ライフサイエンスコーパス: prostate carcinoma

1 cells); T24 (bladder carcinoma); and DU 145 (prostate carcinoma).

2 es of AFAP-110 in the tumorigenic process of prostate carcinoma.

3 ncer and serum prostate-specific antigen for prostate carcinoma.

4 patients with newly diagnosed and recurrent prostate carcinoma.

5 l neoplasia, and remaining at high levels in prostate carcinoma.

6 in the detection, staging, and restaging of prostate carcinoma.

7 FACBC is a promising radiotracer for imaging prostate carcinoma.

8 p21.2, and one copy is frequently deleted in prostate carcinoma.

9 carcinoma, the 3LL lung carcinoma, and RM-1 prostate carcinoma.

10 show that PDGF D and uPA colocalize in human prostate carcinoma.

11 feratve function of adaptor protein GRB10 in prostate carcinoma.

12 ncluding curative antitumor activity against prostate carcinoma.

13 MIC is widely expressed in prostate carcinoma.

14 It is called squamous cell prostate carcinoma.

15 ing diagnostic or therapeutic strategies for prostate carcinoma.

16 region that has been shown to be involved in prostate carcinoma.

17 nt improvement to targeted radiotherapies of prostate carcinoma.

18 sion molecule, acts as a tumor suppressor in prostate carcinoma.

19 he androgen-insensitive state of progressive prostate carcinoma.

20 l test to examine the relationship of PIN to prostate carcinoma.

21 ribute to the development and progression of prostate carcinoma.

22 ily of cytokines, plays an important role in prostate carcinoma.

23 ding glioblastoma, endometrial carcinoma and prostate carcinoma.

24 rable disease control for men with high-risk prostate carcinoma.

25 iR-106b dependent downregulation of RBMS1 in prostate carcinoma.

26 o upregulated, and miR-107 downregulated, in prostate carcinoma.

27 vide high contrast in a mouse model of human prostate carcinoma.

28 molog (PTEN) is frequently involved in human prostate carcinoma.

29 astases from orthotopically implanted PC3LN3 prostate carcinoma.

30 movement are commonly mutated or deleted in prostate carcinomas.

31 c hyperplasia but significantly increased in prostate carcinomas.

32 ility for developing aggressive, spontaneous prostate carcinomas.

33 applied to an independent set of 30 primary prostate carcinomas.

34 xpressing tumor cells in invasive breast and prostate carcinomas.

35 minished the apoptotic effect of Ad.mda-7 in prostate carcinomas.

36 ed staining method for the identification of prostate carcinomas.

37 expression is lost in metastatic bladder and prostate carcinomas.

38 and numerically abnormal in the majority of prostate carcinomas.

39 uring transformation, as well as in advanced prostate carcinomas.

40 ll malignant human cancers, including 90% of prostate carcinomas.

41 peripheral zone and primary peripheral zone prostate carcinomas.

42 quired for mda-7/IL-24-mediated apoptosis of prostate carcinomas.

43 icity as seen in advanced hormone-refractory prostate carcinomas.

44 tions of IRDye 800CW 2-DG for epithelial and prostate carcinomas.

45 = 21), compared with levels in patients with prostate carcinoma (0.12 +/- 0.03 ng/mg U(Cr); P < 0.02;

46 ects of apigenin on androgen-sensitive human prostate carcinoma 22Rv1 tumor xenograft subcutaneously

47 1A promoter in 63% of primary microdissected prostate carcinomas (7 of 11 samples).

48 Cyst(e)inase suppressed the growth of prostate carcinoma allografts, reduced tumor growth in b

49 We hypothesized that metastatic prostate carcinomas also use the SDF-1/CXCR4 pathway to

50 pha and EBV LMP1 enhance XMRV replication in prostate carcinoma and B-lineage cells through the kappa

51 virus (XMRV) is a gammaretrovirus linked to prostate carcinoma and chronic fatigue syndrome.

