ライフサイエンスコーパス: PSA

1 PSA concentration values directly measured in 35 human s

2 PSA flare-up during (177)Lu-PSMA treatment is very uncom

3 PSA had reduced by 58% from baseline at 3 months.

4 PSA levels, clinical data, and reference standards were

5 PSA-binding peptides exhibited specific binding to polym

6 sed three-dimensional polar surface area (3D-PSA) studies showed that ensemble-based 3D-PSA is a good

7 D-PSA) studies showed that ensemble-based 3D-PSA is a good predictor of passive permeability.

8 -specific antigen (PSA) levels (ng/mL): 50% (PSA < 0.5), 69% (0.5 <= PSA < 1), 100% (1 <= PSA < 2), 9

9 ) and high-risk features (Gleason score > 7, PSA doubling time < 10 mo, or PSA > 1.0 ng/mL) with nega

10 approach for the identification of alpha-2,8-PSA-binding peptides, involving design from the endogeno

11 (1 <= PSA < 2), 91% (2 <= PSA < 5), and 96% (PSA >= 5).

12 A PSA decline of at least 50% was achieved in 32 of 50 pat

13 s (95% CI 13.8-23.8) in patients achieving a PSA decline >= 50%.

14 5% CI, 13.8-23.8 mo) in patients achieving a PSA decline of at least 50%.

15 ne >= 50%) was observed in 7 patients, and a PSA decline of any amount was observed in 11 patients.

16 d on the basis of conventional imaging and a PSA doubling time of <=10 months) who were continuing to

17 r patients with biochemical recurrence and a PSA level of less than 1 ng/mL.

18 Methods: Twenty-four patients with BCR and a PSA level of less than 2.0 ng/mL were included.

19 FFP was defined as a PSA rise <= 0.2ng/mL above nadir post sRT, with no addit

20 FFP was defined as a PSA rise of no more than 0.2 ng/mL above nadir after sRT

21 temic therapies on progression experienced a PSA decline of at least 50%.

22 37% (95% CI: 25%, 49%), respectively, for a PSA level less than 0.5 ng/mL (P = .46); 59% (95% CI: 52

23 : 52%, 66%) and 48% (95% CI: 34%, 61%) for a PSA level of 0.5-0.9 ng/mL (P = .19); and 80% (95% CI: 7

24 : 75%, 85%) and 62% (95% CI: 54%, 70%) for a PSA level of 1.0-1.9 ng/mL (P = .01).

25 Only a PSA decline of greater than or equal to 50% remained sig

26 treatment, death from prostate cancer, or a PSA level of at least 2.0 ng/mL at any time after random

27 In 70% of patients, a PSA decline of greater than or equal to 50% was obtained

28 Conclusion: In this study, a PSA decline of greater than or equal to 50% after treatm

29 The best PSA response after TAT (a PSA decline >= 50%) was observed in 7 patients, and a PS

30 es commencing 359 d from enrollment), with a PSA decline of at least 50% in 11 patients (73%).

31 detected; in 26 of 40 (65%) patients with a PSA level between 0.2 and 0.5 ng/mL and in 10 of 26 (38.

32 g/mL and in 10 of 26 (38.5%) patients with a PSA level less than 0.2 ng/mL.

33 tion of recurrent disease in patients with a PSA level of 0.5-1.0 ng/mL.

34 is positive in about 50% of patients with a PSA level of less than 0.5 ng/mL, which could substantia

35 , it showed limited value in patients with a PSA level of less than 0.5 ng/mL.

36 ing was positive in 59.1% of patients with a PSA level of less than 1.0 ng/mL and in 88.9% of patient

37 an 1.0 ng/mL and in 88.9% of patients with a PSA level of more than 1.0 ng/mL.

38 less than 0.5 ng/mL, 56% of patients with a PSA of 0.5-0.99 ng/mL, 70% of patients with a PSA of 1.0

39 SA of 0.5-0.99 ng/mL, 70% of patients with a PSA of 1.0-1.99 ng/mL, and 90% of patients with a PSA of

40 f 1.0-1.99 ng/mL, and 90% of patients with a PSA of at least 2.0 ng/mL scored either 1 or 2 on (11)C-

41 In 32% patients (7/22) with a PSA of less than 0.2 ng/mL, suggestive lesions were pres

42 sorted by PSA level, 45% of patients with a PSA of less than 0.5 ng/mL, 56% of patients with a PSA o

43 11 PET/MRI for biochemical recurrence with a PSA value no higher than 0.5 ng/mL at our institution.

