ライフサイエンスコーパス: prostate tumor

1 th MR imaging (brain, liver, pancreatic, and prostate tumors).

2 opper uptake can be used as a means to image prostate tumors.

3 ose overexpression is highly associated with prostate tumors.

4 d, prostate-specific oncolytic virus (OV) to prostate tumors.

5 of ETS transcription factors are frequent in prostate tumors.

6 al-derived or luminal-derived Pten-deficient prostate tumors.

7 nd 14-3-3epsilon were overexpressed in human prostate tumors.

8 ic activation of the ETS factor ESE1/ELF3 in prostate tumors.

9 n and inhibit growth of castration-resistant prostate tumors.

10 xypropyl)methacrylamide (HPMA) copolymers in prostate tumors.

11 a striking suppression in the development of prostate tumors.

12 stently down-regulated miRs in primary human prostate tumors.

13 ve genomic hybridization (CGH) on 86 primary prostate tumors.

14 nd we found that AIF protein is increased in prostate tumors.

15 membrane proteoglycan overexpressed in human prostate tumors.

16 lar localization have been detected in human prostate tumors.

17 arcomas, as well as in metastatic breast and prostate tumors.

18 tures that are associated with cell types of prostate tumors.

19 crofluidic cards in an extended series of 30 prostate tumors.

20 compared with progenitor cells from control prostate tumors.

21 s TRAMP mice, that is predisposed to develop prostate tumors.

22 e against pre-established mouse melanoma and prostate tumors.

23 has a functional role in the development of prostate tumors.

24 ed fibroblasts (CAF) that characterize TRAMP prostate tumors.

25 tanding of the de-differentiation process of prostate tumors.

26 SF2 inactivation we have observed in primary prostate tumors.

27 useful in predicting the prognosis of human prostate tumors.

28 sed the extent and the histological grade of prostate tumors.

29 pregulate EMT transcription factors in mouse prostate tumors.

30 d with Gleason score and metastasis in human prostate tumors.

31 s with the aggressiveness and progression of prostate tumors.

32 riptional changes and results in age-related prostate tumors.

33 , but distinct from CSCs obtained from frank prostate tumors.

34 d upon castration of mice carrying xenograft prostate tumors.

35 on of cell growth in vitro and in orthotopic prostate tumors.

36 mpared to their levels in hormone-responsive prostate tumors.

37 t affect skin wound healing or the growth of prostate tumors.

38 and our findings reveal utility in assessing prostate tumors.

39 mbryonic stem cells and in highly metastatic prostate tumors.

40 expression is lost in >60% of human primary prostate tumors.

41 s another compensatory inhibitory pathway in prostate tumors after ipilimumab therapy.

42 a(1) has been demonstrated to correlate with prostate tumor aggressiveness and metastatic potential.

43 ay component that itself was associated with prostate tumor aggressiveness.

44 TAMs surrounding murine prostate tumors also expressed argI(high)iNOS(low) early

45 in athymic nude mice: a human PC-3 M-luc-C6 prostate tumor and a human BxPc3-luc2 pancreatic tumor m

46 al model to explore the interactions between prostate tumor and immune microenvironment.

47 e not been compared on a large scale between prostate tumor and normal prostate, and the mechanisms b

48 Here, we sequenced the exomes of 112 prostate tumor and normal tissue pairs.

49 rrelated with metastasis in a mouse model of prostate tumor and that in human prostate cancer, CFL ex

50 ons by MMPs to the progression of aggressive prostate tumor and to helping tumors cleverly find alter

51 carried out gene-expression profiling of 98 prostate tumors and 52 benign adjacent prostate tissue s

52 study, we quantitatively profiled 95 primary prostate tumors and 86 benign adjacent prostate tissue s

53 n are reactivated in mouse and human primary prostate tumors and are further enriched in human metast

54 response-1 (Egr-1) is overexpressed in human prostate tumors and contributes to cancer progression.

55 ssion in primary tumors, we analyzed primary prostate tumors and found a significant correlation betw

56 deep genomic analysis of advanced metastatic prostate tumors and has revealed candidate somatic alter

57 r ESE3/EHF in the development of a subset of prostate tumors and highlight the clinical importance of

58 layed the growth of androgen-dependent human prostate tumors and impaired androgen-induced cell migra

59 us-related virus) has been detected in human prostate tumors and in blood samples from patients with

60 f established MCA-induced tumors or TRAMP-C1 prostate tumors and inhibited the development of TRAMP-C

61 ely activated in a substantial proportion of prostate tumors and is considered a key mechanism suppor

62 We sequenced the genomes of 57 prostate tumors and matched normal tissues to characteri

63 f both PI3-kinase and Ras signaling in human prostate tumors and metastases.

