ライフサイエンスコーパス: androgen-dependent

1 Initially, prostate cancer is androgen dependent.

2 ial juncture in prostate development that is androgen dependent.

3 dustrialized countries and it is known to be androgen-dependent.

4 Furthermore, the mutant Bag-1L increases androgen-dependent activation of a subset of AR targets

5 man CaP LNCaP sublines: LNCaP(nan), which is androgen dependent (AD), and LNCaP-HP, which is androgen

6 tal LNCaP cell line, whose proliferation was androgen dependent (AD), was used to explore the mechani

7 significantly elevated in PCa tissues and in androgen-dependent (AD) and androgen-independent (AI) ce

8 easing peptide (GRP) receptor (GRPR) in both androgen-dependent (AD) and androgen-independent (AI) hu

9 t is initiated by androgens and patterned by androgen dependent and independent signals.

10 Prostate cancer is initially androgen dependent and there is evidence that androgen r

11 the direct AR-dependent target genes in both androgen-dependent and -independent cancer cells by gene

12 recruitment to the PSA gene promoter in both androgen-dependent and -independent cell lines.

13 te cancer cells significantly decreases both androgen-dependent and -independent cellular proliferati

14 Proepithelin promoted the migration of androgen-dependent and -independent human prostate cance

15 -2 significantly inhibits the growth of both androgen-dependent and -independent LNCaP cells.

16 The growth suppressor MST1 kinase modulates androgen-dependent and -independent nuclear YAP1-AR inte

17 induction of the heat-shock response in both androgen-dependent and -independent prostate cancer cell

18 inhibits AR transcriptional activity in both androgen-dependent and -independent prostate cancer cell

19 echanisms underlying the differences between androgen-dependent and -independent prostate cancer rema

20 the p160 coactivator ACTR/AIB1 increase both androgen-dependent and -independent PSA expression, by f

21 gulating the expression of genes involved in androgen-dependent and -independent tumour formation.

22 l of PCa progression to study AR activity in androgen-dependent and ADI PCa cells.

23 The cyclic AMP-induced increase in androgen-dependent and androgen-independent AR transcrip

24 sion severely compromises the growth of both androgen-dependent and androgen-independent AR-positive

25 Androgen-dependent and androgen-independent human prosta

26 This positive effect is observed in both androgen-dependent and androgen-independent LNCaP cells.

27 ion of PAGE4 can lead to transitions between androgen-dependent and androgen-independent phenotypes b

28 rface antigen specifically expressed on both androgen-dependent and androgen-independent prostate can

29 bitor rapamycin caused growth arrest in both androgen-dependent and androgen-independent prostate can

30 ed underlying functional differences between androgen-dependent and androgen-independent prostate can

31 demonstrate that HIPK1 is expressed in both androgen-dependent and androgen-independent prostate can

32 porter should enable in vivo imaging of both androgen-dependent and androgen-independent prostate tum

33 s revealed that (18)F-FPA can delineate both androgen-dependent and androgen-independent prostate xen

34 erences in MAPK levels were detected between androgen-dependent and androgen-independent xenografts,

35 st that AR promotes the invasiveness of both androgen-dependent and androgen-refractory prostate canc

36 sely correlated with the invasiveness of the androgen-dependent and androgen-refractory prostate canc

37 candidates to treat prostate cancer at both androgen-dependent and androgen-refractory stages, we de

38 ition of AR by Arr2 knockdown occurs in both androgen-dependent and castration-resistant PCa (CRPC) c

39 which the AR regulates cell proliferation in androgen-dependent and castration-resistant PCa are inco

40 5 overexpression promotes the growth of both androgen-dependent and castration-resistant PCa xenograf

41 d, importantly, reduced the proliferation of androgen-dependent and castration-resistant prostate can

42 androgen receptor (AR) is a mediator of both androgen-dependent and castration-resistant prostate can

43 It occurred in both androgen-dependent and castration-resistant prostate can

44 itical role in the growth and progression of androgen-dependent and castration-resistant prostate can

