ライフサイエンスコーパス: PSA

1 PSA and ALP were measured before each treatment cycle an

2 PSA levels in midlife strongly predict future lethal PCa

3 PSA levels were quantitatively analyzed by using electro

4 PSA values have been widely used to predict biological t

5 PSA velocity was 0.32 +/- 0.59 ng/mL/y (range, 0.04-1.9

6 PSA was assessed 2 mo after RLT.

7 io [aHR], 1.72; 95% CI, 1.17-2.52; P = .01), PSA doubling time less than 9 months (aHR, 2.06; 95% CI,

8 nsor had an extremely low LOD of 1.0pgmL(-1) PSA within the detection range of 0.005-20ngmL(-1) and 0

9 zed to the surface of a microtiter well, (2) PSA, and (3) an anti-PSA antibody-UCNP conjugate were co

10 ients were randomly assigned to detect a 20% PSA RR improvement.

11 61 treated patients, 33 (54.1%) had >/= 30% PSA declines by C4 and did not switch taxane, 15 patient

12 patients (24.6%) who did not achieve >/= 30% PSA declines by C4 switched taxane, and 13 patients (21.

13 mary clinical endpoint was confirmed >/= 50% PSA decline versus historical control (TAX327).

14 was associated with a higher rate of >/= 50% PSA decrease at C4 ( P = .009).

15 taxane, 46.7% subsequently achieved >/= 50% PSA decrease.

16 l, 35 patients (55.6%) had confirmed >/= 50% PSA responses, exceeding the historical control rate of

17 tudy did not reach its prescribed level of 6 PSA responses of 0.2 ng/mL or lower, although 5 response

18 A PSA decline of more than 50% was observed significantly

19 A PSA nadir value of greater than 0.5 ng/mL following radi

20 Five (13%) patients achieved a PSA level of 0.2 ng/mL or lower (95% CI, 4%-27%).

21 axel increased the likelihood of achieving a PSA </= 0.2 ng/mL at 7 months (45.3% v 28.8% of patients

22 atients had metastatic prostate cancer and a PSA level higher than 4.0 ng/mL between 6 and 12 months

23 (PR) was a secondary end point, defined as a PSA level reduction to lower than 4.0 ng/mL but higher t

24 rostatectomy without prior radiotherapy at a PSA level of less than 1 ng/mL.

25 For a PSA less than 3.5 mug/L, most relapses were diagnosed at

26 For a PSA of 0.5-3.5 mug/L, PSA-stratified sensitivity was 88%

27 82,429 men 50 to 69 years of age received a PSA test; 2664 received a diagnosis of localized prostat

28 e, of whom 2 patients and 1 patient showed a PSA decline of more than 30% and more than 50%, respecti

29 Forty-seven patients (64%) showed a PSA decline, including 23 (31%) with a decline by more t

30 st, in group 2, 14 patients (43.8%) showed a PSA decline, of whom 10 and 8 patients showed a decline

31 In group 1, 4 patients (12.9%) showed a PSA decline, of whom 2 patients and 1 patient showed a P

32 nse, no patient with increasing ALP showed a PSA response (P = 0.036).

33 Here, we show that a PSA-carrying NCAM fragment is generated at the plasma me

34 The primary end point was a PSA level of 0.2 ng/mL or lower within 12 months of star

35 .0 ng/mL (n = 341), and 37% for those with a PSA > 2.0 ng/mL (n = 323); P < .001.

36 Patients with a PSA level of at least 75 ng/mL (75 mug/L) 24 hours after

37 to 0.2 ng/mL (n = 441), 63% for those with a PSA of 0.21 to 0.50 ng/mL (n = 822), 54% for those with

38 o 0.50 ng/mL (n = 822), 54% for those with a PSA of 0.51 to 1.0 ng/mL (n = 533), 43% for those with a

39 to 1.0 ng/mL (n = 533), 43% for those with a PSA of 1.01 to 2.0 ng/mL (n = 341), and 37% for those wi

40 than (18)F-choline PET/CT in patients with a PSA of less than 1 ng/mL.