64 reased levels of both proteins in aggressive prostate tumors and metastatic deposits.

65 howed that CASP7 is downregulated in primary prostate tumors and metastatic lesions across multiple d

66 molecules with higher expression/activity in prostate tumors and play critical role in PCa growth and

67 ith high-fat diet-accelerated progression of prostate tumors and that Src kinases mediate this pathol

68 recurrent Treg cell clones, one prevalent in prostate tumors and the other associated with prostatic

69 ese results demonstrate interactions between prostate tumors and the psychosocial environment mediate

70 GRHL2 colocalized with AR in prostate tumors and was frequently amplified and upregul

71 tected at membranes in some high-grade human prostate tumors, and PTK6 and E-cadherin expression leve

72 st time the epigenetic silencing of SLIT2 in prostate tumors, and supported SLIT2 as a potential biom

73 owever, MTDH is predominantly cytoplasmic in prostate tumors, and this localization correlates with p

74 ime that Ron promotes prostate tumor growth, prostate tumor angiogenesis and prostate cancer cell sur

75 gen hexasaccharide that was proposed to be a prostate tumor antigen.

76 Using the prostate tumor antigens PSMA and PSCA, we show that co-t

77 hough several preclinical models of advanced prostate tumors are available, a model that recapitulate

78 or its role in development or progression of prostate tumors are scarce.

79 insensitive to ADT, as well as high-grade/NE prostate tumors, are characterized by elevated FOXC2, an

80 However, it is unknown whether prostate tumors arise well differentiated and then progr

81 localization for focal therapy of aggressive prostate tumors as well as assessment of the therapy res

82 ic modulation of p-Akt in PTEN-deficient PC3 prostate tumor bearing mice after oral administration an

83 g expansion occurred following castration of prostate tumor-bearing mice.

84 Eleven Dunning R3327-AT prostate tumor-bearing nude rats were immobilized in cus

85 ic acne in normal mice and also in tumors in prostate-tumor-bearing, severe combined immunodeficient

86 Volumes of interest (VOIs) for prostate tumors, benign prostatic hyperplasia (BPH) nodu

87 nding of the mechanistic functions of ERG in prostate tumor biology and towards development of early

88 The paucity of biomarkers to predict prostate tumor biology makes it important to identify ke

89 in IGFBP-3 exhibit weaker growth of primary prostate tumors but higher incidence of metastatic disea

90 miR-21 axis exerts its oncogenic effects in prostate tumors by downregulating TGFBR2, hence inhibiti

91 stromal cell-conditioned media to stimulate prostate tumor cell growth.

92 ic proteins (BMP) are critical regulators of prostate tumor cell growth.

93 derstand the mechanism of action of SPDEF in prostate tumor cell invasion and metastasis.

94 uced expression of endogenous SMC genes in a prostate tumor cell line (LNCaP), none could induce the

95 tion, and utilization of a novel human LNCaP prostate tumor cell line, N-AR, which stably expresses w

96 Forced expression of ERG in prostate tumor cell lines resulted in significantly incr

97 By dissecting the underlying mechanism in prostate tumor cell lines we show the ERG-mediated up-re

98 Mst1 in a LNCaP or castration-resistant C4-2 prostate tumor cell model, as revealed by a mutagenesis

99 dependent transcription is a major driver of prostate tumor cell proliferation.

100 ects of SPDEF on tumor cell metastasis using prostate tumor cells as a model.

101 In untreated specimens, 50% prostate tumor cells exhibited nuclear accumulation of A

102 involved in ligand-mediated AR activation in prostate tumor cells have not been clearly defined.

