ライフサイエンスコーパス: ERG

1 ERG binds to chromatin regions occupied by TEAD/YAP1 and

2 ERG controls the Wnt/beta-catenin pathway by promoting b

3 ERG currents have been previously studied primarily in t

4 ERG fusions retaining interstitial sequences occurred mo

5 ERG inhibitory peptides (EIPs) and derived peptidomimeti

6 ERG is not expressed in normal prostate epithelia, but w

7 ERG recruits PRMT5 to AR-target genes, where PRMT5 methy

8 ERG results are consistent with the structural analyses

9 ERG's oncogenic potential is well known because of its i

10 ERGs recorded after mice Kir7.1 suppression by shRNA, or

11 13.12 (near PCIF1/MMP9/ZNF335), and 21q22.2 (ERG).

12 13.12 (near PCIF1/MMP9/ZNF335), and 21q22.2 (ERG).

13 er, among whom 884 were assayed for ERG (426 ERG-positive).

14 channels contribute directly to the abnormal ERG associated with blindness via alterations in sub-ret

15 the heart; relatively little is known about ERG function in the brain, although mutations in ERG cha

16 ne responses (the a-wave of the dark-adapted ERG protocol of 12.0 cd/s/m2) was longer (mean differenc

17 muV]; P=.003; the a-wave of the dark-adapted ERG protocol of 12.0 cd/s/m2: mean difference, -55.7 muV

18 ne responses (the a-wave of the dark-adapted ERG protocol of 3.0 cd/s/m2: mean difference, -48.9 muV

19 Our findings highlight an ERG-regulated mechanism capable of repopulating the pare

20 rachloride (CCL4)-induced fibrogenesis in an ERG-dependent manner in mice.

21 ivities of oncogenic factors, such as AR and ERG in prostate cancer.

22 VEGF-responsive and ERG-dependent genes, and ERG chromatin immunoprecipitation (ChIP)-seq revealed th

23 Comparison of SPOP-mutant and ERG-fusion organoid models showed evidence of divergent,

24 OCT and ERG parameters, as well as AO-SLO cone densities, were s

25 identified a network of VEGF-responsive and ERG-dependent genes, and ERG chromatin immunoprecipitati

26 ts both the juxtaposition of the TMPRSS2 and ERG gene loci and also their recombination.

27 on of interstitial genes between TMPRSS2 and ERG has been reported to influence tumor progression in

28 the interstitial regions between TMPRSS2 and ERG Identifying these patients at biopsy might improve p

29 ype of parental cells upon restoration of AR/ERG signaling.

30 ring triggering stimuli appears to attenuate ERG currents, leading to membrane potential depolarizati

31 The EIPs attenuated ERG-mediated transcription, chromatin recruitment, prote

32 In all carriers, the average ERG amplitude to 30-Hz flashes was approximately 50% of

33 r both, 53 of 55 (96%) had abnormal baseline ERG results.

34 r toxicity, peak-to-peak comparisons between ERG studies before and after OAC treatment and CTCAE 4.0

35 s of MMP9, with a direct interaction between ERG and MMP9.

36 competition model, ERF overexpression blocks ERG-dependent tumour growth, and ERF loss rescues TMPRSS

37 des (EIPs) and derived peptidomimetics bound ERG with high affinity and specificity, leading to prote

38 Pten loss that yields oncogenic activity by ERG.

39 TMPRSS2:ERG was assessed by ERG immunohistochemistry on tumor tissue microarrays con

40 e and the risk of prostate cancer defined by ERG protein expression subtype.

41 es, obligate carriers could be identified by ERG testing.

42 peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) K(+) channels in carbon monoxide-induced pr

43 Because XLRP carrier ERG amplitudes and decay rates over time were on average

44 in human luminal-type prostate cancer cells, ERG binds to the promoter of YAP1 and is necessary for Y

45 ual acuity at presentation and abnormal cone ERG results.