45 NO) levels lead to growth inhibition of both androgen-dependent and castration-resistant prostate tum

46 Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a repro

47 HRH antagonist MIA-602 for treatment of both androgen-dependent and CRPC.

48 , ENZA) or bicalutamide induced autophagy in androgen-dependent and in castration-resistant CaP (cast

49 found differential expression of miR-125b in androgen-dependent and independent CaP cells, as well as

50 nel of cell lines, hSef was detected in both androgen-dependent and independent cells but was signifi

51 it growth of various malignancies, including androgen-dependent and independent prostate cancer, by s

52 Both androgen-dependent and more aggressive androgen-independ

53 Ad-ARR(2)PB/hNIS-infected LNCaP cells showed androgen-dependent and perchlorate-sensitive iodide upta

54 Our data demonstrate androgen-dependent and tissue-specific siRNA-mediated ge

55 ty of human prostate cancer cell line LNCaP (androgen-dependent) and its androgen-independent variant

56 tions with three competing cancer "species": androgen dependent, androgen producing, and androgen ind

57 was less than wild-type AR and refractory in androgen-dependent AR NH(2)- and carboxyl interaction tr

58 R FXXLF motif of the AR dimer engages in the androgen-dependent AR NH(2)- and carboxyl-terminal inter

59 dual functions of the AR FXXLF motif in the androgen-dependent AR NH(2)- and carboxyl-terminal inter

60 mumol/L) or nocodazole (5 mug/mL) inhibited androgen-dependent AR nuclear translocation by targeting

61 analyses to ascertain that SD70 inhibits the androgen-dependent AR program, and prostate cancer cell

62 that epidermal growth factor (EGF) increases androgen-dependent AR transactivation in the recurrent p

63 hibition of the MAGE-A11-induced increase in androgen-dependent AR transcriptional activity and const

64 y analysis indicated that UGT2B17 suppressed androgen-dependent AR transcriptional activity and enhan

65 rmal growth factor (EGF) signaling increases androgen-dependent AR transcriptional activity through t

66 -602, MIA-606, and MIA-690--on the growth of androgen-dependent as well as castration-resistant prost

67 ith the antiandrogen bicalutamide sensitized androgen-dependent, as well as AR-sensitive androgen-ind

68 AAS exposure during puberty affects several androgen-dependent behaviors.

69 eptor (AR) stimulates the growth of not only androgen-dependent but also of androgen-refractory prost

70 was observed at the transcriptional level in androgen-dependent but not in androgen-independent prost

71 in the absence of a competitive advantage of androgen-dependent cancer cells over castration-resistan

72 ed SRC-1 expression in clinically localized, androgen-dependent cancer is associated with clinical an

73 ndrogen ablation are effective therapies for androgen-dependent CaP, metastatic castration-resistant

74 6 promoter that is functionally required for androgen-dependent Cdc6 transcription.

75 gen receptor (AR)-mediated transcription and androgen-dependent cell growth.

76 ant prostate cancer where it is required for androgen-dependent cell growth.

77 atment (ATRA), but this did not occur in the androgen-dependent cell line expressing low levels of Bc

78 on of miR-221 or miR-222 in LNCaP or another androgen-dependent cell line, LAPC-4, significantly redu

79 tumorigenic prostate epithelial cells or the androgen-dependent cell line, LNCaP.

80 (TC-AR) is inducibly expressed in LNCaP, an androgen-dependent cell line, which expresses little tru

81 cds2, and cds3) and tumors compared with the androgen-dependent cell lines (LNCaP and MLC-SV40) and t

82 e higher in androgen-independent compared to androgen-dependent cell lines.

83 , with no detectable secretion in normal and androgen-dependent cell lines.

