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 ch in the human prostate and resident of the prostate tumor.

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

4 s with the aggressiveness and progression of prostate tumors.

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

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

7 d upon castration of mice carrying xenograft prostate tumors.

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

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

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

11 and our findings reveal utility in assessing prostate tumors.

12 mbryonic stem cells and in highly metastatic prostate tumors.

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

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

15 ose overexpression is highly associated with prostate tumors.

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

17 of ETS transcription factors are frequent in prostate tumors.

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

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

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

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

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

23 a striking suppression in the development of prostate tumors.

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

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

26 ATM loss occurs in a subset of prostate tumors.

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

28 membrane proteoglycan overexpressed in human prostate tumors.

29 lar localization have been detected in human prostate tumors.

30 are present in approximately 5% of advanced prostate tumors.

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

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

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

34 compared with progenitor cells from control prostate tumors.

35 omatic single-nucleotide variants in primary prostate tumors.

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

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

38 c strategies for the treatment of metastatic prostate tumors.

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

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

41 rs that is downregulated in aggressive human prostate tumors.

42 prostatic basal cell carcinomas in the above prostate tumors.

43 romosome-arm gains and losses in 333 primary prostate tumors.

44 ms on the somatic epigenome of 589 localized prostate tumors.

45 siveness in lean and obese mice grafted with prostate tumors.

46 igher expression of PCAT1, PVT1 and c-myc in prostate tumors.

47 omising agents for the specific targeting of prostate tumors.

48 uence management decisions for patients with prostate tumors.

49 pregulate EMT transcription factors in mouse prostate tumors.

50 e prostate, and the loss of GRK2 function in prostate tumors accelerates disease progression toward t

51 In human prostate tumors, ACO2 activity was significantly elevate

52 ETS fusions, the most common alteration in prostate tumors, affect different genes and pathways in

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

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

55 genesis and provide mechanistic insight into prostate tumor aggressiveness and progression mediated b

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

57 Prostate tumor allografts in ASPN-null mice had a reduce

58 ocus (eQTL) association meta-analysis on 496 prostate tumor and 602 normal prostate samples with 117

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

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

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

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

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

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

65 response (DDR) genes are common in advanced prostate tumors and are associated with unique genomic a

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

67 ver, CD8-MP cells infiltrate oncogene-driven prostate tumors and express high densities of PD-1, whic

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

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

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

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

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

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

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

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

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

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

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

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

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

81 n mixtures of cell lines, nuclei from frozen prostate tumors, and biopsy washes.

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

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

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

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

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

87 Prostate tumors are known to remain undetected or dorman

88 The perception that prostate tumors are more lethal in AAs than in EAs is re

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

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

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

92 es reveals the enrichment of somatic SNVs in prostate tumors as opposed to adjacent normal tissue cis

93 s within the FOXA1 plexus mutated in primary prostate tumors as potential targets for therapeutic int

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

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

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

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

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

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

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

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

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

103 xpression signature of patients with primary prostate tumors by investigating the co-expression profi

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

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

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

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

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

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

110 the accumulation of FOXO3A in the cytosol of prostate tumor cells and downregulation of its target ge

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

112 mor microenvironments, we injected mice with prostate tumor cells either subcutaneously or intraosseo

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

114 we showed that ectopic expression of RGN in prostate tumor cells induced dormancy in vivo, while fol

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

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

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

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

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

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

121 60 coactivator to the nuclear compartment of prostate tumor cells.

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

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

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

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

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

127 We noted loss of expression of miR-299-3p in prostate tumors compared to noncancerous prostate tissue

128 levels were upregulated in advanced primary prostate tumors compared to normal tissue or tumors with

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

130 1 was highly expressed in primary breast and prostate tumors compared with adjacent normal epithelial

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

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

133 peutic efficacy of targeting FAO in clinical prostate tumors cultured ex vivo, and identify DECR1, en

134 To define the role of ATM loss in prostate tumor DDR function and sensitivity to DDR-direc

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

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

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

138 Prostate tumors develop resistance to androgen deprivati

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

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

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

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

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

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

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

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

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

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

149 These compound mice displayed accelerated prostate tumor formation and invasion compared with thei

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

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

152 tages of tumorigenesis, autophagy suppresses prostate tumor formation.

153 ecurrently mutated in primary and metastatic prostate tumors, FOXA1 encodes a pioneer transcription f

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

155 iously identified as up-regulated in primary prostate tumors from African American patients, who are

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

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

158 essions positively correlated with increased prostate tumor Gleason score.

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

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

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

162 complete loss of Phlpp2 paradoxically blocks prostate tumor growth and disease progression.

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

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

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

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

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

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

169 et obesity and tumor itself in inhibition of prostate tumor growth at a lower concentration compared

170 ifferentiation in cultured cells and reduced prostate tumor growth in a xenograft model.

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

172 A inhibitor treatment effectively suppressed prostate tumor growth in mice in a stroma-specific targe

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

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

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

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

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

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

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

180 reported that survivin levels increase with prostate tumor growth.

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

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

183 PARP have demonstrated activity in advanced prostate tumors harboring DDR gene alterations, particul

184 xpression of vitamin K-dependent proteins in prostate tumors has been linked to their aggressiveness

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

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

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

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

189 bition of KPNB1 could suppress the growth of prostate tumor in vivo.

190 ic intraepithelial neoplasia and accelerated prostate tumors in comparison with mice harboring only t

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

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

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

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

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

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

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

198 Prostate tumors invariably overexpress prostate surface

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 hen applied to H3K27AC ChIP-seq from just 28 prostate tumor/normal samples.

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

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

222 Advanced and therapy-resistant prostate tumors often display neural or neuroendocrine b

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

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

225 Prostate tumors predominantly express a novel, extraneur

226 Prostate tumors produce various soluble factors, includi

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

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

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

230 PTEN loss stimulates prostate tumor progression by sustaining AKT activation.

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

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

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

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

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

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

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

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

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

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

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

242 signaling pathways were robustly enriched in prostate tumor samples from the compound mice.

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

244 d genes displayed differential expression in prostate tumor samples, were vulnerable to expression al

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

246 159 metastatic CRPC samples and 2142 primary prostate tumors showed that the level of c-Myc is positi

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

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

249 d genes (DEGs) in the proximity of the human prostate tumor-specific AR binding sites.

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

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

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

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

254 findings describe how downregulation of the prostate tumor suppressor PGC1 drives invasiveness and m

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

256 ARgamma coactivator 1 alpha (PGC1alpha) is a prostate tumor suppressor that controls the balance betw

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 repeatability of radiomics features on small prostate tumors using test-retest Multiparametric Magnet

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

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

284 MX2 expression in primary prostate tumors was evaluated using immunohistochemistry

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

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

287 PD-1/PD-L1 pathway is minimally expressed in prostate tumors, we previously demonstrated that PD-1/PD

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 Prostate tumors with beta-catenin activation relied on t

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

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

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

295 g dynamic bioluminescence imaging in a human prostate tumor xenograft growing in a rat.

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

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

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

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

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