103 showed rapid and specific internalization in prostate tumor cells in vitro and accumulation in prosta

104 binding and rapid internalization into human prostate tumor cells in vitro and tumor homing in vivo u

105 lanted s.c. with TROP-2-expressing PC3 human prostate tumor cells or with PC3 metastases in the scapu

106 n of mice with irradiated Mobilan-transduced prostate tumor cells protected mice against subsequent t

107 Inhibiting Prx1 expression in prostate tumor cells reduced tumor vascular formation an

108 In contrast, silencing SIRT1 in metastatic prostate tumor cells restores cell-cell adhesion and ind

109 he antitumor effects of aflibercept in DU145 prostate tumor cells that displays high endogenous IL6R

110 We successfully analyze and classify prostate tumor cells, first in cultured cells, and ultim

111 ulates the nuclear translocation of PAR-4 in prostate tumor cells, providing a mechanism for its biol

112 and early metastatic spread of basal-luminal prostate tumor cells.

113 s from the nucleus to the cytoplasm in human prostate tumor cells.

114 be upregulated by hypoxic condition in PC-3 prostate tumor cells.

115 in67R receptors, which are over expressed in prostate tumor cells.

116 beled UA20 scFv was taken up specifically by prostate tumor cells.

117 protein complexes linked to AR activation in prostate tumor cells.

118 60 coactivator to the nuclear compartment of prostate tumor cells.

119 involved in ligand-mediated AR activation in prostate tumor cells.

120 and genetically-induced primary lung tumors, prostate tumors, colon xenografts, and lung metastases,

121 peractivation of YAP in castration-resistant prostate tumors compared to their levels in hormone-resp

122 1 was highly expressed in primary breast and prostate tumors compared with adjacent normal epithelial

123 veries of recurrent FoxA1 mutations in human prostate tumors, comprehensive understanding of FoxA1 fu

124 -> mTOR and MAPK signaling pathways in these prostate tumors cooperate to upregulate c-Myc.

125 sed proangiogenic potential, suggesting that prostate tumor-derived PTHrP potentiates this activity o

126 immune system, have never been isolated from prostate tumors, despite their suspected role in disease

127 It is unknown whether human prostate tumors develop a similar metabolic response to

128 Prostate tumors develop resistance to androgen deprivati

129 ts show that loss of BRCA2 expression during prostate tumor development is strongly correlated with b

130 Spontaneous prostate tumors did not develop in IGFBP-3KO mice, but s

131 efine the temporal and spatial occurrence of prostate tumors, disseminated tumor cells, and metastase

132 We asked the simple question of whether a prostate tumor driven by MT depends on p110alpha, which

133 uding MT and HER2, while p110beta was key in prostate tumors driven by Pten loss.

134 They observed that metabolic asymmetry in prostate tumors drives aggressive disease with high p62

135 oding RNA frequently expressed in aggressive prostate tumors, drives cancer by directly disrupting SN

136 were elevated in approximately 60% of human prostate tumors evaluated relative to adjacent normal ti

137 %) and no expression was detected in primary prostate tumors examined (0/73; P < 0.001).

138 Moreover, TK-/- TRAMP+ prostate tumors exhibited decreased tumor vascularizatio

139 uminal cells, luminal-derived Pten-deficient prostate tumors exhibited slower disease progression, co

140 rmal mouse prostate tissue and human LuCaP35 prostate tumor explants display an EMT as well as increa

141 GR-Pten(Delta/Delta) mice developed invasive prostate tumors featuring Akt activation and extensive i

142 esents a useful preclinical model of primary prostate tumors for their biological characterization, b

143 genic AR expression by Osr1 promoter induces prostate tumor formation in mice.

144 overexpression of AR is sufficient to induce prostate tumor formation in vivo.

145 growth and invasion, as well as the in vivo prostate tumor formation, local invasion and distant met

146 tages of tumorigenesis, autophagy suppresses prostate tumor formation.

147 s in aggressive (Gleason >/=7, stage >/=T2b) prostate tumors from 24 African American patients.

148 In this model, we show that prostate tumors from 30-week-old TRAMP mice have increas

149 d similar changes in mesenchymal features in prostate tumors from patients treated with androgen-depr

150 rammed the AR cistrome to resemble that of a prostate tumor, functionally linking these specific fact

151 essions positively correlated with increased prostate tumor Gleason score.

152 RM1 prostate tumors grown in kindlin-2(+/-) mice had fewer b

153 ith hSef-b plasmid, significantly suppressed prostate tumor growth (60%) through inhibition of cell p

154 g STAT3 in tumor cells significantly reduced prostate tumor growth and CSCs.