84 ulatory events associated with inhibition of androgen-dependent cell proliferation by 2,3,7,8-tetrach

85 Hyperthermia abrogates AR expression in androgen-dependent cells and might thus promote malignan

86 growth kinetics, which could be reversed in androgen-dependent cells by treatment with a UDP-glucuro

87 n of ABCA1 expression by RNA interference in androgen-dependent cells increased their rate of prolife

88 curonide, DHT-G, at a 6-fold higher level in androgen-dependent cells relative to androgen-independen

89 estern blot analysis, expression of ABCA1 in androgen-dependent cells was inhibited by androgen.

90 Pur alpha knockdown in androgen-dependent cells yielded higher AR and reduced p

91 AR activation promotes ErbB3 degradation in androgen-dependent cells, and that this effect is mediat

92 In contrast to what is found in androgen-dependent cells, AR selectively upregulates M-p

93 ed UGDH expression approximately 2.5-fold in androgen-dependent cells.

94 R and were more invasive than their parental androgen-dependent cells.

95 whereas CLK2 and PAGE4 are expressed only in androgen-dependent cells.

96 We show here that androgen-dependent cellular proliferation and transcript

97 l expansion of tumor cells by enhancement of androgen-dependent cellular proliferation by reducing DH

98 cells markedly decreases Cdc6 expression and androgen-dependent cellular proliferation.

99 he prevention and treatment of estrogen- and androgen-dependent conditions.

100 we show that the corepressor LCoR acts as an androgen-dependent corepressor that represses human PCa

101 There is a direct, androgen-dependent correlation between the levels of act

102 of CRPC cells to a greater extent than their androgen-dependent counterparts.

103 mmary tumors, male athymic nude mice bearing androgen-dependent CWR22 prostate cancer xenografts, and

104 fatty acids (PUFAs; at 1.5 wt%) on growth of androgen-dependent (CWR22) and androgen-independent (CWR

105 We show that this androgen-dependent death reflects decreased expression o

106 Although this regimen effectively regresses androgen-dependent disease, relapse often occurs in an a

107 Prostate cancer is an androgen-dependent disease; metastatic prostate cancer i

108 n and treatment of prostate cancer and other androgen-dependent diseases.

109 ancerous rat prostate tissues, nonmetastatic/androgen-dependent Dunning G and metastatic/androgen-ind

110 cated by decreased human AR regulation of an androgen-dependent endogenous gene using lentivirus shor

111 y RNA interference specifically affected the androgen-dependent expression of AR-targeting genes in L

112 sponsive reporter genes, as well as inhibits androgen-dependent expression of endogenous AR target ge

113 uciferase specifically in the prostate in an androgen-dependent fashion.

114 tric oxide synthase (NOS) is involved in the androgen-dependent gating of male-typical copulatory beh

115 ember of the Rhox gene cluster, Rhox5, is an androgen-dependent gene expressed in Sertoli cells that

116 AR, form a regulatory hierarchy that governs androgen-dependent gene expression and prostate cancer g

117 ndependent cancer cells is not to direct the androgen-dependent gene expression program without andro

118 n, and the effect of cyclin D1 on subsequent androgen-dependent gene expression was determined using

119 n deprivation does not consistently suppress androgen-dependent gene expression.

120 tivation of aryl hydrocarbon receptor blocks androgen-dependent gene induction in LNCaP cells as well

121 interacts with coregulatory proteins during androgen-dependent gene regulation.

122 xpression include increased transcription of androgen-dependent genes in prostate cancer cells that c

123 te-stage prostate cancer, and could regulate androgen-dependent genes in the absence or with very low

124 s-acting elements required for expression of androgen-dependent genes while inhibiting the AR N- and

125 sponse factor), representing less than 6% of androgen-dependent genes.

126 The results show that foot flagging is an androgen-dependent gestural signal, and its emergence is

127 en-dependent transgene expression as well as androgen-dependent growth in soft agar and in mice.

128 tumor suppressive and that the disruption of androgen-dependent growth inhibition via U19 down-regula

129 box region had a dominant-negative effect on androgen-dependent growth of PCa cells that were insensi

130 ivity is one mechanism by which PHB inhibits androgen-dependent growth of prostate cells.