44 s fragilis, but not with a polysaccharide A (PSA) deficient isogenic strain.

45 form of the polysaccharide polysialic acid (PSA) has widespread implications in physiological and pa

46 phosphonic acid (PPA), phenyl sulfonic acid (PSA), and benzoic acid (BA) using N-3,5-bis-(trifluorome

47 Complex polysialic acids (PSAs) exist naturally and provide a means to enhance the

48 rgy, polymeric pressure-sensitive adhesives (PSAs) have now been synthesized by copolymerizing tradit

49 Numbers of MCs after PSA are similar between genotypes in different tissue re

50 A propensity score analysis (PSA) was used to compare outcomes between these 4 groups

51 Probability sensitivity analysis (PSA) of the societal model for the EK was robust, with 9

52 onduct a probabilistic sensitivity analysis (PSA), consisting of 10 000 model runs with 1 000 000 wom

53 ouse models of passive systemic anaphylaxis (PSA) and active systemic anaphylaxis were applied to wil

54 nts demonstrated a decline in aBSI, ALP, and PSA, respectively.

55 Surprisingly, PPA and PSA have rarely been directly compared in detail.

56 within and between other subtypes of PPA and PSA.

57 ecular forms, total (t) and free (f) PSA and PSA complexed to alpha(1)-antichymotrypsin (complexed PS

58 all patients with biochemical recurrence and PSA values no higher than 0.5 ng/mL to assess the detect

59 rgical patients, PSA, PSA doubling time, and PSA velocity correlated with PET results, but the same w

60 correlates with PSA, PSA doubling time, and PSA velocity, suggesting it may have prognostic value.

61 dary endpoints were PSA changes at 12 wk and PSA flare-up.

62 Two different aptamers, PSAG-1 and anti-PSA, are immobilized onto two adjacent nanostructured go

63 We aimed to characterize eight anti-PSA monoclonal antibodies (mAbs) to assess the prostate

64 L (PSAG-1) and from 0.64 to 62.5 ng/mL (anti-PSA), with a reproducibility of 5.4 %.

65 elevated level of prostate-specific antigen (PSA) (>0.2 ng/mL) and high-risk features (Gleason score

66 a rising level of prostate-specific antigen (PSA) after RP.

67 uroflowmetry and prostate specific antigen (PSA) at one, 3 and 6 months and one year following the p

68 radiotherapy for prostate-specific antigen (PSA) biochemical progression.

69 We simulate prostate-specific antigen (PSA) dynamics, with enrichment of PCa stem-like cell (PC

70 logy, imaging, or prostate-specific antigen (PSA) follow up, defined as composite reference standard.

71 ic specificity of prostate specific antigen (PSA) is limited.

72 Prostate specific antigen (PSA) is the common biomarker for prostate cancer (PCa).

73 ing system, where prostate-specific antigen (PSA) is used as a model analyte.

74 Prostate-specific antigen (PSA) is widely used to monitor treatment response in pat

75 hip between serum prostate-specific antigen (PSA) level categories (<5, 5-10, 10-20, and >20 ng/mL) a

76 r less, and serum prostate-specific antigen (PSA) level less than 10 ng/mL.

77 n patients with a prostate-specific antigen (PSA) level less than 2 ng/mL.

78 recurrence with a prostate-specific antigen (PSA) level of less than 1 ng/mL.

79 ed with patients' prostate-specific antigen (PSA) level, primary Gleason score, and prior therapy (an

80 ptomatic men with Prostate-Specific Antigen (PSA) levels < 20 ng ml(-1), of whom 31 had benign diseas

81 l based on rising prostate-specific antigen (PSA) levels (mean, 3.43 ng/mL; median, 0.94 ng/mL; range

82 eased with higher prostate-specific antigen (PSA) levels (ng/mL): 50% (PSA < 0.5), 69% (0.5 <= PSA <

83 ostatectomy serum prostate-specific antigen (PSA) levels of at least 0.2 ng/mL and negative conventio

84 apidly increasing prostate-specific antigen (PSA) levels while taking androgen-deprivation therapy.