155 depletion leads to a profound repression of prostate tumor growth and distal metastasis and substant

156 h the importance of Runx2 phosphorylation in prostate tumor growth and highlight its value as a poten

157 knockdown of MAOA reduced or even eliminated prostate tumor growth and metastasis in PCa xenograft mo

158 ells, but also sufficient to promote primary prostate tumor growth and metastasis upon exogenous expr

159 n of the signaling domain of beta4 inhibited prostate tumor growth and progression in response to los

160 therapeutic strategy in effectively managing prostate tumor growth and provides a framework of system

161 wever, whether osteogenesis is necessary for prostate tumor growth in bone is unknown.

162 but not CD4(+) T cells, was able to restore prostate tumor growth in hosts devoid of myeloid-specifi

163 g paclitaxel and rubone inhibited orthotopic prostate tumor growth in nude mice, compared with monoth

164 microenvironment; however, their function in prostate tumor growth in the skeleton has not been explo

165 bitors resulted in synergistic inhibition of prostate tumor growth in vitro and in vivo.

166 ostate compared with other tissues, inhibits prostate tumor growth in vivo.

167 in human CaP specimens and that it regulates prostate tumor growth through TLR4-dependent regulation

168 nimal model, sHA strongly inhibited LNCaP-AI prostate tumor growth without causing weight loss or app

169 Despite early success to suppress prostate tumor growth, ADT eventually fails leading to r

170 is a potential option for the management of prostate tumor growth, microinvasion, and metastasis.

171 ta show for the first time that Ron promotes prostate tumor growth, prostate tumor angiogenesis and p

172 and reduced both subcutaneous and orthotopic prostate tumor growth, whereas Stat3 had a predominant r

173 reported that survivin levels increase with prostate tumor growth.

174 evaluated the functional role of survivin in prostate tumor growth.

175 rt antiandrogens into AR agonists, promoting prostate tumor growth.

176 s CD11b(+)Gr1(+) cells in the bone marrow of prostate tumor hosts.

177 Metabolic profiling of human prostate tumors identified a massive increase in the SRC

178 In human normal prostates and prostate tumors, IL-17 mRNA levels were positively corre

179 copolymers were administered to mice bearing prostate tumors immediately before treatment of the righ

180 eoblastic bone lesions induced by metastatic prostate tumors in humans.

181 obilan into subcutaneously growing syngeneic prostate tumors in immunocompetent hosts improved animal

182 lished the posttreatment regrowth of primary prostate tumors in mice and their spread to the lungs fo

183 P in cancer, coupled with the development of prostate tumors in mice lacking PHLPP1, identifies PHLPP

184 of PARP efficiently kill breast, ovarian, or prostate tumors in patients carrying hereditary mutation

185 Prostate tumors in TK(-/-) hosts exhibited an increase i

186 dependent radical prostatectomy cohorts (822 prostate tumors in total) by immunohistochemistry.

187 er a human tumor suppressor gene, hSef-b, to prostate tumors in vivo.

188 eta signaling potentiated castrate-resistant prostate tumors, in a Wnt-dependent manner.

189 hed in both fat and cholesterol--accelerated prostate tumor incidence and tumor burden compared to mi

190 ed to explore its functional significance in prostate tumor initiation and its link to androgen recep

191 Prostate tumors invariably overexpress prostate surface

192 ioral stress inhibited apoptosis and delayed prostate tumor involution both in phosphatase and tensin

193 High VDR expression in prostate tumors is associated with a reduced risk of let

194 ow that higher UGT2B17 protein expression in prostate tumors is associated with higher Gleason score,

195 , serine 2 (TMPRSS2) in approximately 40% of prostate tumors, is a key driver of prostate carcinogene

196 es have reported complementary data in human prostate tumor lines, suggesting that p110beta activatio

197 ed LC-MS/MS spectra of protein extracts from prostate tumor LNCaP cells.

198 In contrast, we found that, in Pten(-/-) prostate tumors, loss of Nkx3.1 expression is mediated a

199 - TRAMP+ mice show a significant decrease in prostate tumor mass relative to TRAMP mice containing fu

200 models, we further show that FoxA1 inhibits prostate tumor metastasis in vivo.

201 The expression of WNT16B in the prostate tumor microenvironment attenuated the effects o

202 changes to stromal signaling by an enriched prostate tumor microenvironment cell population, adipose

203 nt roles of BM-MSCs as key components in the prostate tumor microenvironment to promote PCa metastasi

204 , which regulate extracellular matrix in the prostate tumor microenvironment.

