ライフサイエンスコーパス: TTP

1 TTP affected the NOX2 luciferase activity by binding to

2 TTP also inhibited NOX2 and decreased the oxidative stre

3 TTP is approximately 2-fold more frequent in women, and

4 TTP is specifically related to a severe deficiency in AD

5 TTP knockout mice exhibit a profound inflammatory syndro

6 TTP negatively regulates PD-L1 expression through AU-ric

7 TTP targets AU-rich elements in the NLRP3 3'-untranslate

8 TTP was a more sensitive measure of bacterial burden tha

9 TTP was extended to 47.5 d (P <= 0.0199 vs. monotherapie

10 TTP was inversely correlated with vascular patency and v

11 TTP-bound mRNAs are targeted for destruction via recruit

12 xed-effects regression modelling of log(10) (TTP) over time.

13 erved, thus confirming the role of the MK2/3/TTP signaling axis in cytokine production also in vivo.

14 OS (HR 0.93 (95% CI 0.49-1.76), P = 0.822), TTP (HR 0.81 (95% CI 0.42-1.54), P = 0.512), and DFS (HR

15 ter matching, the overall CR rate (P = .94), TTP (P = .83), and overall survival (P > .99) were not s

16 with immunosuppressive agents, for acquired TTP.

17 nset of microvascular thrombosis in acquired TTP and potentially other immune thrombotic disorders.

18 gies for the TMA findings including acquired TTP will allow for a more accurate diagnosis and prevent

19 Most patients with acquired TTP respond to a combination of plasma exchange and ritu

20 we randomly assigned patients with acquired TTP to subcutaneous caplacizumab (10 mg daily) or placeb

21 HLA-DRB1*03-positive subjects with acquired TTP.

22 in a DRB1*03-positive patient with acquired TTP.

23 Activated TTP-deficient neutrophils exhibited decreased apoptosis

24 3.1%) developed stroke unrelated to an acute TTP episode over a median observation period of 3.08 yea

25 The first-line therapy for acute TTP is based on daily therapeutic plasma exchange supply

26 evalence of stroke after recovery from acute TTP and to test the hypothesis that lower ADAMTS13 activ

27 Stroke after recovery from acute TTP occurred in 0% (0 of 22) of patients with normal rem

28 not effective in resolving preexistent acute TTP signs in mice and baboons.

29 mab induced a faster resolution of the acute TTP episode than did placebo.

30 mbocytopenic purpura (TTP) survive the acute TTP episode.

31 In addition, TTP reduced the NOX2 mRNA stability.

32 est the hypothesis that VitE, not just alpha-TTP, is necessary for nervous system development, adult

33 in [alpha-tocopherol transfer protein (alpha-TTP)] in zebrafish embryos causes death within 24 h post

34 Although TTP's effects on gene expression have been well studied

35 for recruitment of the CCR4-NOT complex and TTP-directed decay of an mRNA containing an AU-rich elem

36 y of the transcriptomes of TTP-deficient and TTP-expressing macrophages upon short LPS stimulation su

37 n the cooperation between MK2/3 deletion and TTP mutation ex vivo.

38 nes over purines, whereas effectors dGTP and TTP select for substrates ADP and GDP, respectively.

39 elet count recovery and reduce mortality and TTP-related ischemic events.

40 ssociation between exonic SNP rs12422149 and TTP in patients treated with ADT was confirmed in univar

41 he current knowledge on pregnancy-associated TTP and describe how we manage TTP during pregnancy in o

42 -3 in most patients with acquired autoimmune TTP at presentation (median, approximately 170 ng/mL; ra

43 Because TTP also represses IL-1beta expression, it is a dual inh

44 located in the descending colon had a better TTP compared with ES group (HR 0.44 (95% CI 0.20-0.97),

45 clinical and pathogenic distinctions between TTP and aHUS are often quite challenging.

46 ere we show that a novel interaction between TTP and the CCR4-NOT subunit, CNOT9, is required for rec

47 od-oxygen-level-dependent time-to-peak (BOLD-TTP; a physiological measure of vascular dysfunction) we

48 gene RS is independently prognostic for both TTP and 2-year OS in ER-positive/HER2-negative de novo s

49 that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engag

50 tocytes, and tissue injury that characterize TTP.

51 dazole Cobalt(II) [Co(TPP)(2-MeHIm)] and [Co(TTP)(2-MeHIm)], and the corresponding 2-methylimidazolat

52 We compared TTP expression and cytokine production in mouse bone mar

53 ed a less severe phenotype than the complete TTP KO mice.

54 In conclusion, TTP protects against dopaminergic oxidative injury by pr

55 RIP-qPCR confirmed TTP binding to both sites, with a higher affinity for si

56 t is based on plasma infusion for congenital TTP, or plasma exchange, often in combination with immun

57 lization patterns of lipid binding-defective TTP mutants highlight the importance of protein-lipid in

58 or Tnfaip3, in the absence of MK2-dependent TTP neutralization resulted in a strong reduction of the

59 a proposed mechanistic model that describes TTP-facilitated trafficking of alpha-tocopherol through

60 Although they are rare, diagnosing TTP and aHUS associated with pregnancy, and postpartum,

61 2/3 double deletion (MK2/3 double KO [DKO]), TTP-S52A-S178A (TTPaa) knock-in, as well as combined MK2

62 through its tandem zinc finger (TZF) domain, TTP promotes the deadenylation and ultimate decay of tar

63 Knocking down TTP in primary macrophages leads to an increased inducti

64 Engagement of the DUSP1-TTP regulatory axis by PGE2 is likely to contribute to t

65 stitution of 2 amino acids of the endogenous TTP protein renders it constitutively active as an mRNA-

66 MAs is particularly difficult when the first TTP event occurs during pregnancy; a high index of suspi

67 and in vivo These data have implications for TTP family members throughout the eukarya, since species

68 ell-established murine and baboon models for TTP.