41 s was significantly associated with absolute PSA levels (P = 4.3 x 10(-3)).

42 s was significantly associated with absolute PSA levels (P = 4.3 x 10(-3)).

43 Polysialic acid (PSA) and its major protein carrier, the neural cell adhe

44 Polysialic acid (PSA) is a large negatively charged glycan mainly attache

45 AM) is the major carrier of polysialic acid (PSA) which modulates NCAM functions of neural cells at t

46 by plotting the peak current and Rct against PSA concentration, respectively.

47 s then cleaned by a primary-secondary amine (PSA), GCB, and MgSO4.

48 s CaCl2 (100mg) and primary-secondary amine (PSA, 25mg) as sorbents.

49 y 7.7%; OR, 2.32; 95% CI, 1.04 to 5.15), and PSA concern (mean score 52.8; OR, 1.01 per point change;

50 1 to 20 ng/mL; T2b to 2c, Gleason </= 6, and PSA </= 20 ng/mL; or T1 to 2, Gleason = 7, and PSA </= 2

51 risk group) (T1-T2; Gleason score, </=6; and PSA, <10 ng/mL), and intermediate-risk disease (T1-T2 wi

52 A </= 20 ng/mL; or T1 to 2, Gleason = 7, and PSA </= 20 ng/mL).

53 cles (PLLA NPs) for signal amplification and PSA detection.

54 quations to compute nutrient consumption and PSA production.

55 say system that can reliably measure NEM and PSA in patient samples.

56 required at least 7 months of follow-up and PSA levels at 7 months from ADT initiation.

57 ch immunocomplexes consisting of (1) an anti-PSA antibody immobilized to the surface of a microtiter

58 a microtiter well, (2) PSA, and (3) an anti-PSA antibody-UCNP conjugate were counted under a wide-fi

59 of the PSA-antigen (1-30 ng/mL) between anti-PSA immobilized on the l-Cys modified electrode using la

60 The Au/Cys/FcPAMAM/anti-PSA immunosensor showed excellent performance for PSA at

61 a rising level of prostate-specific antigen (PSA) (range, 0.3-119.0 ng/mL; mean, 10.1 +/- 21.3 ng/mL)

62 ponse measured by prostate-specific antigen (PSA) 2 mo after RLT.

63 as determined by prostate-specific antigen (PSA) and alkaline phosphatase (ALP), as well as the corr

64 Serum prostate-specific antigen (PSA) and Expanded Prostate Index Composite (EPIC) scores

65 , clinical stage, prostate-specific antigen (PSA) and extent of disease, as well as poor patient surv

66 men with elevated prostate-specific antigen (PSA) and negative transrectal ultrasonography (US)-guide

67 ationship between prostate-specific antigen (PSA) and overall survival in the context of a prospectiv

68 ntibodies against prostate specific antigen (PSA) and prostate specific membrane antigen (PSMA), and

69 The prostate-specific antigen (PSA) assays currently employed for the detection of pros

70 tive detection of prostate specific antigen (PSA) at clinically relevant concentrations.

71 the detection of prostate specific antigen (PSA) based on three different generations (G1, G2 and G3

72 ms use presenting prostate-specific antigen (PSA) concentration, biopsy Gleason grade, and clinical s

73 fe, health worry, prostate-specific antigen (PSA) concern, and outlook on life.

74 t achieve >/= 30% prostate-specific antigen (PSA) decline by cycle 4 (C4) switched taxane.

75 this study was a prostate-specific antigen (PSA) doubling time of less than 12 mo after initial trea

76 e demonstrate how prostate specific antigen (PSA) expression varies over several orders of magnitude

77 used in men with prostate-specific antigen (PSA) failure after radical prostatectomy (RP) to triage

78 as performed with prostate-specific antigen (PSA) follow-up every 3 months, with repeated imaging at

79 ible detection of prostate specific antigen (PSA) from 1 to 1,000 nM in 100 mM phosphate buffer.

80 e measurements of prostate-specific antigen (PSA) in 50% serum using the proposed method, we achieve

81 factor (VEGF) and prostate-specific antigen (PSA) in human serum for early diagnosis of PCa.