131 n mature rats, BMS-641988 strongly inhibited androgen-dependent growth of the ventral prostate and se

132 nstrument, a visual scoring method assessing androgen-dependent hair growth in 9 body areas.

133 tic alopecia (AGA) is a common heritable and androgen-dependent hair loss condition in men.

134 reactive oxygen species (ROS) production in androgen-dependent human CaP cells.

135 Androgen-dependent human LNCaP 104-S tumor xenografts pr

136 Ectopic expression of Vav3 in androgen-dependent human prostate cancer cells conferred

137 oliferative and antiandrogenic properties in androgen-dependent human prostate cancer cells.

138 The androgen-dependent human prostate tumor, CWR22, was impl

139 nally, PTP1B depletion delayed the growth of androgen-dependent human prostate tumors and impaired an

140 essin/vasotocin (AVP/AVT) system is strongly androgen dependent in many species and critically mediat

141 e anti-IL-6 antibody-treated mice were still androgen dependent in vitro and in vivo.

142 The production of male calls is androgen dependent in Xenopus; to test the effects of an

143 We show a significant androgen-dependent increase of Foxp3 expression in human

144 hether sex differences in spinal cord DA are androgen dependent, influenced by adult or perinatal and

145 of the cyclin B1 promoter coincides with an androgen-dependent interaction between AR and E2F1 as we

146 e very effective at inhibiting the growth of androgen-dependent LAPC4 human prostate tumor xenograft,

147 ripts under standard culture conditions, the androgen-dependent line LnCaP expressed Nestin only on a

148 ficient to confer ADI growth to the normally androgen dependent LNCaP line.

149 ls, respectively, during the transition from androgen-dependent LNCaP (model for early-stage prostate

150 ntribution of SRC-1, we examined its role in androgen-dependent LNCaP and androgen-independent C4-2 p

151 ll-associated kinase (hMAK), as read-outs in androgen-dependent LNCaP and androgen-independent C4-2B

152 tic effects on the induction of apoptosis in androgen-dependent LNCaP and androgen-independent DU-145

153 an nonmetastatic prostate cancer cell lines, androgen-dependent LnCaP and androgen-independent DU145.

154 aspirin, enhances TRAIL-induced apoptosis in androgen-dependent LNCaP and androgen-independent LNCaP-

155 gainst two human prostate cancer cell lines, androgen-dependent LNCaP and androgen-independent PC-3.

156 Androgen-dependent LNCaP and VCaP cells expressed higher

157 olved in this PKC-mediated effect, using the androgen-dependent LNCaP cell line as a model.

158 line C4-2, established by inoculation of the androgen-dependent LNCaP cell line into castrated mice,

159 ed in decreased proliferation rates for both androgen-dependent LnCaP cells and the LnCaP-derived and

160 mediated knockdown of paxillin expression in androgen-dependent LnCAP cells as well as in androgen-in

161 ated this question in a novel model of human androgen-dependent LNCaP cells cultured for long periods

162 FACS analysis demonstrated that the androgen-dependent LNCaP cells express PAR1, PAR2, and P

163 that the AR is transcriptionally inactive in androgen-dependent LNCaP cells in the absence of androge

164 tional SVs conferred a survival advantage of androgen-dependent LNCaP cells under castration-simulate

165 PI3K/Akt pathway can suppress AR activity in androgen-dependent LNCaP cells with low passage numbers.

166 by androgen receptor protein suppression (in androgen-dependent LNCaP cells) and apoptosis induction.

167 U145 cells compared with the less aggressive androgen-dependent LNCaP cells.

168 en-independent DU145 cells compared with the androgen-dependent LNCaP cells.

169 induced AR suppression and apoptosis only in androgen-dependent LNCaP cells.

170 rs of prostate-specific antigen secretion by androgen-dependent LNCaP cells.

171 , p21(CIP1), compared to the less-malignant, androgen-dependent LNCaP cells.