85 ts with different prostate-specific antigen (PSA) levels, Gleason scores, marital statuses and bone m

86 1), a decrease in prostate-specific antigen (PSA) of 50% or more (PSA50) from baseline, or conversion

87 tient cohort with prostate-specific antigen (PSA) persistence after salvage lymph node dissection (SL

88 nd at the time of prostate-specific antigen (PSA) progression, standard radiographic or clinical prog

89 ates with reduced prostate-specific antigen (PSA) recurrence-free survival.

90 locally assessed prostate-specific antigen (PSA) response (>= 50% decrease from baseline) rate.

91 ndpoints included prostate-specific antigen (PSA) response (Prostate Cancer Working Group 2), toxicit

92 fy those for whom prostate-specific antigen (PSA) testing is likely to be most valuable.

93 Prostate specific antigen (PSA) tests and digital rectal exams cannot differentiate

94 istration) is the prostate specific antigen (PSA) that is detected by conventional biochemical assays

95 ease at low serum prostate specific antigen (PSA) values below 0.5 ng/mL compared with the already hi

96 patients with low prostate-specific antigen (PSA) values.

97 Prostate-specific antigen (PSA) was measured for response assessment.

98 Serial prostate-specific antigen (PSA) was obtained for PSA response assessment.

99 Here, prostate-specific antigen (PSA) was selected as a template model.

100 residual volume, prostate-specific antigen (PSA), and prostate volume were assessed.

101 ere evaluated for prostate-specific antigen (PSA), lactate dehydrogenase (LDH), and CgA at baseline a

102 cancer biomarkers prostate specific antigen (PSA), vascular endothelial growth factor-D (VEGF-D), ETS

103 (EFS), an earlier prostate-specific antigen (PSA)-based composite end point, may further expedite tri

104 The prostate-specific antigen (PSA)-stratified detection rate of (18)F-JK-PSMA-7 after

105 phatase (ALP) and prostate-specific antigen (PSA).

106 ry end point of a prostate-specific antigen (PSA)50 response (PSA decline >=50% at 12 wk vs. baseline

107 ical progression (prostate-specific antigen [PSA] >=0.4 ng/mL and rising after completion of any post

108 cT1 to cT2bN0M0, prostate-specific antigen [PSA] <=20 ng/mL, and Grade Group 1-2) prostate cancer an

109 tently measurable prostate-specific antigen [PSA] values after robot-assisted laparoscopic radical pr

110 ecurrence (median prostate-specific antigen [PSA], 2.5 ng/mL; range, 0.21-35.5 ng/mL) and negative re

111 ts with PSA progression at 6 wk achieved any PSA decline at 12 wk (1% of the entire cohort).

112 to 50% was obtained; 82% of patients had any PSA decline.

113 analyses, factors such as baseline PSA, any PSA decline, PSA decline of greater than or equal to 50%

114 with prior (177)Lu-PSMA treatment showed any PSA decline in 8 patients and a decline of at least 50%

115 ments caused by stroke (post-stroke aphasia, PSA) and neurodegeneration (primary progressive aphasia,

116 using projected superposition approximation (PSA), the Ion Mobility Projection Approximation Calculat

117 ion of miR-299-3p induced a reduction of AR, PSA and VEGFA expression.

118 e to progression; progression was defined as PSA level of 10 ng/mL or greater, PSA doubling time of l

119 tratified PSA levels (P = 0.005), as well as PSA nadir after prostatectomy (P < 0.001).

120 86% (44/51), 86% (42/49), and 95% (76/80) at PSA levels of 0.2 to <0.5 ng/mL, 0.5 to <1 ng/mL, 1 to <

121 program at our institution and had available PSA values at baseline and at 6 wk after treatment initi

122 Baseline PSA had no prognostic value for response prediction.

123 Baseline PSA was 112 ng/mL (range, 20.5-818 ng/mL).

124 Baseline PSA was inversely related with recurrence (hazard ratio,

125 nivariate analyses, factors such as baseline PSA, any PSA decline, PSA decline of greater than or equ

126 Conclusion: In our cohort, baseline PSA had no prognostic value for response prediction.

127 The best PSA response after TAT (a PSA decline >= 50%) was observ

128 and PFS, and a positive association between PSA decline of greater or equal to 50% and PFS.