52 One of these variants was identified in a prostate carcinoma and is altered from isoleucine to met

53 etide SPECT/CT in the detection of recurrent prostate carcinoma and is highly accurate in the differe

54 One hundred four men with newly diagnosed prostate carcinoma and no previous therapy were included

55 nhibits progression to poorly differentiated prostate carcinoma and pulmonary metastasis multiplicity

56 developed from a nodal metastasis of a human prostate carcinoma and that has been propagated as seria

57 patients are at risk for developing advanced prostate carcinoma and therefore would gain the most fro

58 itivity of two human tumor cell lines (DU145 prostate carcinoma and U251 glioma).

59 ents who had metastatic castration-resistant prostate carcinoma and who had exhausted available thera

60 tor inhibitor-1 promoter (in NRP-154 and PC3 prostate carcinoma and WPMY-1 prostate myofibroblast cel

61 fied tumor suppressor geneRASSF1A in primary prostate carcinomas and in prostate cell lines.

62 NKX3.1 protein expression is common in human prostate carcinomas and prostatic intraepithelial neopla

63 and restricted expression on the surface of prostate carcinomas and the neovasculature of most other

64 nd tissue microarrays demonstrates that both prostate carcinomas and the presumed precursor lesion (h

65 or androgen deprivation in hormone-dependent prostate carcinoma, and it has been examined as a chemop

66 prostatic intraepithelial neoplasia, primary prostate carcinoma, and metastases.

67 ternative source of cAMP, was found in human prostate carcinoma, and therefore, the contribution of t

68 terolemia directly accelerates the growth of prostate carcinomas, and that the pharmacological reduct

69 ls of a neuroendocrine/small cell variant of prostate carcinoma are available for experimental studie

70 The late stages of progression of prostate carcinoma are typically characterized by an and

71 Breast and prostate carcinomas are among those cancers that respond

72 setting of earlier detection, a majority of prostate carcinomas are still clinically localized and o

73 a/K-ATPase is significantly reduced in human prostate carcinoma as well as in several human cancer ce

74 (FAS) has been found to be overexpressed in prostate carcinomas, as well as other cancers, and it is

75 tion data of (125)I-labeled ligands in human prostate carcinoma bearing (PC-3) mice revealed two comp

76 U118 (human glioblastoma), and DU145 (human prostate carcinoma), but not that of M14-Mel xenografts

77 utant, Bax-negative) and PC-3 (p53-negative) prostate carcinomas, but not in HuPEC.

78 se, is overexpressed in androgen-independent prostate carcinoma C4-2 cells.

79 an +/-s.d.), and results in human breast and prostate carcinoma cell arrest and retention in the micr

80 ostate tumor growth and drastically enhances prostate carcinoma cell interaction with surrounding str

81 In this report, we characterized the human prostate carcinoma cell line 22Rv1 in an orthotopic syst

82 sion, using as our model the PA DU-145 human prostate carcinoma cell line and a highly invasive subli

83 excellent in vitro uptake within the DU-145 prostate carcinoma cell line and orthotopically implante

84 (223Leu) and p53(274Phe), from Fas-resistant prostate carcinoma cell line DU145.

85 ma incidence, restoration of expression in a prostate carcinoma cell line homozygous for the frameshi

86 at the PEITC-induced apoptosis in PC-3 human prostate carcinoma cell line is mediated by ERKs.

87 d differential display analysis of the human prostate carcinoma cell line PC-3 and its highly metasta

88 sed in many cancers including the metastatic prostate carcinoma cell line PC-3-M.

89 elial growth factor (VEGF) in vitro in human prostate carcinoma cell line PC-3.

90 In the DU-145 prostate carcinoma cell line, rhIL-11 stimulates a trans

91 t activated by PEITC treatment in PC-3 human prostate carcinoma cell line.

92 ) disseminating variants from the human PC-3 prostate carcinoma cell line.

93 l and apoptotic responses in the NRP-154 rat prostate carcinoma cell line.