172 ke cells functioned to sustain the remaining androgen-dependent LNCaP cells.

173 ion of these miRs had the opposite effect in androgen-dependent LNCaP cells.

174 N) root and nine other Oriental herbs in the androgen-dependent LNCaP human prostate cancer cell mode

175 Knockdown of SAFB1 in androgen-dependent LNCaP PCa cells increased AR and pros

176 ition of miR-23b/-27b in the less aggressive androgen-dependent LNCaP prostate cancer cell line resul

177 Here, we demonstrate that in androgen-dependent LNCaP prostate cancer cells, the clea

178 gly, the depletion of mitochondrial DNA from androgen-dependent LNCaP resulted in a loss of androgen

179 45 and PC-3 prostate cancer cells but not in androgen-dependent LNCaP-FGC cells, although both cell t

180 (PC3, DU145, PPC1, LNCaP-SF, and 22Rv1) and androgen-dependent (LNCaP and VCaP) and/or normal prosta

181 duces growth arrest and apoptosis in various androgen-dependent (LNCaP) and -independent (DU145 and P

182 variant 9 expression were increased in both androgen-dependent (LNCaP) and androgen-independent (DU-

183 at H(2)S inhibits cell proliferation of both androgen-dependent (LNCaP) and antiandrogen-resistant pr

184 dent to androgen independent, we established androgen-dependent LuCaP 35 human prostate cancer xenogr

185 Prostate cancer starts as androgen-dependent malignancy and responds initially to

186 n receptor (AR) coactivator proteins in this androgen-dependent malignancy is only beginning to emerg

187 epithelial cell growth and development in an androgen-dependent manner, and that functional different

188 ontinued to produce secretory proteins in an androgen-dependent manner, they responded poorly to andr

189 that suppresses AR protein expression in an androgen-dependent manner, while de-repressing AR expres

190 ilitated interactions of AR with SRC-1 in an androgen-dependent manner.

191 1-AR degradation pathway may represent a new androgen-dependent mechanism for regulating AR levels in

192 other predominantly within cell nuclei by an androgen-dependent mechanism in a hormone naive and an a

193 Unexpectedly, these mice display androgen-dependent muscle weakness and early death, show

194 thermore, knocking down PTEN can convert the androgen-dependent Myc-CaP cell into androgen independen

195 nal (23)FQNLF(27) sequence that mediates the androgen-dependent N/C interaction.

196 se, a degenerative disorder characterized by androgen-dependent neuromuscular weakness, is caused by

197 for the AR NH(2)-terminal FXXLF motif in the androgen-dependent NH(2)-terminal and carboxyl-terminal

198 rinibs, caused rapid and complete killing of androgen-dependent or -independent prostate cancer, but

199 uld be considered for the management of both androgen-dependent or -independent prostate cancers.

200 for the prostate to develop into a strictly androgen-dependent organ with respect to tissue homeosta

201 Our study suggests that androgen-dependent outcome of apoptotic treatment can oc

202 Targeting of androgen-dependent pathways in CRPC postchemotherapy has

203 l death induced by low-dose TPA in the LNCaP androgen-dependent PCa cell line and that TPA-induced ce

204 of dsRNA poly(I:C) induces apoptosis in the androgen-dependent PCa cell line LNCaP in a TLR3-depende

205 stein, and their combinations on early-stage androgen-dependent PCa cells (LNCaP) and bone metastatic

206 In androgen-dependent PCa cells, the well characterized C-t

207 Compared to androgen-dependent PCa cells, these cells showed increas

208 normal prostate-derived pRNS-1-1 cells, and androgen-dependent PCa lines LNCaP, PC346C, and CWR22 mo

209 nteractions may be a potent intervention for androgen-dependent PCa therapy.