46 aviour is comparable between normal and cone ERG(absent) RPGRIP1 (ins/ins) littermates.

47 Immunohistochemically, cone ERG(absent) RPGRIP1 (ins/ins) retinas have extensive L/M

48 Despite marked changes in cone ERG and retinal morphology, photopic vision-guided behav

49 Cone morphology of the dogs lacking cone ERG are truncated with shortened outer and inner segment

50 Ophthalmoscopically, cone ERG(absent) RPGRIP1 (ins/ins) eyes show discolouration o

51 Implicit times of the red cone ERGs were slightly faster for the Neuroline skin electro

52 proaches demonstrate that a highly conserved ERG-bound enhancer located upstream of HLX (which encode

53 ChIP)-seq revealed the presence of conserved ERG-bound putative enhancer elements near these target g

54 In contrast, 11-cis-retinal content, ERGs and retinal histology were normal in mice with Atg7

55 However, in the past decade ERG has become highly associated with prostate cancer de

56 Decreased ERG expression also correlates with EndMT in tissues fro

57 Mechanistic studies of deregulated ERG in prostate cancer and other cancers continue to enh

58 ween the number of injections and diminished ERG responses, such that on average each intravitreous m

59 These tumors also frequently displayed ERG gene fusions involving alternative 5'-partners to TM

60 re subtypes of CSNB and demonstrate distinct ERG features.

61 multiple cancer lineages harboring distinct ERG fusions within a single cancer nodule.

62 Three chemically diverse ERG channel blockers (terfenadine, ErgToxin-1, and E-403

63 Transcription of DLL4 coincides with dynamic ERG-dependent recruitment of the transcriptional co-acti

64 that prostate-specific activation of either ERG or YAP1 in mice induces similar transcriptional chan

65 Electroretinogram (ERG) was recorded from MPS IIIB and wild-type (WT) mice

66 inal inflammation, and an electroretinogram (ERG) illustrated decreased amplitude of the b wave in bo

67 rders with characteristic electroretinogram (ERG) abnormalities.

68 B1 patients have a normal electroretinogram (ERG) a-wave, indicative of photoreceptor function, but l

69 - and b-wave responses of electroretinogram (ERG) are abolished.

70 Recordings of electroretinogram (ERG) oscillatory potentials and scotopic threshold respo

71 ase of photopic b-wave of electroretinogram (ERG).

72 e opsin, loss of photopic electroretinogram (ERG) responses and loss of cone cells.

73 n the eye as assessed by electroretinograms (ERG), corneal and retinal tomography, and histology.

74 out (KO) mice, recording electroretinograms (ERG) and performing immunocytochemical staining.

75 ther variability in cone electroretinograms (ERGs) ranging from normal to absent in an extended RPGRI

76 ing DTL electrodes and electroretinographic (ERG) protocols with flash strengths of 0.009, 0.17, 3.0,

77 scotopic and photopic electroretinographic (ERG) responses to single-flash stimuli also show no diff

78 ated by TUNEL assay and electroretinography (ERG) analysis.

79 y clinical findings and electroretinography (ERG) on 244 evaluable injections in 63 patients using 30

80 n microscopy (TEM), and electroretinography (ERG) were used to analyze 6 genotypes including WT at th

81 ation, full-field flash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-

82 re performed, including electroretinography (ERG), multifocal ERG (mfERG), perimetry, optical coheren

83 an abnormal response on electroretinography (ERG) in UBE3D(+/-) heterozygous mice.

84 Scotopic electroretinography (ERG) showed a diminished c-wave amplitude in the CLN5 de

85 neration using scotopic electroretinography (ERG), optical coherence tomography (OCT), and immunohist

86 ckness were found using electroretinography (ERG), fundus photography (FP), fundus fluorescein angiog

87 Visual acuity (VA), electroretinography (ERG), and spectral-domain optical coherence tomography (

88 otype was assessed with electroretinography (ERG), optical coherence tomography, psychophysics, and p

89 man leukemias according to Evi1/EVI1 and Erg/ERG expression, reflecting aggressiveness and cell of or

90 irm that this network of genes requires ERK, ERG and p300 activity.