94 Utilizing prostate carcinoma cell lines (C1, C2, and C3) derived f

95 ave observed HSP70 release from intact human prostate carcinoma cell lines (PC-3 and LNCaP) by a mech

96 ecreted MDA-7/IL-24 in inducing apoptosis in prostate carcinoma cell lines and displayed transformed

97 We show here in both pancreatic and prostate carcinoma cell lines cobalt chloride (used to m

98 tion of this cyclase was investigated in the prostate carcinoma cell lines LNCaP and PC3.

99 ion of Hsp72 did not reduce viability of the prostate carcinoma cell lines PC-3 and DU-145.

100 ibitor, significantly inhibited migration of prostate carcinoma cell lines, demonstrating that tumor

101 ates tumor metastasis, we used two different prostate carcinoma cell lines, DU145 and PC3, in which t

102 kDa PRL transfection in DU145 and PC-3 human prostate carcinoma cell lines, we demonstrated that expr

103 1A promoter was observed in five widely used prostate carcinoma cell lines, which acquired the abilit

104 silencing of RASSF1A was found in four other prostate carcinoma cell lines, which were adapted for ce

105 tivities against LNCaP, DU145, and PC3 human prostate carcinoma cell lines.

106 of human prostate tumors, mouse tumors, and prostate carcinoma cell lines.

107 protein and O-GlcNAc levels are elevated in prostate carcinoma cell lines.

108 odel showed that some rapidly promoted LNCaP prostate carcinoma cell tumorigenesis and others had no

109 omote angiogenesis and growth of LNCaP human prostate carcinoma cell tumors, and that these increases

110 e epithelial cells (PZ-HPV-7); several human prostate carcinoma cells (22Rv1, DU145, LNCaP, and PC3);

111 oration of CEACAM1(a)-4L expression in human prostate carcinoma cells (PC-3) suppresses tumorigenicit

112 ls (PrECs) compared with their expression in prostate carcinoma cells (PC-3).

113 NV1023 had significant oncolytic effect on prostate carcinoma cells (PC3, DU145, and LNCap) in vitr

114 In PC-3 prostate carcinoma cells (with overexpression of Bcl-2),

115 The murine prostate carcinoma cells 148-1,LMD and 148-1,PA were der

116 , we show that androgen deprivation of human prostate carcinoma cells activates the small GTPase, Ral

117 PN-1 levels increased in prostate carcinoma cells after downregulation of MMP-9 a

118 of wild-type p53 with increased survival of prostate carcinoma cells after fractionated exposure to

119 ted the suppression of GSK-3beta activity in prostate carcinoma cells and enhanced the turnover of be

120 esions because of high expression of PSMA in prostate carcinoma cells and in bone metastases and lymp

121 (3-Cl-AHPC), induces apoptosis in breast and prostate carcinoma cells and inhibits AKT activity in th

122 First, using a series of human prostate carcinoma cells and normal human prostate epith

123 Here, we used PC3M prostate carcinoma cells as a model to overexpress wild

124 Here, using PC3 human prostate carcinoma cells as a model, we provide direct e

125 in both human normal prostate epithelial and prostate carcinoma cells as well as in clinical prostate

126 egulation of NAG-1 expression in LNCaP human prostate carcinoma cells by 12-O-tetradecanoylphorbol-13

127 by MT1-MMP enhanced the migration of DU-145 prostate carcinoma cells by 2-fold compared with uncleav

128 MMP-9) activation promoted invasion of human prostate carcinoma cells by dissolving basement membrane

129 ndicate that EGCG induces apoptosis in human prostate carcinoma cells by shifting the balance between

130 The growth of normal prostate as well as of prostate carcinoma cells depends on functional androgen

131 n-tyrosine phosphatase, PTPmu, whereas LNCaP prostate carcinoma cells do not.