210 nst PCa proliferation and the progression of androgen-dependent PCa to the castration-resistant stage

211 els of the receptor tyrosine kinase ErbB3 in androgen-dependent PCa, resulting in AW-resistant cell c

212 rCa) is characterized by progression from an androgen-dependent phenotype to one that is inevitably a

213 nal nucleus of the bulbocavernosus (SNB), an androgen-dependent population of motoneurons in the lumb

214 , sexual function, erythropoiesis, and other androgen-dependent processes remains poorly understood.

215 pathways of androgen-independent as well as androgen-dependent progression, and highlight substantia

216 and highly heritable trait characterized by androgen-dependent, progressive hair loss from the scalp

217 epression of AR transcriptional activity and androgen-dependent proliferation of PC cells.

218 sion in LNCaP cells strongly compromises the androgen-dependent proliferation of these cells.

219 -3 in LNCaP cells significantly enhances the androgen-dependent proliferation of these cells.

220 drogen receptor (AR) activity and thus limit androgen-dependent proliferation.

221 AP-1 transactivation, significantly enhances androgen-dependent proliferation.

222 nvolvement in transcriptional recycling with androgen dependent promoters.

223 s of BPA block proliferation of AR-positive, androgen-dependent prostate adenocarcinoma cells (LNCaP

224 cs analysis of master TFs CREB1 and FoxA1 in androgen-dependent prostate cancer (ADPC) and castration

225 drogen-regulated transcriptional programs of androgen-dependent prostate cancer and CRPC, and recent

226 line LNCaP-Abl), compared with those in the androgen-dependent prostate cancer cell line (LNCaP).

227 cell lines PC-3 and DU 145 compared with the androgen-dependent prostate cancer cell line LNCaP.

228 In this study, we used the androgen-dependent prostate cancer cell line MDA PCa 2b,

229 Androgen-dependent prostate cancer cell lines (LNCaP) an

230 AR target genes and inhibit proliferation in androgen-dependent prostate cancer cell lines.

231 , BIPep expression was sufficient to inhibit androgen-dependent prostate cancer cell proliferation in

232 ion and methylation and as a major driver of androgen-dependent prostate cancer cell proliferation.

233 osome 8q24, is highly induced by androgen in androgen-dependent prostate cancer cells and xenograft t

234 Similarly, Protac-A treatment of androgen-dependent prostate cancer cells induced G(1) ar

235 It is established that androgen-dependent prostate cancer cells undergo apoptos

236 diacylglycerol mimetics induces apoptosis in androgen-dependent prostate cancer cells, an effect that

237 , inhibiting ligand-dependent AR activity in androgen-dependent prostate cancer cells, while enhancin

238 lex with AR and acts as an AR corepressor in androgen-dependent prostate cancer cells.

239 wed the growth rate and induced apoptosis in androgen-dependent prostate cancer cells.

240 nced by androgen stimulation in AR-positive, androgen-dependent prostate cancer cells.

241 PKC) by phorbol esters promotes apoptosis in androgen-dependent prostate cancer cells.

242 on of the microRNAs or induction of IGF1R in androgen-dependent prostate cancer cells.

243 ological treatment of choice for progressive androgen-dependent prostate cancer is the nonsteroidal a

244 Androgen-dependent prostate cancer lines, which express

245 c expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castrat

246 hibitors might be more effective in treating androgen-dependent prostate cancer patients.

247 Androgen-dependent prostate cancer typically progresses

248 in A2 genes in CRPC but not in earlier stage androgen-dependent prostate cancer, establishing a stage

249 ession by antiandrogens has been reported in androgen-dependent prostate cancer, its roles in regulat

250 g of choice for the treatment of progressive androgen-dependent prostate cancer.

251 The clinical significance of INPP4B in androgen-dependent prostate cancers was determined in no

252 ere not necessary for growth or viability of androgen-dependent prostate cells.

253 ntify kinases that enable tumor formation by androgen-dependent prostate epithelial (LHSR-AR) cells u

254 delayed prostate growth and had no effect on androgen-dependent prostate regeneration, suggesting an

255 effective than castration in suppression of androgen-dependent prostate tumor growth.