129 quilibrium dissociation constant K(d)between PSA and its imprint was estimated at K(d) = (1.02 +/- 0.

130 When sorted by PSA level, 45% of patients with a PSA of less than 0.5 n

131 tive model including age, fPSA and complexed PSA, outperformed tPSA detection efficacy.

132 exed to alpha(1)-antichymotrypsin (complexed PSA).

133 Conclusion: PSA changes at 6 wk after (177)Lu-PSMA initiation are an

134 The confirmed PSA response rate was 54.8% (95% CI, 45.2% to 64.1%; 63

135 , Pseudomonas aeruginosa exposed to CSE (CSE-PSA) had increased resistance to oxidative stress, which

136 Finally, CSE-PSA had increased virulence in a model of pneumonia, wit

137 pneumonia, with 0% of mice infected with CSE-PSA alive at day 6, while 28% of controls survived.

138 Patients with a pre-PET/CT PSA level of more than 0.5 ng/mL (98/111; 88%) had PET-p

139 h unfavorable-risk (clinical stage cT2cN0M0, PSA of 20-50 ng/mL, or Grade Group 3-5) prostate cancer

140 ctors such as baseline PSA, any PSA decline, PSA decline of greater than or equal to 50%, prior chemo

141 cancer (PCa) diagnostic utility of different PSA molecular forms, total (t) and free (f) PSA and PSA

142 Of 31 patients who experienced early PSA progression at 6 wk, 29 (94%) showed biochemical pro

143 ed to evaluate the prognostic value of early PSA changes after (177)Lu-labeled prostate-specific memb

144 MA PET performed for a persistently elevated PSA level (>=0.1 ng/mL) at least 6 wk after SLND (post-S

145 the Prostate-ICECaP-database with evaluable PSA and disease follow-up data were analyzed.

146 PSA molecular forms, total (t) and free (f) PSA and PSA complexed to alpha(1)-antichymotrypsin (comp

147 ction rates were 31.8%, 44.9%, and 71.4% for PSA < 0.2 ng/mL, 0.2 <= PSA < 0.5, and 0.5 <= PSA < 1, r

148 0), 88.9% (n = 8/9), and 94% (n = 47/50) for PSA levels of >0.2 to <0.5, 0.5 to <1.0, 1 to <2.0, and

149 Among the various techniques employed for PSA detection, aptamer-based biosensors (aptasensors) ha

150 nd fluency-related components were found for PSA and PPA.

151 No benefit was found for PSA-based screening in men aged 70 years and older.

152 e voltammetry technique was investigated for PSA detection in standard solution in the concentration

153 tate-specific antigen (PSA) was obtained for PSA response assessment.

154 rvation policy with salvage radiotherapy for PSA biochemical progression (PSA >=0.1 ng/mL or three co

155 rvation policy with salvage radiotherapy for PSA biochemical progression should be the current standa

156 genetic risk significantly influenced future PSA testing.

157 did not reduce the overall number of future PSA tests.

158 rostate cancer in general practice on future PSA testing.

159 A C18 SPE cartridge paired with SPE GCB/PSA proved to be the most effective clean-up method and

160 luted serum samples of specific glycosylated-PSA to the first sensor and total PSA to the second one

161 defined as PSA level of 10 ng/mL or greater, PSA doubling time of less than 3 years, or upgrading (de

162 Higher PSA levels after RARP and positive pathologic lymph node

163 a BRCA1 or BRCA2 alteration, while a higher PSA response rate was observed in patients with a BRCA2

164 On multivariable analysis, higher PSA values after RARP (P = 0.004) and positive pathologi

165 , who were living in rural places had higher PSA levels, and T1 and N0 stages have a high OR for bone

166 l status, lower socioeconomic status, higher PSA level, T1 and N0 stage, and bone metastasis were ind

167 However, PSA measurements are considered only after 12 wk of trea

168 ficant changes were demonstrated (p <.05) in PSA, peak urinary flow, QoL (quality of life) questionna

169 The percentage changes in PSA at 6 and 12 wk were highly associated (r = 0.90; P <

170 th a greater than or equal to 30% decline in PSA at 6 wk also had a lower risk of imaging-based progr

171 A greater than or equal to 30% decline in PSA at 6 wk was associated with longer overall survival

172 66% (19/29) progressed, with a mean rise in PSA of 1.59 ng/mL over the 3 y.