91 bability weighting to account for evaluating ERG status only in surgically treated cases.

92 of human SPOP-mutant cancers do not express ERG.

93 Whole-eye ERGs and multielectrode arrays confirmed a major retinal

94 the degradation of the transcription factor ERG and that translocations of ERG or mutations in SPOP

95 e overexpression of the transcription factor ERG are present in approximately 50% of all prostate can

96 Here we identify the transcription factor ERG as a key regulator of endothelial Notch signalling.

97 The ETS transcription factor ERG drives expression of VE-cadherin and controls juncti

98 ormation-specific (ETS) transcription factor ERG in prostate cells.

99 MT in liver disease.The transcription factor ERG is key to endothelial lineage specification and vasc

100 , the gene encoding the transcription factor ERG is recurrently rearranged and plays a critical role

101 s of the megakaryocytic transcription factor ERG to target genes.

102 d activation of the ETS transcription factor ERG, a prerequisite for DLL4 induction.

103 o overexpression of the transcription factor ERG, while a mutually exclusive 10% of prostate cancers

104 We recover seven transcription factors (ERG, HOXA5, HOXA9, HOXA10, LCOR, RUNX1 and SPI1) that ar

105 electrode types allow successful full-field ERG recording, although separate normative data for both

106 Comparison of full-field ERG recordings with microfiber DTL and Neuroline skin el

107 Full-field flash ERG findings were normal in both eyes.

108 etic transcription factors (TFs) PU.1, FLI1, ERG, C/EBPalpha, C/EBPbeta, and MYB at nucleosome-deplet

109 of the isolated cone response (30-Hz flicker ERG: mean difference, -12.1 muV [95% CI, -22.5 to -1.6 m

110 e the isolated cone responses (30-Hz flicker ERG: mean difference, 1.2 milliseconds [95% CI, 0.5-1.8

111 tate cancer, among whom 884 were assayed for ERG (426 ERG-positive).

112 est that SPOP acts as a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic

113 rs were ERG-positive, and being negative for ERG staining was associated with higher Gleason score.

114 iated phosphorylation of ERG is required for ERG functions in prostate cells, but the reason for this

115 of a novel ERG isoform, ERGalt, and frequent ERG deletion.

116 RSS2-ERG-positive prostate cancer cells from ERG dependency.

117 Epithelial cells derived from ERG transgenic mouse prostates have increased prostasphe

118 Furthermore, ERG traces from regenerated retinas displayed waveforms

119 modified ISCEV protocol in the Mini Ganzfeld ERG.

120 e DUX4 and the ETS transcription factor gene ERG is a hallmark of a subtype of B-progenitor ALL that

121 rent mediated by Ether-a-go-go-Related Gene (ERG) channels.

122 ETS-related gene (ERG) is a member of the E-26 transformation-specific (ET

123 ally mediated by Ether-a-go-go-Related Gene (ERG) K(+) channels contributes to persistent firing in n

124 elial transcription factor ETS-related gene (ERG) promotes liver homoeostasis by controlling canonica

125 oblast transformation-specific-related gene (ERG), or TMPRSS2:ERG, in prostate cancer varies by race.

126 S mutant form of ether-a-go-go-related gene (ERG; Kv11.1).

127 entification of early redox-regulated genes (ERGs) in the nucleus of the model organism Arabidopsis t

128 erythroblastosis virus E26 oncogene homolog (ERG).

129 tation thresholds and lower 0.5-Hz and 30-Hz ERG amplitudes.

130 Network analyses identified ERG, IL6R, and LDLR as modifiers of MMP9, with a direct

131 ts (36%) had a greater than 20% asymmetry in ERG values between the 2 eyes.