205 ssed in mouse and human stromal cells of the prostate tumor microenvironment.

206 apies that restore NK cell efficiency in the prostate tumor microenvironment.

207 additional immune-inhibitory pathways in the prostate-tumor microenvironment, we evaluated untreated

208 adenocarcinoma of mouse prostate (TRAMP)-C2 prostate tumor model.

209 heme cellular iron revealed that preclinical prostate tumor models could be differentiated according

210 analyses of transcription in multiple murine prostate tumor models featuring PI3K/AKT pathway activat

211 s, and external data on genes with recurrent prostate tumor mutations.

212 depots achieved >95% tumor regression in the prostate tumors (n=8); with a median survival of more th

213 eal adenocarcinoma, glioblastoma multiforme, prostate tumors, non-small cell lung tumors, and ovarian

214 To interrogate the redox status of prostate tumors noninvasively, we developed hyperpolariz

215 enografts treated with PI3K inhibitor and in prostate tumors of mice with prostate-restricted express

216 levels in Pten/Trp53 double-null MEFs and in prostate tumors of Pten/Trp53 double-null mutant mice.

217 Prostate tumors often contain neuroendocrine differentia

218 ontaneously disintegrated over time when DKO prostate tumor organoids grew larger, setting the stage

219 ocket inhibitor preferentially collapsed DKO prostate tumor organoids over AADKO organoids, which spo

220 1 in metastatic tissue compared with primary prostate tumors (P < 0.0001).

221 Prostate tumors produce various soluble factors, includi

222 romote transactivation of ErbB2 and c-Met in prostate tumor progenitor cells and human cancer cell li

223 xtual signals that regulate the expansion of prostate tumor progenitor cells are poorly defined.

224 on of ErbB2 and c-Met reduced the ability of prostate tumor progenitor cells to undergo self-renewal

225 new paradigm for RB function in controlling prostate tumor progression and lethal tumor phenotypes.

226 ficient phenotype and delayed Pten-deficient prostate tumor progression in both castrate-naive and ca

227 and Id3 genes that are crucially involved in prostate tumor progression through PI3K-dependent and mT

228 ion levels of CCND2 markedly correlated with prostate tumor progression to high Gleason score and ele

229 n1 immunoreactivity directly correlated with prostate tumor progression to metastasis in the transgen

230 ost abundantly expressed variant that drives prostate tumor progression under ADT conditions.

231 istic acid stimulates high-fat diet-mediated prostate tumor progression.

232 We report known prostate tumor regulatory drivers and nominate novel tra

233 control mice increased the aggressiveness of prostate tumors relative to noncastrated counterparts, d

234 xpression in cells of primary and metastatic prostate tumors relative to the normal prostate epitheli

235 e mechanism by which nerves are attracted to prostate tumors remains unknown.

236 ly, our preclinical studies demonstrate that prostate tumor resistance to cabazitaxel can be overcome

237 pression, and NCoA2 overexpression in murine prostate tumors resulted in hyperactivation of PI3K/AKT

238 Analyses of genome-wide gene expression in prostate tumors revealed frequent alterations in the exp

239 Integration of multi-omics data from 521 prostate tumor samples indicated a stronger regulatory i

240 s of tissue microarrays containing 112 human prostate tumor samples revealed that Etk expression is e

241 h genotype and gene expression data from 602 prostate tumor samples.

242 as downregulated in a majority of metastatic prostate tumors, showing a negative correlation with EZH

243 graphy techniques as the contrast numbers in prostate tumor sites are severalfold higher as compared

244 f canonical Wnt signaling is shown to reduce prostate tumor size and restore regression following cas

245 We hypothesized that prostate tumor specific epigallocatechin-gallate (EGCg)

246 e (198)AuNPs utilizes the redox chemistry of prostate tumor specific phytochemical EGCg as it convert

247 co-occurs with expression of beta-catenin in prostate tumor specimens.

248 degradation may be an effective therapeutic prostate tumor strategy in the context of AR mutations t

249 Here we show they function in prostate tumor suppression in the mouse.

250 eta activated kinase-1 (Tak1), is a putative prostate tumor suppressor gene within this region whose

251 NKX3.1, a prostate tumor suppressor that accelerates the DNA repai

252 ) cell lines (LAPC4) and in 1 out of 24 (4%) prostate tumors surveyed.