132 to identify gene expression changes in LNCaP prostate carcinoma cells exposed to PC-SPES and estrogen

133 We also found that the prostate carcinoma cells expressing high levels of MT1-M

134 ilencing in vitro and extend tests to target prostate carcinoma cells following systemic administrati

135 ditional PLCgamma1 knockdown in PC3LN3 human prostate carcinoma cells for further evaluation of PLCga

136 vivo, and in vivo that metastatic breast and prostate carcinoma cells form multicellular homotypic ag

137 of highly malignant viable circulating human prostate carcinoma cells from orthotopic but not ectopic

138 d hormone-related protein) overexpression by prostate carcinoma cells has been implicated in tumor pr

139 Green fluorescent protein-positive prostate carcinoma cells in a hydrogel or excised tumor

140 vo model of NI was established by implanting prostate carcinoma cells in the sciatic nerves of nude m

141 ous than sequential treatment in human DU145 prostate carcinoma cells infected with an adenovirus con

142 density the migration speed of DU-145 human prostate carcinoma cells is a balance between tractile a

143 show that N-cadherin mRNA expression in PC-3 prostate carcinoma cells is dependent on beta(1) integri

144 ven by the CDKN1A and CDH1 promoters in PC-3 prostate carcinoma cells is sensitive to treatment with

145 Here, we report that prostate carcinoma cells LNCaP and PC3 autoactivate late

146 Preferential bone metastasis of prostate carcinoma cells may therefore be facilitated by

147 Therefore, expression of PARP-DBD in prostate carcinoma cells offers a strategy to achieve se

148 c approach and generated an isogenic pair of prostate carcinoma cells PC3 (p53-/-) by stably introduc

149 Fas expression and converting Fas-sensitive prostate carcinoma cells PC3 into Fas-resistant ones.

150 Here we show that 22Rv1 prostate carcinoma cells produce high-titer virus that i

151 F4/p130 association after IR was observed in prostate carcinoma cells regardless of their sensitivity

152 r prostate stromal cells cotransplanted with prostate carcinoma cells s.c. into nude mice reduced tum

153 Here we show that the metastatic human prostate carcinoma cells selected for survival in the ci

154 TGFbeta and the medium conditioned by the prostate carcinoma cells stimulated myofibroblast differ

155 s increased and accumulated in the nuclei of prostate carcinoma cells subjected to ionizing radiation

156 d receptor expressed at the surface of human prostate carcinoma cells that plays central roles in ang

157 y be responsible for enhanced sensitivity of prostate carcinoma cells to a variety of anticancer trea

158 cells to proteasome and Hsp90 inhibitors and prostate carcinoma cells to proteasome inhibitors.

159 sitized the apoptotic response of breast and prostate carcinoma cells to various drugs, ranging from

160 SAT was conditionally overexpressed in LNCaP prostate carcinoma cells via a tetracycline-regulatable

161 Alone, LNCaP prostate carcinoma cells were essentially nontumorigenic

162 Breast and prostate carcinoma cells with activated PI(3) kinase los

163 as well as the effects of depleting Pim1 in prostate carcinoma cells with high levels of MYC.

164 Conversely, breast and prostate carcinoma cells with minimal PI(3) kinase activ

165 Treatment of prostate carcinoma cells with the novel retinoid 6-[3-(1

166 n were internalized by Siglec-XII-expressing prostate carcinoma cells, allowing targeting of a toxin

167 We show here that EGR1 binds to the AR in prostate carcinoma cells, and an EGR1-AR complex can be

168 MMP-9, highly invasive and metastatic human prostate carcinoma cells, androgen-repressed prostate ca

169 ceptor 1 (FGFR1) is ectopically expressed in prostate carcinoma cells, but its functional contributio

170 In HCA7 colon and C4-2 prostate carcinoma cells, ERBB2 is constitutively activa

171 transfection prevented the proliferation of prostate carcinoma cells, led to lactate dehydrogenase r

172 SRB12-p9 skin SCC cells, as well as with PC3 prostate carcinoma cells, revealed that RXRalpha transcr

173 The present study shows that in prostate carcinoma cells, the mda-7/IL-24-induced ER str

174 ydrazine (laromustine)-resistant DU145 human prostate carcinoma cells, which express high levels of A

175 n specifically induced in vitro apoptosis in prostate carcinoma cells, with innate resistance to chem

176 in androgen receptor-positive and -negative prostate carcinoma cells.