132 on was associated with a 5.3-muV decrease in ERG amplitude (P < 0.001).

133 Wnt signaling is decreased in ERG-deficient endothelial cells; activation of Wnt signa

134 associated, on average, with a decrement in ERG response.

135 nstream effectors Grp78/BiP and eIF2alpha in ERG transgenic mouse prostate glands indicate the presen

136 be exploited for therapeutic intervention in ERG-positive prostate cancers.

137 function in the brain, although mutations in ERG channels have recently been linked to schizophrenia.

138 s, and over 90% of these fusions occurred in ERG exons 3 or 4.

139 significantly associated with a reduction in ERG (P = 0.045).

140 - drusen-like deposits, severe reduction in ERG responses, photoreceptor cell loss and gliosis.

141 se (PI3K)/Akt-dependent manner, resulting in ERG enrichment at Dll4 promoter and multiple enhancers.

142 We show that Ang1 induces ERG phosphorylation in a phosphoinositide 3-kinase (PI3K

143 In infant ERG recordings skin electrodes frequently result in a be

144 es showed that DTL electrodes produce larger ERGs.

145 el was associated with a reduction in mature ERG expression and an increase in the expression of seve

146 molecular mechanisms involving ERK-mediated ERG activation that could be exploited for therapeutic i

147 Moreover, ERG represents a promising candidate biomarker for asses

148 s that were not coimmunolocalized with mouse ERG cells.

149 ed on light-adapted perimetry and multifocal ERG but with near-normal rod-mediated vision according t

150 ash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-color dark-adapted p

151 luding electroretinography (ERG), multifocal ERG (mfERG), perimetry, optical coherence tomography (OC

152 l deregulation of ERG, expression of a novel ERG isoform, ERGalt, and frequent ERG deletion.

153 xpression of ERG channels and the ability of ERG blocks to abolish persistent firing evoked by both s

154 Ablation of ERG expression results in endothelial-to-mesenchymal tra

155 In the absence of ERG-28, SLO-1 channels undergo aspartic protease DDI-1-d

156 plex 2 (PRC2), transcriptional activation of ERG target genes, and increased cell migration.

157 des a selection pressure in the continuum of ERG dependent neoplastic process.

158 expression and the clinicopathologic data of ERG and IL-6 using immunohistochemical double staining a

159 prevent CRL3(SPOP)-dependent degradation of ERG in prostate cancer cells.

160 ow that constitutive endothelial deletion of ERG (Erg(cEC-KO)) in mice causes embryonic lethality wit

161 Inducible endothelial deletion of ERG (Erg(iEC-KO)) results in defective physiological and

162 companied by transcriptional deregulation of ERG, expression of a novel ERG isoform, ERGalt, and freq

163 specifically with the DNA binding domain of ERG.

164 e DNA-binding and transactivation domains of ERG, but it inhibits wild-type ERG transcriptional activ

165 suggesting that the proliferative effects of ERG and PRMT5 are mediated through attenuating AR's abil

166 Expression of ERG and IL-6 correlated strongly in prostate tissue samp

167 The broad expression of ERG channels and the ability of ERG blocks to abolish pe

168 vely, our study shows that the expression of ERG in prostate cancer is linked to the expression of IL

169 Forced expression of ERG in prostate tumor cell lines resulted in significant

170 e cancer did not result in the expression of ERG protein in histologically normal prostate glands, hi

171 the morphological and phenotypic features of ERG gain in normal mouse prostate cells, including expan

172 serine 2) gene to the open reading frame of ERG, encoding an ETS family transcription factor.

173 deregulation results in loss of function of ERG, either by deletion or induced expression of an isof

174 nderstanding of the mechanistic functions of ERG in prostate tumor biology and towards development of

175 c reticulum stress in the prostate glands of ERG transgenic mice.