82 time detection of prostate specific antigen (PSA) in human serum using silicon nanowire field effect

83 ect the biomarker prostate specific antigen (PSA) in serum.

84 cal data, and the prostate-specific antigen (PSA) level at baseline and 8 wk after therapy applicatio

85 as reflected by a prostate-specific antigen (PSA) level higher than 4.0 ng/mL after 7 months of ADT,

86 Prostate-specific antigen (PSA) level in midlife predicted future prostate cancer (

87 His prostate-specific antigen (PSA) level was 7.1 ng/mL.

88 24-hour post-PAE prostate-specific antigen (PSA) level was registered in 133 patients with sPVA.

89 gs with increased prostate-specific antigen (PSA) level, or (c) had a prior history of prostate cance

90 s, including age, prostate-specific antigen (PSA) level, PSA density, race, digital rectal examinatio

91 urrently elevated prostate-specific antigen (PSA) level.

92 0.001) and higher prostate-specific antigen (PSA) levels (P = 0.024) were associated with management

93 use of increasing prostate-specific antigen (PSA) levels after radical prostatectomy were included in

94 l of longitudinal prostate-specific antigen (PSA) levels and risks for biopsy upgrading.

95 Prostate-specific antigen (PSA) levels have been used for detection and surveillanc

96 nts with a median prostate-specific antigen (PSA) of 6.4 ng/mL (range, 2.2-158.4 ng/mL; interquartile

97 gic, clinical, or prostate-specific antigen (PSA) progression; otherwise, treatment was to continue f

98 or cell (CTC) and prostate-specific antigen (PSA) response end points in five prospective randomized

99 s were: confirmed prostate-specific antigen (PSA) response rate (RR) and whether ETS fusions predicte

100 examined >/= 50% prostate-specific antigen (PSA) responses, PSA progression-free survival, clinical

101 with a continued prostate-specific antigen (PSA) rise after enzalutamide treatment discontinuation.

102 free detection of prostate specific antigen (PSA) still remains a challenge in prostate cancer diagno

103 evelopment of the prostate specific antigen (PSA) test, and a continuing decrease in the rates of oth

104 the cancer marker prostate specific antigen (PSA) using photon-upconversion nanoparticles (UCNPs) as

105 The median prostate-specific antigen (PSA) value was 1.0 ng/mL (mean, 4.7 ng/mL; range, 0.13-1

106 y, on considering prostate-specific antigen (PSA) value, (64)CuCl2 PET/CT had a higher DR than (18)F-

107 imaging at serum prostate-specific antigen (PSA) values low enough to affect target volume delineati

108 ared with current prostate-specific antigen (PSA) values, Gleason score (GS), and d'Amico risk classi

109 shed affinity for prostate specific antigen (PSA) was complexed with PSA prior to being immobilised o

110 Prostate-specific antigen (PSA) was determined every 4 wk.

111 d increase in the prostate-specific antigen (PSA), commonly referred to as biochemical recurrence.

112 inoma (PC), serum prostate-specific antigen (PSA), greatly overestimates PC population.

113 score </= 6, and prostate-specific antigen [PSA] 10.1 to 20 ng/mL; T2b to 2c, Gleason </= 6, and PSA

114 idate surrogates (prostate-specific antigen [PSA] failure, PSA nadir >0.5 ng/mL, PSA doubling time <9

115 ason score, </=6; prostate-specific antigen [PSA], <10 ng/mL; PSA density <0.15 ng/mL/cm3; and <8-mm

116 ggests that at least half of the 40 SNPs are PSA-associated independent of PCa.

117 e analogs had calculated polar surface area (PSA), measured LogD7.4, aqueous kinetic solubility, and

118 unds 5-nonyloxytryptamine and vinorelbine as PSA mimetics.

119 -up every 3 months, with repeated imaging at PSA progression or clinical suspicion for progression.

120 Our purpose was to determine if a baseline PSA level during midlife predicts lethal PCa in a US pop

121 95% CIs, of the association between baseline PSA and risk of lethal PCa.

122 ent did not significantly differ by baseline PSA level.