173 results with enzalutamide were also seen in PSA progression-free survival (174 and 333 events, respe

174 n established clinical predictors, including PSA, T stage, surgical margin status, or Gleason score (

175 s interference of biomolecular interactions, PSA-binding ligands have important implications for both

176 y cause, or was censored at the date of last PSA assessment.

177 mprehensive Cancer Network stage, PSA level, PSA doubling time, PSA velocity, and time between initia

178 vision and differentiated into higher levels PSA expression cells in organoid assays compared with OL

179 CR localization in patients with BCR and low PSA values (reader consensus).

180 yL PET/CT scans in patients with BCR and low PSA values.

181 e for recurrent prostate cancer, even at low PSA levels no higher than 0.5 ng/mL.

182 Even at those low PSA values, only 8 of 66 (12.1%) patients had exclusive

183 PCa recurrence even among patients with low PSA levels when interpretation accounts for the clinical

184 atectomy, especially among patients with low PSA values.

185 rried, were living in urban areas, had lower PSA levels, underwent surgery, and radiation had lower O

186 n urban areas, married marital status, lower PSA levels and lower Gleason scores were better prognost

187 PSA < 0.5), 69% (0.5 <= PSA < 1), 100% (1 <= PSA < 2), 91% (2 <= PSA < 5), and 96% (PSA >= 5).

188 44.9%, and 71.4% for PSA < 0.2 ng/mL, 0.2 <= PSA < 0.5, and 0.5 <= PSA < 1, respectively.

189 <= PSA < 1), 100% (1 <= PSA < 2), 91% (2 <= PSA < 5), and 96% (PSA >= 5).

190 levels (ng/mL): 50% (PSA < 0.5), 69% (0.5 <= PSA < 1), 100% (1 <= PSA < 2), 91% (2 <= PSA < 5), and 9

191 SA < 0.2 ng/mL, 0.2 <= PSA < 0.5, and 0.5 <= PSA < 1, respectively.

192 h the analogue readout can routinely measure PSA concentrations in human serum samples, very low conc

193 The sensors are able to measure PSA in serum with a dynamic range between 0.26 and 62.5

194 Median PSA level was 0.23 ng/mL (range, 0.03-0.5 ng/mL).

195 Median PSA was 1.2 ng/mL (interquartile range, 0.6-2.8 ng/mL).

196 Results: The 261 patients had a median PSA level of 0.96 ng/mL (range, 0.01-400 ng/mL).

197 sults: A total of 532 patients with a median PSA level of 0.97 ng/mL (interquartile range: 0.41-2.46

198 sults: PSMA PET/CT was performed at a median PSA value of 0.60 ng/mL (interquartile range, 0.3-2.4) a

199 features of the cohort included short median PSA doubling time (2.3 mo) and extensive prior treatment

200 Results: The median PSA was 0.26 ng/mL (interquartile range, 0.15-0.59 ng/mL

201 Results: The median PSA was 0.26ng/mL (IQR 0.15 - 0.59) and follow-up 38 mon

202 The median PSA-PFS and overall survival were 3.2 mo (95% confidence

203 sent a viable alternative to complex natural PSAs in increasing the stability of therapeutic peptides

204 Polysialylated NCAM (PSA-NCAM) and perineuronal nets, highly glycosylated mol

205 Three patients had no PSA decline at any time.

206 pid and sensitive determination of these non-PSA markers.

207 s for diagnosis of prostate cancer using non-PSA markers.

208 e patients were classified as nonresponders (PSA decline <50%), and 25 patients were classified as re

209 ts were assigned to 3 groups on the basis of PSA changes: response (>=30% decline), progression (>=25

210 events accounted for successful detection of PSA in plasma, indicate the high specificity of the sens

211 s PSA is critical for expanding knowledge of PSA interactions and achieving selective glycan targetin

212 ed changes in the core-fucosylation level of PSA between PCa patients and healthy controls.

213 d ratio, 0.9 per nanograms per milliliter of PSA; 95% confidence interval [CI], 0.8, 0.9; P < .001).

