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

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

2 ific membrane antigen (PSMA)-617 therapy for metastatic prostate cancer.

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

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

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

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

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

8 ressor gene PTEN to promote the emergence of metastatic prostate cancer.

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

10 DNA repair defects are found in primary and metastatic prostate cancer.

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

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

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

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

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

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

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

18 patients diagnosed with locally advanced and metastatic prostate cancer.

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

20 ntial target of therapeutic intervention for metastatic prostate cancer.

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

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

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

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

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

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

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

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

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

30 ling circuit with functional significance in metastatic prostate cancer.

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

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

33 , such as (177)Lu-PSMA-617, is used to treat metastatic prostate cancer.

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

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

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

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

38 al as an imaging biomarker for recurrent and metastatic prostate cancer.

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

40 hylation is significantly more pronounced in metastatic prostate cancer.

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

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

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

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

45 1 are correlated with hormone-refractory and metastatic prostate cancer.

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

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

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

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

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

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

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

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

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

55 antitumor activity in patients with castrate metastatic prostate cancer.

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

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

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

59 ational clinical trials against advanced and metastatic prostate cancer.

60 ts FASN as a potential therapeutic target in metastatic prostate cancer.

61 apy (Prostate-Specific Membrane Antigen) for metastatic prostate cancer.

62 al as an imaging biomarker for recurrent and metastatic prostate cancer.

63 dy of CTT1057 in patients with localized and metastatic prostate cancer.

64 onuclide therapy, and radioguided surgery of metastatic prostate cancer.

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

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

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

68 pendent quantification of bone metastasis in metastatic prostate cancer.

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

70 ated by Pten heterozygosity, elicited lethal metastatic prostate cancer.

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

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

73 sensitivity and specificity for detection of metastatic prostate cancer.

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

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

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

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

78 rapy and ablative therapies in patients with metastatic prostate cancer.

79 e biodistribution and kinetics for targeting metastatic prostate cancer.

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

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

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

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

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

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

86 g pathways has been observed in advanced and metastatic prostate cancers.

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

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

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

90 ); 16 had CIM evidence of new or progressive metastatic prostate cancer and 1 had high clinical suspi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 tase activity in the development of advanced metastatic prostate cancer and suggests that blocking SR

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

108 atory tumor microenvironment in a subtype of metastatic prostate cancer, and show that a PRC1 inhibit

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

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

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

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

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

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

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

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

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

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

119 MA-11 performed well for the localization of metastatic prostate cancer at initial staging and at the

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

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

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

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

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

125 in a significant proportion of patients with metastatic prostate cancer, but the clinical implication

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

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

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

129 -culture of primary MSCs with validated bone metastatic prostate cancer cell line models.

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

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

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

133 Metastatic prostate cancer cell lines and bone metastasi

134 We also found that metastatic prostate cancer cell lines have a reduced lev

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

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

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

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

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

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

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

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

149 lso found that the upregulation of MAP4K4 in metastatic prostate cancer cells is driven by the MYC pr

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

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

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

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

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

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

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

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

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

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

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

161 ion of 276 kinase proteins in a pair of bone metastatic prostate cancer cells.

162 Metastatic prostate cancer commonly presents with target

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

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

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

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

167 ass-3 genomic rearrangements are enriched in metastatic prostate cancers, consist of duplications and

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

169 Metastatic prostate cancer continues to pose a difficult

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

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

172 Metastatic prostate cancer demonstrated significantly hi

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

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

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

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

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

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

179 100 kinases potentially implicated in human metastatic prostate cancer for functional evaluation.

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

181 Metastatic prostate cancers from anorchid men express tr

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

183 Heterogeneity in the genomic landscape of metastatic prostate cancer has become apparent through s

184 otent treatment strategies for patients with metastatic prostate cancer has been a major research foc

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

186 ast decade, a revolution in the treatment of metastatic prostate cancer has occurred with the advent

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

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

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

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

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

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

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

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

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

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

197 Metastatic prostate cancer is characterized by recurrent

198 Metastatic prostate cancer is differentiated by expressi

199 The evolutionary progression from primary to metastatic prostate cancer is largely uncharted, and the

200 Metastatic prostate cancer is treated with drugs that an

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

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

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

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

205 ut of 8 samples from patients diagnosed with metastatic prostate cancer (mean +/- SEM = 21 +/- 2.957

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

207 Smokers develop metastatic prostate cancer more frequently than nonsmoke

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

209 ividual treatment decisions in patients with metastatic prostate cancer (mPC), molecular diagnostics

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

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

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

213 For patients with metastatic prostate cancer, noninvasive serial measureme

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

215 l value by improving diagnostic accuracy for metastatic prostate cancer on (68)Ga-PSMA-11 PET/MRI and

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

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

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

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

220 A metastatic prostate cancer patient treated with the PARP

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

222 verlap significantly with those expressed in metastatic prostate cancer patients and in three individ

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

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

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

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

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

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

229 the role of IL-7 in tumor invasiveness using metastatic prostate cancer PC-3 cell line derivatives, a

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

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

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

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

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

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

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

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

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

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

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

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

242 Bone metastatic prostate cancer provokes extensive osteogenes

243 Fourteen patients with metastatic prostate cancer received escalating amounts (

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

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

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

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

248 RCK to existing approaches on 17 primary and metastatic prostate cancer samples.

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

250 Lethal metastatic prostate cancer seems to arise from a single

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

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

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

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

255 Analysis of human bone metastatic prostate cancer specimens reveals heterogeneo

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

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

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

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

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

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

262 Eligible patients had metastatic prostate cancer threatening enough to justify

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

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

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

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

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

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

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

270 class-2 activating mutations are acquired in metastatic prostate cancers, truncate the C-terminal dom

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

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

273 Methods: Subjects with metastatic prostate cancer underwent 2 PET/CT scans with

274 Methods: Subjects with metastatic prostate cancer underwent two PET/CT scans wi

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

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

277 In this report, a mouse model of metastatic prostate cancer was generated through the del

278 Metastatic prostate cancer was two times as likely among

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

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

281 engineered mouse model of Pten/Trp53 mutant metastatic prostate cancer, we found that complete loss

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

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

292 Patients with metastatic prostate cancer who undergo androgen-ablation

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

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

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

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

297 These mice developed early-onset metastatic prostate cancer with complete penetrance.

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

299 Trop2 as a driver and therapeutic target for metastatic prostate cancer with neuroendocrine phenotype

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