123 al PCa was strongly associated with baseline PSA in midlife: odds ratios (95% CIs) comparing PSA in t

124 ase, prior local therapy, and lower baseline PSAs (all P </= .01).

125 52 of 270 patients (19%) with PCa early BCR (PSA < 1.0 ng/mL).

126 Treatment response was defined as both PSA </= 0.1 ng/mL and >50% reduction in PSA.

127 The detection rates were stratified by PSA.

128 t, 59.1% had low-risk tumor characteristics (PSA < 10 ng/mL and Gleason score < 7), and 89.2% underwe

129 in midlife: odds ratios (95% CIs) comparing PSA in the > 90th percentile versus less than or equal t

130 Conclusion PSA </= 0.2 ng/mL at 7 months is prognostic for longer o

131 currently accepted but rather controversial PSA indicator.

132 Standardization of seminal plasma derived PSA calibrant molecular form mass concentrations and pur

133 talyze hydrogen peroxide reduction to detect PSA and PSMA.

134 ule), no nodal involvement, and a detectable PSA level of 0.2 to 4.0 ng per milliliter to undergo rad

135 We determined PSA-stratified sensitivity rates for both tracers and co

136 rade, stage, presence of metastatic disease, PSA velocity, or PSA doubling time.

137 hages never used in transport studies (i.e., PSA-HM1, PSA-HP1, PSA-HS2, and H3/49).

138 ogression to high Gleason score and elevated PSA levels, and served as an independent predictor of bi

139 rements of free prostate specific antigen (f-PSA), which is similar in size to BSA, were performed to

140 ced dynamically on the basis of two factors: PSA doubling time (</= 3 v > 3 months) and nodal versus

141 es (prostate-specific antigen [PSA] failure, PSA nadir >0.5 ng/mL, PSA doubling time <9 months, and i

142 generation antiandrogen agent with a falling PSA level at the time of enrollment; this therapy was co

143 limit of detection of 1.2 pg mL(-1) (42 fM) PSA in 25% blood serum, which is about ten times more se

144 ilure (BCF) defined by any of the following: PSA failure (nadir + 2), hormonal intervention, clinical

145 nstructed multivariable models adjusting for PSA, Gleason sum, number of prior hormone therapies, pri

146 NPs): 19 novel, 15 previously identified for PSA (14 of which were also PCa-associated), and 6 previo

147 The LOD for PSA was 1000-fold better than the only previous report o

148 ortant information about genetic markers for PSA that may improve PCa screening, thereby reducing ove

149 st or cytostatic drug to act as mimetics for PSA to stimulate regeneration after injury in the mammal

150 llent detection limits (LOD) of 15 fg/mL for PSA and 4.8 fg/mL for PSMA were achieved in serum.

151 s (0.05-100ng/mL for VEGF and 1-100ng/mL for PSA), as well as high levels of sensitivity and selectiv

152 from mouse to human and used parameters for PSA shedding and prostate cancer.

153 mmunosensor showed excellent performance for PSA at the pulse amplitude; 50mV and the scan rate; 10mV

154 The performance for PSA detection therefore well meets the clinical requirem

155 nt, only strategies with biopsy referral for PSA levels higher than 10.0 ng/mL or age-dependent thres

156 40 years of age underwent 18 strategies for PSA screening.

157 mplex formation with antibodies was used for PSA detection.

158 re the use of PSA values, such as the % free PSA and Prostate Health Index by increasing the accuracy

159 treatment response, compared with a further PSA increase in 65% (22/34) in those not treated.

160 ern blot (WB) and in multiple research grade PSA ELISAs.

161 The variables used to define the groups (PSA concentration, Gleason grading, and clinical stage)

162 Patients with high PSA levels have to undergo unnecessary but physically pa

163 as comparably low (PSA < 0.5 mug/L) or high (PSA > 3.5 mug/L).

164 atic disease at diagnosis ( P = .01), higher PSA ( P < .01), prior abiraterone or enzalutamide use (

165 s 75.4 cm(3), respectively; P < .01), higher PSA density (0.16 vs 0.10, respectively; P < .01), and h

166 ositive (68)Ga-PSMA scan results, and higher PSA levels.