214 These results demonstrate the potential of PSA-binding peptides for selective targeting and highlig

215 The most robust predictor of PSA progression was change in SUV(hetero) (PET1 to PET3;

216 state health index employs quantification of PSA in its free and bound forms to enumerate the risk of

217 amer-based sensor to the dual recognition of PSA.

218 acterization of nanopore blockade sensing of PSA by (1) tuning on/off the electromagnet, (2) varying

219 tes active delivery and selective sensing of PSA to the nanopore.

220 d cognitive tasks across the full spectra of PSA and PPA.

221 igh electronegativity and excluded volume of PSA often promotes interference of biomolecular interact

222 In multivariate analysis, only PSA level was significantly associated with scan positiv

223 n, 11.8 mo; 95% CI, 8.6-15.1) (P = 0.007) or PSA progression (median, 6.5 mo; 95% CI, 5.2-7.8) (P < 0

224 son score > 7, PSA doubling time < 10 mo, or PSA > 1.0 ng/mL) with negative or equivocal conventional

225 orical boundaries for any subtypes of PPA or PSA.

226 ence on correlative CT/MRI/bone scanning, or PSA response after focal therapy.

227 In postsurgical patients, PSA, PSA doubling time, and PSA velocity correlated with

228 tatectomy varied among 54.5% (6/11 patients; PSA < 0.5 mug/L), 87.5% (14/16 patients; PSA 0.5-2 mug/L

229 ts; PSA < 0.5 mug/L), 87.5% (14/16 patients; PSA 0.5-2 mug/L), and 90.9% (20/22 patients; PSA > 2 mug

230 PSA 0.5-2 mug/L), and 90.9% (20/22 patients; PSA > 2 mug/L).

231 rimary radiotherapy, and 70 had a persistent PSA elevation after receiving initial treatment (69 afte

232 e of 7-10, positive margins, or preoperative PSA >=10 ng/mL) for biochemical progression after radica

233 Its CDR is dependent on the prescan PSA value with excellent CDR in patients with PSA >= 1 n

234 TWEAK and Fn14 deficiencies prevent PSA-related symptoms, resulting in resistance to decreas

235 lue of Information tool were used to process PSA outcomes.

236 adiotherapy for PSA biochemical progression (PSA >=0.1 ng/mL or three consecutive rises).

237 and any amino-acid location in the protein, PSA molecules remain strongly inserted in the PPy polyme

238 In postsurgical patients, PSA, PSA doubling time, and PSA velocity correlated with PET

239 ts, (18)F-DCFPyL PET/CT correlates with PSA, PSA doubling time, and PSA velocity, suggesting it may h

240 sion detection rate was correlated with PSA, PSA kinetics, and original primary tumor grade.

241 latform is the ratio between PSAG-1 reactive PSA and total PSA, defined as the glycan score.

242 was the proportion of men having a repeated PSA test within 2 years.

243 ic risk had a higher propensity for repeated PSA testing within 2 years than men with normal genetic

244 d 25 patients were classified as responders (PSA decline >=50%).

245 prostate-specific antigen (PSA)50 response (PSA decline >=50% at 12 wk vs. baseline).

246 sistant prostate cancer and a rapidly rising PSA level.

247 ized (mean [SD] age, 64 [7] years; mean [SD] PSA level, 4.9 [2.1] ng/mL), 443 eligible patients (93%)

248 Although screening by serum PSA levels can reduce prostate cancer-specific mortality

249 CP was defined as any detectable first serum PSA value after RARP (>=0.1 ng/mL) at least 6 wk after s

250 n patterns correlate with longitudinal serum PSA measurements in 70 PCa patients.

251 ation for accurate bone staging at low serum PSA levels.

252 foci of suggestive uptake, even at low serum PSA levels.

253 re prevalent even in patients with low serum PSA levels.

