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 patients with newly diagnosed and recurrent prostate carcinoma.

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

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

5 FACBC is a promising radiotracer for imaging prostate carcinoma.

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

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

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

9 ncluding curative antitumor activity against prostate carcinoma.

10 MIC is widely expressed in prostate carcinoma.

11 ing diagnostic or therapeutic strategies for prostate carcinoma.

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

13 nt improvement to targeted radiotherapies of prostate carcinoma.

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

15 he androgen-insensitive state of progressive prostate carcinoma.

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

17 ribute to the development and progression of prostate carcinoma.

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

19 ding glioblastoma, endometrial carcinoma and prostate carcinoma.

20 proliferation and reduced differentiation in prostate carcinoma.

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

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

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

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

25 astases from orthotopically implanted PC3LN3 prostate carcinoma.

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

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

28 movement are commonly mutated or deleted in prostate carcinomas.

29 c hyperplasia but significantly increased in prostate carcinomas.

30 ility for developing aggressive, spontaneous prostate carcinomas.

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

32 xpressing tumor cells in invasive breast and prostate carcinomas.

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

34 ed staining method for the identification of prostate carcinomas.

35 and numerically abnormal in the majority of prostate carcinomas.

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

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

38 peripheral zone and primary peripheral zone prostate carcinomas.

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

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

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

42 expression is lost in metastatic bladder and prostate carcinomas.

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

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

45 1A promoter in 63% of primary microdissected prostate carcinomas (7 of 11 samples).

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

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

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

49 of renal cell carcinomas, as well as in some prostate carcinoma and breast carcinoma lines.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 the IL-11 receptor system is up-regulated in prostate carcinoma, and may be one part of a cytokine ne

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

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

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

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

69 Breast and prostate carcinomas are among those cancers that respond

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

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

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

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

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

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

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

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

78 ng cancer (H69) cell lines or a variant of a prostate carcinoma cell line (PC3-N).

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

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

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

82 (223Leu) and p53(274Phe), from Fas-resistant prostate carcinoma cell line DU145.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 We have shown previously that the putative prostate carcinoma cell lines TSU-Pr1 and JCA-1 share a

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

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

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

102 1A promoter was observed in five widely used prostate carcinoma cell lines, which acquired the abilit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 (3-Cl-AHPC), induces apoptosis in breast and prostate carcinoma cells and inhibits AKT activity in th

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

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

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

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

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

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

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

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

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

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

131 stable maspin-expressing transfectants using prostate carcinoma cells DU145 as the parental cell line

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

140 e molecules in the death of the DU-145 human prostate carcinoma cells induced by methylseleninic acid

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 Prostate carcinoma cells metastasizing to bone must init

148 transfection and treatment on production by prostate carcinoma cells of IL (interleukin)-8, which ca

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 Alone, LNCaP prostate carcinoma cells were essentially nontumorigenic

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

165 Treatment of T24 bladder and PC3 prostate carcinoma cells with full-length and 3'-truncat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 optosis particularly in androgen-independent prostate carcinoma cells.

184 sistance of the circulating metastatic human prostate carcinoma cells.

185 has antiproliferative consequences in LNCaP prostate carcinoma cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 rolled by translational efficiency in murine prostate carcinoma cells.

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

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

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

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

207 looxygenase-2 (COX-2) inhibitor celecoxib in prostate carcinoma cells.

208 ontribute to preferential bone metastasis by prostate carcinoma cells.

209 oncosuppressive effect of DLC1 in metastatic prostate carcinoma cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 Prostate carcinoma is linked to osteoblastic metastasis.

238 Prostate carcinoma is the most commonly diagnosed cancer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 -LOX-2 and 15S-HETE formation are reduced in prostate carcinoma (Pca).

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

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

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

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

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

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

273 Whether such therapies impact on prostate carcinoma remains to be determined through addi

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

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

276 led with color Doppler US, is inadequate for prostate carcinoma screening; therefore, targeted biopsy

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

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

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

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

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

282 nd therapeutic value of maspin in breast and prostate carcinoma, the lack of a suitable animal model

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

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

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

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

287 RM1 murine prostate carcinoma tumors transduced with human prostate

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

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

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

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

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

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

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

295 Of 133 consecutive patients with prostate carcinoma who were referred to the radiation on

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

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

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

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.