metastatic prostate cancer were available for this study

284 Patients with new metastatic prostate cancer were randomly assigned within

285 -5alpha-dihydrotestosterone in patients with metastatic prostate cancer were reviewed.

286 multiple SSX family members are expressed in metastatic prostate cancers which are amenable to simult

287 ted androgen signaling signature, similar to metastatic prostate cancer, which may reflect dedifferen

288 of men with relapsing, locally advanced, or metastatic prostate cancer who achieve a good initial re

289 onate, improves overall survival in men with metastatic prostate cancer who are starting hormone ther

290 Patients with newly diagnosed metastatic prostate cancer who had adequate hematologic,

291 Men with metastatic prostate cancer who have a poor response to i

292 eatment options are needed for patients with metastatic prostate cancer who have not received chemoth

293 Patients with metastatic prostate cancer who undergo androgen-ablation

294 uits men with high-risk, locally advanced or metastatic prostate cancer who were initiating long-term

295 We recruited 692 men with documented metastatic prostate cancer who were unselected for famil

296 Current and new therapies in metastatic prostate cancer will comprise a multitargeted

297 -line hormonal treatment, most patients with metastatic prostate cancer will succumb to a hormone-ref

298 ic agent to improve the treatment outcome of metastatic prostate cancer with docetaxel.

299 alities that have been tested in humans with metastatic prostate cancer, with consideration of the st

300 conducted in patients with bone pain due to metastatic prostate cancer, with disease progression aft