254 were 75 men (median age, 69 y; median serum PSA, 3.69 mug/L) with 232 metastatic nodes less than 12

255 ce that was positively associated with serum PSA level (<10 ng/mL, 21%; 10-20 ng/mL, 41%; >=20 ng/mL,

256 A-positive regions also increased with serum PSA level (P < 0.001).

257 ian, 16.7 mo; 95% CI, 14.4-19.0) than stable PSA (median, 11.8 mo; 95% CI, 8.6-15.1) (P = 0.007) or P

258 -based progression than patients with stable PSA (hazard ratio, 0.60; 95% CI, 0.38-0.94) (P = 0.02),

259 -based progression than patients with stable PSA (hazard ratio, 3.18; 95% CI, 1.95-5.21) (P < 0.001).

260 National Comprehensive Cancer Network stage, PSA level, PSA doubling time, PSA velocity, and time bet

261 e polymorphisms) in addition to the standard PSA test that informed them about lifetime genetic risk

262 A-7 PET/CT detection efficacy and stratified PSA levels (P = 0.005), as well as PSA nadir after prost

263 gave a much better predictive accuracy than PSA alone.

264 Search for novel biomarkers other than PSA has resulted in the identification of several promis

265 The PSA confirmed that FM100 was associated with better post

266 ANOVA, but there was a large overlap in the PSA values for number of lesion categories.

267 oped sensitive and specific ELISAs for these PSA molecular forms and measured them in 301 PCa patient

268 Network stage, PSA level, PSA doubling time, PSA velocity, and time between initial treatment and PET

269 ositive examination, stratified according to PSA tier.

270 racteristics influencing peptide affinity to PSA, and carbohydrate-peptide binding was further quanti

271 mber of lesions was significantly related to PSA by ANOVA, but there was a large overlap in the PSA v

272 late to the amount of glycosylated and total PSA in the sample.

273 ycosylated-PSA to the first sensor and total PSA to the second one leads to changes in the charge tra

274 ratio between PSAG-1 reactive PSA and total PSA, defined as the glycan score.

275 ee-to-total (FPR) and the complexed-to-total PSA (CPR) ratios significantly increased the diagnostic

276 nd characterisation of novel ligands towards PSA is critical for expanding knowledge of PSA interacti

277 en synthesized by copolymerizing traditional PSA monomers, butyl acrylate and acrylic acid, with muss

278 e, surface charge, and morphology of the TRH-PSA NPs were determined using dynamic light scattering (

279 r surgery, in the absence of an undetectable PSA value after RARP.

280 The secondary endpoints were PSA changes at 12 wk and PSA flare-up.

281 re significantly associated with OS, whereas PSA values were not (P = 0.059).

282 ted with ALP (r = 0.60, P < 0.0001) and with PSA (r = 0.38, P = 0.003).

283 rious conditions, including competition with PSA of alternating 2,8/9-linkages and screening with PSA

284 ET lesion detection rate was correlated with PSA, PSA kinetics, and original primary tumor grade.

285 atients, (18)F-DCFPyL PET/CT correlates with PSA, PSA doubling time, and PSA velocity, suggesting it

286 MAbs were obtained by immunization with PSA and characterized by competition studies, ELISAs and

287 Mice with PSA and active systemic anaphylaxis had increased Fn14 a

288 SA value with excellent CDR in patients with PSA >= 1 ng/mL.

289 2%, and 81%, respectively, for patients with PSA < 0.5 ng/mL, 0.5-0.99 ng/mL, 1.0-1.99 ng/mL, and >=

290 2%, and 81%, respectively, for patients with PSA <0.5 ng/mL, 0.5-0.99 ng/mL, 1.0-1.99 ng/mL, and >=2.

291 nd is positive in about 50% of patients with PSA <0.5 ng/mL, which could substantially impact clinica

292 In patients with PSA levels >= 1 ng/mL the DR and PPV were 90% and 91%, r

293 In patients with PSA levels < 1 ng/mL, the DR and PPV were 69% and 85%, r

294 ncer lesions in 88% (14/16) of patients with PSA persistence after SLND.

295 Patients with PSA progression after 6 wk of treatment could benefit fr

296 Overall, only 1 (3%) of 36 patients with PSA progression at 6 wk achieved any PSA decline at 12 w

297 0.38-0.94) (P = 0.02), whereas patients with PSA progression had a higher risk of imaging-based progr

298 ts: We identified 124 eligible patients with PSA values at 6 wk.

299 lternating 2,8/9-linkages and screening with PSA-expressing cells.

300 ng and duration of androgen deprivation; 3-y PSA results; and clinical events were documented.