167 Patients with higher PSA, higher GS, and higher d'Amico risk score had statis

168 His PSA was monitored every 6 months and gradually increased

169 er used in transport studies (i.e., PSA-HM1, PSA-HP1, PSA-HS2, and H3/49).

170 between single prostate cancer cells and how PSA expression shifts with genetic drift.

171 n transport studies (i.e., PSA-HM1, PSA-HP1, PSA-HS2, and H3/49).

172 table concentrations of rabbit IgG and human PSA by the naked eye were down to 0.1 and 4 ng/mL, respe

173 s other than PCa-such as genetics-can impact PSA.

174 switch strategy was associated with improved PSA response rates versus TAX327.

175 (P = 1.0) concordantly paralleled changes in PSA levels.

176 ts were investigator-assessed 50% decline in PSA concentration from baseline (PSA50) for BAT (for all

177 C count; and a 30%, 50%, and 70% decrease in PSA level.

178 An increase in PSA during therapy cycles occurs because of disease prog

179 both PSA </= 0.1 ng/mL and >50% reduction in PSA.

180 after prostatectomy for moderately increased PSA levels.

181 rate was positively associated to increasing PSA as well as concomitant ADT.

182 r history of prostate cancer with increasing PSA level.

183 Increased mass concentrations of intact PSA yielded higher immunoassay absorbance values, even b

184 KD increases prostate-specific antigen (KLK3/PSA) expression.

185 For a PSA of 0.5-3.5 mug/L, PSA-stratified sensitivity was 88% (15/17) for (18)F-DCF

186 apy (n = 85), tracer sensitivity was largely PSA-independent.

187 age, prostate-specific antigen (PSA) level, PSA density, race, digital rectal examination results, a

188 patients with biochemical relapse and a low PSA level, (64)CuCl2 PET/CT shows a significantly higher

189 Early SRT at low PSA levels after RP is associated with improved FFBF and

190 this range, sensitivity was comparably low (PSA < 0.5 mug/L) or high (PSA > 3.5 mug/L).

191 ocetaxel increased the likelihood of a lower PSA and improved survival.

192 be positively affected by using SRT at lower PSA levels, including reductions in BcR, DM, CSM, and al

193 Although mean PSA was 63% higher in those with low oxygen tolerating b

194 Median PSA among controls was 0.68, 0.88, and 0.96 ng/mL for me

195 of 542 men, aged 64.8 years +/- 8.2 (median PSA, 7 ng/mL), were included.

196 The median PSA level at the time of (68)Ga-PSMA-11 PET/CT was 0.48

197 The median age was 67 years, and the median PSA level was 53 ng per milliliter.

198 s Fourteen men (mean age, 62.8 years; median PSA level, 8.3 ng/mL) underwent treatment, with 12 men c

199 ar detection range from 0.1 pg/mL to 1 ng/mL PSA.

200 antigen [PSA] failure, PSA nadir >0.5 ng/mL, PSA doubling time <9 months, and interval to PSA failure

201 prostate-specific antigen [PSA], <10 ng/mL; PSA density <0.15 ng/mL/cm3; and <8-mm total cancer leng

202 On multivariable analysis, 7-month PSA </= 0.2 and low volume disease were prognostic of lo

203 Patients on ADT alone who achieved a 7-month PSA </= 0.2 ng/mL had the best survival and were more li

204 multivariable analysis, achieving a 7-month PSA </= 0.2 ng/mL was more likely with docetaxel, low-vo

205 survival was significantly longer if 7-month PSA reached </= 0.2 ng/mL compared with > 4 ng/mL (media

206 the adjusted model for all-cause mortality: PSA nadir greater than 0.5 ng/mL (adjusted hazard ratio

207 tion (AUC 0.71 and 0.75) compared to mpMRI + PSA alone (AUC 0.64 and 0.69 respectively).

208 ji cells undergoing apoptosis; (b) in mutant PSA-3 cells with manipulatable PS content; and (c) in Sc

209 Sixteen (40%) patients had no PSA response and 6 (15%) were not assessable and assumed

210 -random assignment incidence of SSEs but not PSA outcomes.