176 lence ratios and 95% confidence intervals of ERG expression in relation to patient characteristics.

177 dentify a pathogenic mechanism where loss of ERG causes endothelial-dependent liver fibrogenesis via

178 Conversely, loss of ERG phosphorylation at Ser-96 resulted in recruitment of

179 s the ERG-cistrome and a genome-wide loss of ERG-mediated transcriptional activation and cell migrati

180 in retinal function was detected by means of ERG.

181 knowledge about the molecular mechanisms of ERG function in prostate cells has hampered efforts to t

182 ular step stimuli suggest that modulation of ERG channels may underlie many forms of persistent activ

183 ta provide evidence that the oncogenicity of ERG is mediated, in part, by competition with ERF and th

184 nism whereby ERK-mediated phosphorylation of ERG at one serine residue causes a conformational change

185 ERK-mediated phosphorylation of ERG is required for ERG functions in prostate cells, but

186 during chronic ER stress due to presence of ERG in prostate epithelium induces survival pathways and

187 tion of IL-6, whereas the down-regulation of ERG decreased IL-6 secretion.

188 to calculate HRs and 95% CIs for the risk of ERG-positive and, separately, ERG-negative disease.

189 take was associated with a decreased risk of ERG-positive disease (HR: 0.54; 95% CI: 0.37, 0.81; P-tr

190 In the more common scenario of ERG upregulation, chromatin immunoprecipitation followed

191 the ERG gene as the established surrogate of ERG fusion genes among 262 prostate cancer biopsies from

192 on in a transgenic mouse model with those of ERG knockdown in a TMPRSS2:ERG-positive PC cell line.

193 iption factor ERG and that translocations of ERG or mutations in SPOP prevent CRL3(SPOP)-dependent de

194 unction that were detectable with the use of ERG.

195 tations; 1 had a cone dystrophy phenotype on ERG and 6 had a cone-rod pattern of dysfunction.

196 Amplitudes and implicit times on ERG, mean deviation on VF, central subfield mean thickne

197 They also suggest that overcoming ERG resistance to SPOP-mediated degradation represents a

198 al, disease-free survival, ERG: peak-to-peak ERG amplitudes in response to 30-Hz photopic flicker sti

199 Photopic ERG, visual evoked potentials, IHC and cell counting ind

200 By contrast, the photopic ERG b-waves in KO mice were hardly affected at any age.

201 native IKr and cross-reacted with guinea pig ERG channel.

202 osphorylation, which correlated with reduced ERG function and decreased photoreceptor survival at bot

203 ression and interaction with the ETS-related ERG protein at enhancer elements.

204 From a screen for functionally relevant ERG interactors, we identify the arginine methyltransfer

205 effect on the ex-vivo isolated mouse retina ERG where the RPE is not attached to the isolated retina

206 We review ERG's structure and function, and its role in prostate c

207 Rod ERG abnormalities (in addition to cone dysfunction) were

208 or the risk of ERG-positive and, separately, ERG-negative disease.

209 Ocular survival, disease-free survival, ERG: peak-to-peak ERG amplitudes in response to 30-Hz ph

210 Interventions/Urinary PCA3 and T2:ERG RNA measurement before prostate biopsy.

211 ined measurement of PCA3 and TMPRSS2:ERG (T2:ERG) RNA in the urine after digital rectal examination w

212 Combined urinary testing for T2:ERG and PCA3 can avert unnecessary biopsy while retainin

213 33-85 years) combining testing of urinary T2:ERG and PCA3 at thresholds that preserved 95% sensitivit

214 s hampered efforts to therapeutically target ERG.

215 al new therapies that are based on targeting ERG.