256 en ablation therapy is effective in treating androgen-dependent prostate tumors; however, tumors that

257 In androgen-dependent prostatic adenocarcinomas, cyclin D1

258 n capability for CRPC in comparison with the androgen-dependent PSA promoter-driven system.

259 immunoprecipitation analysis that showed its androgen-dependent recruitment to the promoter of the st

260 gand-binding domain (LBD) ensures the strict androgen-dependent regulation of androgen receptor (AR):

261 hese results illuminate a mechanism in which androgen-dependent repression of ERRgamma reprograms pro

262 early clinical prostate cancer growth is an androgen-dependent response, the results of the present

263 id production and reduced expression of some androgen-dependent SC genes.

264 ar change correlated with anatomical loss of androgen-dependent sensory vibrissae and penile spines i

265 early androgen-independent phase and a late androgen-dependent sexual differentiation phase.

266 R ligand-binding domain do not fully inhibit androgen-dependent signaling critical for PCa progressio

267 elopment of prostate cancer from the initial androgen-dependent state to a later aggressive androgen-

268 enhance prostate cancer progression from an androgen-dependent state to an androgen-independent stat

269 The evolution of prostate cancer from an androgen-dependent state to one that is androgen-indepen

270 , as well as formation of gap junctions, are androgen-dependent strongly implicate an important role

271 (1) KD is androgen-dependent, suggesting that blocking androgen ac

272 that ARs within LA muscle fibers mediate the androgen-dependent survival and growth of the LA muscle

273 nd activity in cultured ECs, and we named it androgen-dependent TFPI-regulating protein (ADTRP).

274 ter A1 (ABCA1), was 15- to 20-fold higher in androgen-dependent than in androgen-independent LNCaP hu

275 A genomic variant in the human ADTRP [androgen-dependent tissue factor (TF) pathway inhibitor

276 MAGE-11 is expressed in androgen-dependent tissues and in prostate cancer cell l

277 physiologic end points, such as the size of androgen-dependent tissues.

278 ct of IL-6 inhibition on the conversion from androgen dependent to androgen independent, tumor cells

279 le in the conversion of prostate cancer from androgen dependent to androgen independent, we establish

280 ift in androgen receptor (AR) signaling from androgen-dependent to androgen (ligand)-independent.

281 Using the cancer progression model of androgen-dependent to androgen-independent Lymph Node Ca

282 Prostate cancer progresses from an androgen-dependent to androgen-independent stage after a

283 The transition from androgen-dependent to castration-resistant prostate canc

284 Emodin treatment resulted in repressing androgen-dependent transactivation of AR by inhibiting A

285 FKBP51 stimulates androgen-dependent transcription and cell growth, and FK

286 In living cells, NU7026 treatment increases androgen-dependent transcription from endogenous genes t

287 They have also revealed that the androgen-dependent transcription of GRTH expression in L

288 Androgen-dependent transcriptional activity by the andro

289 Androgen-dependent transcriptional activity of AR-R405S

290 nd carboxyl-terminal interaction amplify the androgen-dependent transcriptional response to p300 requ

291 osure to androgen withdrawal and they retain androgen-dependent transgene expression as well as andro

292 tivity in a dose-dependent manner and reduce androgen-dependent tumor growth in an aromatase-transfec

293 The procyanidin B dimers were able to reduce androgen-dependent tumor growth, indicating that these c

294 Neither was elevated in androgen-dependent tumors or benign prostate samples.

295 n vivo and, surprisingly, was sufficient for androgen-dependent tumors to overcome castration-mediate

296 en ablation therapy is effective in treating androgen-dependent tumors, but eventually, androgen-inde

297 levels between the androgen-independent and androgen-dependent tumors, IL-6 inhibition promoted both

298 d higher levels of IL-17RL compared with the androgen-dependent tumors.

299 ion therapy are effective in treating local, androgen-dependent tumors.

300 n ablation causes infiltration of regressing androgen-dependent tumours with leukocytes, including B