211 4 and cofilin, which we identified as novel PSA-binding proteins.

212 icroarray analysis revealed that the nuclear PSA-carrying and -lacking NCAM fragments affect expressi

213 noblot analysis we verified that the nuclear PSA-carrying NCAM fragment increases mRNA and protein ex

214 These results indicate that the nuclear PSA-carrying NCAM fragment is generated by distinct and

215 The 40 SNPs explain 9.5% of PSA variation in non-Hispanic whites, and the remaining

216 ted trial (Southwest Oncology Group 9346) of PSA </= 0.2, > 0.2 to 4, and > 4 ng/mL.

217 The proteolytic activity of PSA towards a small peptide substrate carrying streptavi

218 promising candidate for clinical analysis of PSA.

219 younger men, supporting the genetic basis of PSA levels.

220 phatase (ALP), as well as the correlation of PSA changes with the results of prostate-specific membra

221 s were applied for quantitative detection of PSA in a buffer and human serum diluted 1/100.

222 e FET setup for electrochemical detection of PSA.

223 ptasensing platform for the determination of PSA.

224 Moreover, the expression of PSA-NCAM is reduced by depression, and conversely enhanc

225 V) current were relevant to the formation of PSA-aptamer complex at the modified electrode surface.

226 om a genome-wide association study (GWAS) of PSA in 28,503 Kaiser Permanente whites and 17,428 men fr

227 eads to the generation and nuclear import of PSA-lacking and -carrying NCAM fragments.

228 C3 mediated production of T and induction of PSA in LNCaP-AKR1C3 cells as a model of a CRPC cell line

229 The limit of PSA detection was of 23fg/mL, concentration range of 23f

230 A median reduction of PSA level by 2.9 ng/mL was observed at 6 months.

231 fold better than the only previous report of PSA detection using Fe3O4.

232 e evaluated to determine the significance of PSA changes as a follow-up marker.

233 used to select men for entry at the time of PSA nadir onto randomized trials evaluating the impact o

234 As a next step for clinical translation of PSA based therapeutics, we have previously identified th

235 testing measurements that require the use of PSA values, such as the % free PSA and Prostate Health I

236 o a reagentless, label free, and "signal-on" PSA sensor.

237 disease (T1-T2 with Gleason score, 7 and/or PSA, 10-20 ng/mL).

238 lure was defined as radiologic, clinical, or PSA progression or death from prostate cancer).

239 ence of metastatic disease, PSA velocity, or PSA doubling time.

240 d monitoring of detectable postprostatectomy PSA levels that delay initiation of SRT.

241 on the collection of only four postsurgical PSA values.

242 ore ARS inhibition had resistant posttherapy PSA changes (PTPC), shorter rPFS, shorter time on therap

243 To this end, seminal plasma purified PSA standards from different commercial sources were inv

244 vel in blood is 4ng/mL) and detection range (PSA levels span from < 0.1-10(4)ng/mL in blood), thus sh

245 t management, including SRT, and most recent PSA were recorded using medical records.

246 % prostate-specific antigen (PSA) responses, PSA progression-free survival, clinical and radiologic p

247 We analyzed men with rising PSA after RP with PSA readings between 0.05 and 1.0 ng/m

248 ood), thus showing great promise for routine PSA diagnostics and for other in-situ applications.

249 sted for age, year, race, comorbidity score, PSA level, Gleason score, T stage, N stage, chemotherapy

250 logistic regression analysis, PSMA and serum PSA significantly correlated with treatment response, wh

251 h a potential that outperforms that of serum PSA.

252 (68)Ga-PSMA-11 PET/CT in patients with serum PSA levels of less than 1 ng/mL, determine how often con

253 volumetry technique and compared with serum PSA levels.