216 uorescence and electrophysiological testing (ERG and EOG) may indicate initial stages or more widespr

217 Finally, we demonstrate that ERG directly interacts with Notch intracellular domain (

218 These data demonstrate that ERG is an essential regulator of angiogenesis and vascul

219 We determined that ERG activates the transcriptional program regulated by Y

220 In summary, we found no evidence that ERG is an effector of SPOP mutation in human prostate ca

221 We find that ERG mediates Ang1-dependent regulation of Notch ligands

222 tation followed by sequencing indicates that ERG inhibits the ability of ERF to bind DNA at consensus

223 We propose that ERG coordinates Ang1, beta-catenin and Notch signalling

224 a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic effector of SPOP muta

225 Here we report that ERG ubiquitination and degradation are governed by the C

226 This reveals that ERG represses the expression of a previously unreported

227 Here the authors show that ERG balances TGFbeta signalling through the SMAD1 and SM

228 We show that ERG controls the balance between Notch ligands by drivin

229 Here, we show that ERG, through its physical interaction with androgen rece

230 In C. elegans, we show that ERG-28, an endoplasmic reticulum (ER) membrane protein,

231 Molecular analysis shows that ERG binds to SMAD3, restricting its access to DNA.

232 Our results also suggest that ERG current normally governs cortical neuron responses t

233 y-resistant cell population, suggesting that ERG may have a direct role in preventing resistance to a

234 The ERG a-wave is the light-induced hyperpolarization of ret

235 The ERG gene is fused to TMPRSS2 in approximately 50% of pro

236 6 resulted in recruitment of EZH2 across the ERG-cistrome and a genome-wide loss of ERG-mediated tran

237 etween the TMPRSS2 promoter sequence and the ERG coding sequence (TMPRSS2:ERG) in urine, noninvasive

238 response, binds to androgen receptor at the ERG gene breakpoint and inhibits both the juxtaposition

239 emistry to assess oncoprotein encoded by the ERG gene as the established surrogate of ERG fusion gene

240 easure of photoreceptor-BP connectivity, the ERG, was restored to a normal waveform.

241 inine 761 highlights a mechanism for how the ERG oncogene may coax AR towards inducing proliferation

242 diabetic rats was assessed by monitoring the ERG b-wave and oscillatory potentials, Muller cell react

243 s pathway leads to aberrant elevation of the ERG oncoprotein.

244 y, leading to proteolytic degradation of the ERG protein.

245 ism in prostate tumor cell lines we show the ERG-mediated up-regulation of the prostanoid receptors E

246 wed gliosis and degenerative changes, though ERG responses were minimally affected.

247 TMPRSS2-ERG gene fusions occur in over 50% of prostate cancers,

248 TMPRSS2-ERG gene fusions that occur frequently in human prostate

249 TMPRSS2-ERG gene fusions were observed in 44% of cases, and over

250 issues showed that the presence of a TMPRSS2-ERG rearrangement was highly correlated with lower level

251 SPOP mutations and TMPRSS2-ERG rearrangements occur collectively in up to 65% of hu

252 ites of fusion oncogenes BCR-ABL and TMPRSS2-ERG.

253 Lastly, tumors displaying TMPRSS2-ERG fusions that retained interstitial genes were less l

254 However, TMPRSS2-ERG gene fusions and PTEN losses occurred in only 21% an

255 his study, we analyzed the status of TMPRSS2-ERG fusion genes and interstitial genes in tumors from a

256 ized two mouse models recapitulating TMPRSS2-ERG insertion or deletion events in the background of pr

257 tumour growth, and ERF loss rescues TMPRSS2-ERG-positive prostate cancer cells from ERG dependency.

258 The TMPRSS2-ERG fusion event and the overexpression of the transcrip

259 l prostate cancers are caused by the TMPRSS2-ERG gene-fusion, which enables androgens to drive expres

260 ss along with other genes within the TMPRSS2-ERG interstitial region contributes to disease progressi

261 y genes, which retained interstitial TMPRSS2/ERG sequences.

262 TMPRSS2:ERG phenotyping of larger studies is required to determi

263 TMPRSS2:ERG was assessed by ERG immunohistochemistry on tumor ti

264 ific associations in a total of 1221 TMPRSS2:ERG phenotyped PrCa cases.