253 Mean prostate tumor SUVmax(15-20min) was significantly higher

254 d for 91 human prostate specimens, including prostate tumor (T), matched normal adjacent to tumor (AT

255 A prostate tumor-targeting single-chain antibody fragment

256 age IGFBP-3KO mice tended to exhibit larger prostate tumors than control mice.

257 specific compound mutant mice develop lethal prostate tumors that are inherently resistant to castrat

258 slower-growing, autochthonous PTEN-deficient prostate tumors that did not exhibit a classic Warburg p

259 gs indicate that ETV4 promotes metastasis in prostate tumors that have activation of PI3-kinase and R

260 gulation of ESE1/ELF3 and NF-kappaB in human prostate tumors that was associated with adverse prognos

261 primary localized low- and high-grade human prostate tumors that were implanted under the renal caps

262 se early following the initial occurrence of prostate tumors, there is a significant temporal lag in

263 androgen-dependent and castration-resistant prostate tumors through a mechanism that involves AR fun

264 nofluorescent confocal microscopy of patient prostate tumor tissue and LNCaPs confirmed nuclear local

265 borated with real-time PCR analysis of human prostate tumor tissue arrays that revealed the expressio

266 four miRNAs were also downregulated in human prostate tumor tissue compared with normal prostate.

267 We hypothesized that BRCA1 expression in prostate tumor tissue may be associated with prostate ca

268 In human prostate tumor tissue microarrays, loss of PTEN correlat

269 P3 expression was elevated in multiple human prostate tumor tissue samples and in the human androgen-

270 immunotherapy based on its overexpression in prostate tumor tissue, especially in some metastatic tis

271 Furthermore, prostate tumor tissues and prostate cancer metastasized

272 RecQL4 expression was also detected in human prostate tumor tissues as a function of tumor grade with

273 ors NLRP3, NLRC4, NLRP6, NRLP12, and AIM2 in prostate tumor tissues, and verified their mRNA level in

274 In human prostate tumor tissues, elevated cancer stem-like cell m

275 y result showed that MAK is overexpressed in prostate tumor tissues, suggesting a role of MAK in pros

276 e tumor blood vessels in malignant colon and prostate tumor tissues.

277 ression is elevated during the adaptation of prostate tumors to androgen-targeted therapies (ATTs), a

278 upregulated during the adaptive response of prostate tumors to ATTs and a prognostic biomarker of cl

279 alled Sabutoclax, is sufficient to sensitize prostate tumors to mda-7/IL-24-induced apoptosis, wherea

280 Our findings show how prostate tumors undergo a metabolic reprogramming that r

281 This study aimed to investigate the prostate tumor uptake, photothermal therapy mediated mac

282 ey for somatic events in systemic metastatic prostate tumors using both high-resolution copy number a

283 n, and are protective against neuroendocrine prostate tumor variants.

284 growth through TLR4-dependent regulation of prostate tumor vasculature.

285 are the most promising new developments for prostate tumor visualization.

286 g the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events a

287 ther, in mice bearing orthotopic 22Rv1 human prostate tumors, we did not find a statistically signifi

288 bearing the castration-resistant endogenous prostate tumor, which prevented effector responses to UV

289 mor vascularization relative to TK+/+ TRAMP+ prostate tumors, which correlated with reduced levels of

290 To selectively target advanced prostate tumors with a constitutive activated PI3K/Akt p

291 f ESE3/EHF expression to a distinct group of prostate tumors with distinctive molecular and biologic

292 signaling pathways are often deregulated in prostate tumors with poor prognosis.

293 t samples, as well as their progenitor human prostate tumor xenograft (CWR22) that had been passaged

294 V-1 and PreXMRV-2, during the passaging of a prostate tumor xenograft in nude mice.

295 lyamide demonstrates antitumor activity in a prostate tumor xenograft model with limited host toxicit

296 tumor growth in the mouse PTEN-deficient PC3 prostate tumor xenograft model.

297 DHX15 knockdown inhibited the growth of C4-2 prostate tumor xenografts in mice.

298 ate tumor cells in vitro and accumulation in prostate tumor xenografts in vivo, demonstrating the pot

299 When overexpressed in cells derived from prostate tumor xenografts, delta-catenin gene invariably

300 ntial as a radiosensitizer on cell lines and prostate tumor xenografts.