254 Using a pre-SRT PSA cutoff </= 0.5 versus > 0.5 ng/mL, 5-year and 10-yea

255 Each pre-SRT PSA doubling increased significantly the relative risk o

256 as 56% overall, 71% for those with a pre-SRT PSA level of 0.01 to 0.2 ng/mL (n = 441), 63% for those

257 ogic tumor stage, Gleason score, and pre-SRT PSA were associated with BcR, DM, CSM, and OS; androgen

258 Pre-SRT PSA, GS, SVI, surgical margins, and ADT use were associa

259 These data indicate that PSA-NCAM-mediated neuroplasticity is necessary for antid

260 ragments without and with PSA indicates that PSA-carrying and -lacking NCAM play different functional

261 These data strongly suggest that PSA screening for prostate cancer may be more harmful th

262 The PSA concentrations determined by the NW FETs in serum we

263 The PSA confirmed our findings using both institutional cost

264 The PSA level 24 hours after PAE correlated with prostate is

265 The PSA level could be rising or falling at the time of enro

266 The aim of this study was to assess the PSA-stratified performance of the (18)F-labeled PSMA tra

267 re was a significant correlation between the PSA changes and the therapeutic response according to fo

268 ailable follow-up data, in particular by the PSA series.

269 Results from the PSA give slightly greater mean effects for both the rout

270 a partial response, with a reduction in the PSA level to lower than 4.0 ng/mL but higher than 0.2 ng

271 d have more success regarding changes in the PSA.

272 In the nucleus, the PSA-carrying NCAM fragment interacts via PSA with PC4 an

273 Semi-log plots of the PSA concentration vs. faradaic current are linear from 1

274 plication was performed with analysis of the PSA levels in serum samples obtained from patients with

275 The WB results revealed that all of the PSA standards contained different mass concentrations of

276 ed using sandwich-type immunoreaction of the PSA-antigen (1-30 ng/mL) between anti-PSA immobilized on

277 Here, we show that the nuclear import of the PSA-carrying NCAM fragment is mediated by positive cofac

278 or subfamily 2 group F member 6, whereas the PSA-lacking NCAM fragment increases mRNA and protein exp

279 atients (23%) had progressive disease: their PSA level rose by more than 25%.

280 47%) had stable disease: the change in their PSA level ranged from less than a 50% decline to less th

281 cessary for antidepressant action; therefore PSA-NCAM represents an interesting, and novel, target fo

282 requirements in terms of LOD (the threshold PSA level in blood is 4ng/mL) and detection range (PSA l

283 PSA doubling time <9 months, and interval to PSA failure <30 months) for all-cause mortality using th

284 5% CI, 1.29-3.28; P = .003), and interval to PSA failure less than 30 months (aHR, 1.76; 95% CI, 1.06

285 ion therapy appears to identify men prior to PSA failure who are at high-risk for death.

286 son score, data available for post-treatment PSA and follow-up for at least 3 years in patients witho

287 the PSA-carrying NCAM fragment interacts via PSA with PC4 and cofilin, which are involved in RNA poly

288 Most of the events were PSA failures.

289 Sensitivity increased abruptly, when PSA values exceeded 0.5 mug/L (P = 2.4 x 10(-5)).

290 ext of an RCT, we aimed to determine whether PSA failure is associated with the risk of ACM stratifie

291 HR, 1.76; 95% CI, 1.06-2.92; P = .03); while PSA failure did not.

292 d by nuclear NCAM fragments without and with PSA indicates that PSA-carrying and -lacking NCAM play d

293 d SUVmean were significantly associated with PSA and ADT (P = 0.018 and 0.004 for SUVmax, respectivel

294 te specific antigen (PSA) was complexed with PSA prior to being immobilised on the surface of a gold

295 a statistically significant correlation with PSA levels (P < 0.0001) as a surrogate marker of tumor b

296 nase substrate (MARCKS) which interacts with PSA within the plane of the plasma membrane.

297 iew of prospectively acquired data, men with PSA greater than or equal to 3 ng/mL after negative tran

298 In patients with PSA levels below 0.2 ng/dL, 7 of 12 patients had disease

299 e analyzed men with rising PSA after RP with PSA readings between 0.05 and 1.0 ng/mL, considered elig

300 significant correlation of PSMA uptake with PSA, GS, and risk classification according to the d'Amic