265 alyzed in case-case comparisons (296 TMPRSS2:ERG fusion-positive versus 256 fusion-negative cases) an

266 del with those of ERG knockdown in a TMPRSS2:ERG-positive PC cell line.

267 Additionally, TMPRSS2:ERG variants are detectable in urine to provide non-inva

268 selectively isolating and adsorbing TMPRSS2:ERG mRNA onto bare gold electrodes without requiring any

269 hat combined measurement of PCA3 and TMPRSS2:ERG (T2:ERG) RNA in the urine after digital rectal exami

270 negative (OR = 0.53, P = 0.0007) and TMPRSS2:ERG fusion-positive PrCa (OR = 1.30, P = 0.0016), respec

271 ferences have been described between TMPRSS2:ERG fusion-positive and fusion-negative prostate cancer

272 ical utility by accurately detecting TMPRSS2:ERG in a collection of 17 urinary samples obtained from

273 is that prostate cancers that harbor TMPRSS2:ERG may be etiologically distinct from fusion-negative c

274 9962 (17q24), which were enriched in TMPRSS2:ERG fusion-negative (OR = 0.53, P = 0.0007) and TMPRSS2:

275 or the candidate target gene SOX9 in TMPRSS2:ERG fusion-positive PrCa, which was not evident in TMPRS

276 itive PrCa, which was not evident in TMPRSS2:ERG negative tumors.

277 s a rationale for targeting PRMT5 in TMPRSS2:ERG positive prostate cancers.

278 pared the transcriptional effects of TMPRSS2:ERG expression in a transgenic mouse model with those of

279 ts, such as the multiple variants of TMPRSS2:ERG fusion gene mutations in prostate cancer (PCa), are

280 The lower prevalence of TMPRSS2:ERG fusions in men of African descent implies that alter

281 ta-analysis showed the prevalence of TMPRSS2:ERG fusions in prostate cancer to be highest in men of E

282 stematic review and meta-analysis of TMPRSS2:ERG fusions in relation to race, Gleason score, and tumo

283 ) in urine, noninvasive screening of TMPRSS2:ERG mRNA in patient urine samples could improve the spec

284 emical assay for direct detection of TMPRSS2:ERG mRNA in PCa urinary samples by selectively isolating

285 tion-specific-related gene (ERG), or TMPRSS2:ERG, in prostate cancer varies by race.

286 sumption may play a role in reducing TMPRSS2:ERG-positive disease.

287 equence and the ERG coding sequence (TMPRSS2:ERG) in urine, noninvasive screening of TMPRSS2:ERG mRNA

288 The TMPRSS2:ERG gene fusion is common in androgen receptor (AR) posi

289 y function of PRMT5 is restricted to TMPRSS2:ERG-positive prostate cancer cells.

290 ays for identifying multiple urinary TMPRSS2:ERG variants are potentially useful to aid in early canc

291 of a discovery set of 552 cases with TMPRSS2:ERG data and 7650 unaffected men from five centers we ha

292 an independent set of 669 cases with TMPRSS2:ERG data was established to replicate the top five candi

293 iants differentially associated with TMPRSS2:ERG fusion status.

294 expressing either mutated SPOP or truncated ERG.

295 ion of full-length or N-terminally truncated ERG protein in prostate epithelia.

296 s a dominant-negative inhibitor of wild-type ERG function.

297 on domains of ERG, but it inhibits wild-type ERG transcriptional activity and is transforming.

298 d that 47 of 262 (18%) prostate cancers were ERG-positive, and being negative for ERG staining was as

299 I: 0.37, 0.81; P-trend = 0.004) but not with ERG-negative disease (HR: 0.96; 95% CI: 0.62, 1.50; P-tr

300 tability and mostly occur in tumours without ERG upregulation.