177 nd FB-Aca-BBN(7-14) was tested in PC-3 human prostate carcinoma cells.

178 ligand (TRAIL/Apo2-L)-mediated apoptosis in prostate carcinoma cells.

179 tracellular HSP70 to the cell surface of the prostate carcinoma cells.

180 optosis particularly in androgen-independent prostate carcinoma cells.

181 sistance of the circulating metastatic human prostate carcinoma cells.

182 has antiproliferative consequences in LNCaP prostate carcinoma cells.

183 plex emerges as a new target of radiation in prostate carcinoma cells.

184 e of HSF1 in the malignant phenotype of PC-3 prostate carcinoma cells.

185 ease of clusterin mRNA and protein levels in prostate carcinoma cells.

186 w this altered Ln-5 changes the migration of prostate carcinoma cells.

187 ethods to alleviate GSK-3beta suppression in prostate carcinoma cells.

188 ic survival after ionizing radiation (IR) of prostate carcinoma cells.

189 tal red fluorescent protein-expressing human prostate carcinoma cells.

190 ansmembrane collagen, collagen XXIII, in rat prostate carcinoma cells.

191 elial cells exert an anti-tumour activity on prostate carcinoma cells.

192 n of RASSF1A-expressing construct into LNCaP prostate carcinoma cells.

193 cycle progression and survival of human PC3 prostate carcinoma cells.

194 genes regulated by FKHRL1 and FKHR in LAPC4 prostate carcinoma cells.

195 owth factor (VEGF) expression in DU145 human prostate carcinoma cells.

196 and increases VEGF expression in DU145 human prostate carcinoma cells.

197 ulin-like growth factor (IGF)-1 signaling in prostate carcinoma cells.

198 rolled by translational efficiency in murine prostate carcinoma cells.

199 ated with high levels of HA synthesis by the prostate carcinoma cells.

200 ssion and its pro-survival response in human prostate carcinoma cells.

201 an (HA) pericellular matrix assembled on the prostate carcinoma cells.

202 reased the HGF-driven motility of metastatic prostate carcinoma cells.

203 g pathway that controls the proliferation of prostate carcinoma cells.

204 K1) in an HGF-dependent manner in metastatic prostate carcinoma cells.

205 oncosuppressive effect of DLC1 in metastatic prostate carcinoma cells.

206 ltures of bone marrow stromal cells with PC3 prostate carcinoma cells.

207 However, XMRV has not been found in prostate carcinoma cells.

208 - and for prostate precursor/stem cells and prostate carcinoma cells.

209 stimulates the intraosseous growth of PC-3M prostate carcinoma cells.

210 ssociated with an increased risk of advanced prostate carcinoma compared with the CC genotype [odds r

211 ) signaling persists in castration-resistant prostate carcinomas (CRPC), because of several mechanism

212 the cytotoxicity of PG, EGCG and Q to human prostate carcinoma DU-145 cells, since catalase increase

213 milk thistle extract, against advanced human prostate carcinoma DU145 cells and later identified that

214 ve activation of NF-kappaB in advanced human prostate carcinoma DU145 cells.

215 e NE cell population is greatly increased in prostate carcinomas during androgen ablation therapy tha

216 e show that alpha(6) integrin was present on prostate carcinoma escaping the gland via nerves.

217 n cultured human cancer cells (glioblastoma, prostate carcinoma, Ewing's sarcoma), HCR transduction m

218 majority of breast, colon, lung, ovarian and prostate carcinomas examined.

219 ETV1, a JMJD2A-binding protein, resulted in prostate carcinoma formation in mice haplodeficient for

220 d that the levels of MMP-26 protein in human prostate carcinomas from multiple patients were signific

221 rol subjects, and also from 10 patients with prostate carcinoma (group 2).

222 We report here that hormone-refractory human prostate carcinoma growing orthotopically efficiently de

223 In particular, prostate carcinoma has a high propensity for neural inva

224 s AGS (gastric carcinoma), DU-145 and LNCaP (prostate carcinoma), HCT-116 (colon carcinoma), MCF-7 (b

225 In epithelial prostate carcinomas, high SIRT7 levels are associated wi

226 , PC-3, ND-1, DU-145, 22Rv1, and one primary prostate carcinoma immortalized by overexpression of the

227 metric MR imaging for detection of recurrent prostate carcinoma in patients with suspected recurrence

228 arin and possess anticancer actions on human prostate carcinoma in vitro and in vivo.

229 ation of PKCzeta in mice results in invasive prostate carcinoma in vivo in the context of phosphatase

230 against orthotopically implanted LNCaP human prostate carcinomas in male nude mice and orthotopically

231 Furthermore, development of prostate carcinomas in TRAMP/Rosa26-FoxM1b double TG mic

232 hough SIGLEC12 allele status did not predict prostate carcinoma incidence, restoration of expression

233 NA (miRNA) expression and the development of prostate carcinoma is assumed.

234 Prostate carcinoma is the most commonly diagnosed cancer

235 s; UMUC-3, a bladder carcinoma line, and the prostate carcinoma line, DU145.

236 DU-145 cells, an E-cadherin expressing human prostate carcinoma line, survive loss of integrin-depend

237 bits the growth of androgen-responsive human prostate carcinoma LNCaP cells and provide molecular und

238 report that EGCG-induced apoptosis in human prostate carcinoma LNCaP cells is mediated via modulatio

239 unit permeation of polyamine pools in human prostate carcinoma LNCaP cells.

240 s efficiently than the wild-type XMRV in the prostate carcinoma LNCaP, DU145, and PC-3 cell lines, HE

241 iferative activity against hormone dependent prostate carcinoma LNCaP, with an IC50 value 3 times low

242 usters (breast carcinoma, ovarian carcinoma, prostate carcinoma, lung carcinoma, and melanoma).

243 ia an MET-dependent pathway; however, in two prostate carcinoma models, metastatic colonization was M

244 Fifteen patients with a recent diagnosis of prostate carcinoma (n = 9) or suspected recurrence (n =

245 expression in normal prostate tissue and in prostate carcinoma of increasing Gleason grades in paraf

246 timal markers were also measured for Dunning prostate carcinomas of anaplastic (RHF = 15%-20%) and we

247 er ADAM9 is critical for the pathogenesis of prostate carcinoma, one of the most common cancers in me

248 l (nanocurie) levels into mice bearing solid prostate carcinoma or disseminated human lymphoma induce

249 ssociated with an increased risk of advanced prostate carcinoma (OR, 1.95; 95% CI, 1.09-3.47).

250 or when inoculated with metastatic melanoma, prostate carcinoma, or mammary carcinoma cell lines.

251 Metastatic prostate carcinoma overexpresses prostate-specific membr

252 nce with a series of 73 castration-resistant prostate carcinoma patients treated with (225)Ac-PSMA-61

253 a large cohort of breast, lung, ovarian, and prostate carcinoma patients.

254 The TRAIL-resistant prostate carcinoma PC-3 and melanoma M202 cell lines wer

255 r (AR) signaling is a distinctive feature of prostate carcinoma (PC) and represents the major therape

256 titutively activated in androgen-independent prostate carcinoma (PC) cell lines due to the upregulate

257 roles in prostate tumorigenesis: AR promotes prostate carcinoma (PC) development, whereas GR acts as

258 wing sarcoma (Rh1), glioblastoma (U-373) and prostate carcinoma (PC-3) cells, and concurrently inhibi

259 migration of ovarian carcinoma (SKOV-3) and prostate carcinoma (PC-3) were examined following treatm

260 bladder cancer HTB9, colon cancer HCT116 and prostate carcinoma PC3 cells.

261 ancer 1) tumor-suppressor gene in metastatic prostate carcinoma (PCA) cells increased the expression

262 Prostate carcinoma (PCa) is the second most commonly dia

263 Prostate carcinoma (PCa) was detected in 75 patients in

264 in the development and progression of human prostate carcinoma (Pca).

265 normal prostate tissue samples, 127 primary prostate carcinomas (PCa), and 19 metastatic PCas.

266 c membrane antigen (PSMA), expressed by most prostate carcinomas (PCa), is a promising target for PCa

267 SA) levels after definitive local therapy of prostate carcinoma present a diagnostic dilemma.

268 eminating variants of human fibrosarcoma and prostate carcinoma recruit elevated levels of infiltrati

269 ion, DLC-3 expression was reduced in primary prostate carcinomas relative to normal prostate tissue.

270 Predicting prognosis in prostate carcinoma remains a challenge when using clinic

271 ever, the mechanism of NE cell enrichment in prostate carcinoma remains an enigma.

272 an immunohistochemical analysis of 126 human prostate carcinoma samples using polyclonal anti-NGEP se

273 Nineteen patients with prostate carcinoma scheduled for robot-assisted laparosc

274 7.8%), lymphoma (seven patients, 15.6%), and prostate carcinoma (seven patients, 15.6%).

275 c-MYC/Pim1-induced prostate carcinomas show evidence of neuroendocrine (NE)

276 In contrast, invasive prostate carcinoma showed a loss of beta3 and gamma2 pro

277 as localized primarily in the tumor cells of prostate carcinoma specimens.

278 Differential display of mRNA expression in prostate carcinoma sublines with varying metastatic pote

279 d expression of beta-catenin associated with prostate carcinoma suggests a role for beta-catenin in p

280 Since laminin 5 is lost in prostate carcinoma, the mechanism of control that result

281 oteins were both expressed in the same human prostate carcinoma tissue samples examined.

282 Two hundred seventy four patients with pT3 prostate carcinoma treated by radical prostatectomy and

283 astoma, and human DU145 androgen-independent prostate carcinoma tumor cells indicated that both compo

284 kinase family, was found to be expressed in prostate carcinoma tumor samples and cell lines.

285 RM1 murine prostate carcinoma tumors transduced with human prostate

286 n 5 were investigated in normal and invasive prostate carcinoma using immunohistochemistry, Northern

287 ause the prognosis of histologically similar prostate carcinomas varies, thus creating a need to pred

288 act of human chorionic gonadotropin (hCG) on prostate carcinoma viability was investigated.

289 of the following criteria: (a) Recurrence of prostate carcinoma was suspected after definitive therap

290 own efficacy as a single agent against human prostate carcinoma, we evaluated 2ME2 as a potential rad

291 nces and chemoresistance in lung, colon, and prostate carcinoma, we hypothesized that 14-3-3zeta prom

292 hods: In total, 280 men with newly diagnosed prostate carcinoma were included in the present study.

293 5-85 y) with metastatic castration-resistant prostate carcinoma were treated with 210 cycles of (225)

294 In the 8 patients with newly diagnosed prostate carcinoma who underwent dynamic scanning, visua

295 de that oncolytic therapy effectively treats prostate carcinomas with NI in an in vivo murine model w

296 hypoacetylation at this site is observed in prostate carcinomas with poor prognosis, this suggests t

297 hormone-independent (DU-145 and PC-3) human prostate carcinomas, without altering growth or survival

298 nanoparticles towards glioblastoma (GBM) and prostate carcinoma xenograft lesions in nude mice (eight

299 We report a human neuroendocrine/small cell prostate carcinoma xenograft that was developed from a n

300 and efficacy in a human PTEN-deficient LNCaP prostate carcinoma xenograft tumor model.