69 cancer, RS was independently prognostic for TTP (hazard ratio, 1.40; 95% CI, 1.05 to 1.86; P = .02)

70 n the mouse epithelium to uncover a role for TTP in IECs and to identify target genes in these cells.

71 ing features contained predictive signal for TTP (concordance index = 0.658; P = .0006) and CLOVAR pr

72 nt, is a possible new treatment strategy for TTP, as it was demonstrated to reduce disulfide bonds in

73 Of 170 consecutive patients treated for TTP at The Johns Hopkins Hospital from 1995 through 2018

74 lusion, stroke is common after recovery from TTP and is associated with reduced ADAMTS13 activity dur

75 lower ADAMTS13 activity after recovery from TTP is associated with an increased risk of stroke durin

76 erformed deep RNA sequencing on spleens from TTP knockout mice that were also deficient in both TNF r

77 irs bound (CDP/dATP, UDP/dATP, ADP/dGTP, GDP/TTP) that reveal the conformational rearrangements respo

78 and subsequently, she was diagnosed to have TTP.

79 However, TTP also employs the same mechanism to inhibit the expre

80 In rare cases, however, TTP begins as soon as childhood, with frequent inherited

81 results suggest potential involvement of HuR/TTP RNA binding protein axis in regulation of inflammati

82 s to examine RNA binding protein (RNABP) HuR/TTP axis in endometriosis patients compared to menstrual

83 innovative drugs is still needed to improve TTP management.

84 rmore, MRD negativity significantly improved TTP of patients >75 years (HR, 4.8; P < .001), as well a

85 ir encoded proteins accumulate abnormally in TTP knockout (KO) mice, leading to a severe inflammatory

86 duced the highest daily percentage change in TTP (5.17% [95% Bayesian credibility interval 4.61-5.77]

87 The change in TTP localization is specific to alpha-tocopherol and is

88 xide synthase (iNos or Nos2) was elevated in TTP-knockout IECs.

89 S13 antigen levels correlate with outcome in TTP with increased cardiac and neurological involvement

90 ied several conserved tryptophan residues in TTP that serve as major sites of interaction with two tr

91 l iTTP and could become an important tool in TTP management.

92 f Tnf mRNA and other cytokine transcripts in TTP-deficient mice results in the development of a profo

93 Increased TTP binding to the 3'UTR of feedback inhibitor mRNAs, su

94 tonseed coat extract significantly increased TTP mRNA and protein levels with a magnitude similar to

95 The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of tran

96 H(2) S was observed to inhibit TTP function (binding to TNFalpha mRNA) by an in vitro f

97 From the United Kingdom TTP registry, we undertook a prospective study investiga

98 mated WMH segmentation methods (Cascade, kNN-TTP, Lesion-TOADS, LST-LGA and LST-LPA).

99 ce, both within and across scanners, for kNN-TTP, followed by LST-LPA and LST-LGA, with worse perform

100 sed stability of the otherwise highly labile TTP mRNA.

101 Mice lacking TTP develop a severe, spontaneous inflammatory syndrome

102 although to a lesser extent than full-length TTP.

103 However, local TTP appears to originate from collagen area fraction, as

104 es < 1.0 denote diminished fecundity (longer TTP).

105 embolization to provide significantly longer TTP than cTACE.

106 rvival was significantly associated with low TTP/HuR mRNA ratios and correlated with high levels of t

107 cy-associated TTP and describe how we manage TTP during pregnancy in our clinical practice.

108 d >/=10(-5) vs >/=10(-4) (both with a median TTP of 15 months; 63% and 55% OS at 3 years, respectivel

109 rs, an intermediate-risk group with a median TTP of 4.8 years, and a low-risk group with a median TTP

110 .8 years, and a low-risk group with a median TTP of 9.3 years.

111 stable oscillations of tumor burdens; median TTP is at least 27 months with reduced cumulative drug u

112 lization group had significant longer median TTP (>26 mo) than patients in the cTACE group (6.8 mo; P

113 nt benefit for MRD-negative patients (median TTP not reached, 70% OS at 3 years), and similar poorer

114 In MPTP-treated mice, TTP expression increased and was co-located with dopamin

115 Our data reveal the p38 MAPK-MK2-TTP axis as a key regulator of expression of ARE-bearing

116 Moreover, TTP augmented mitotic cell-cycle arrest as demonstrated

117 nd by a non-MK2-phosphorylatable TTP mutant (TTP-AA) in 1 h LPS-stimulated macrophages and correlated

118 s without obvious MRA lesions showed neither TTP nor TSA time delay.

119 one with abundant collaterals showed neither TTP nor TSA time delay.

120 leotide incorporation, the first nucleotide (TTP) was incorporated at a fast rate (152 s(-1)), wherea

121 Bcl-2 expression; while overexpression (OE)-TTP lentivirus caused opposite effects.

122 necroptosis occurred only in the absence of TTP and was mediated by the expression of TNFalpha and a

123 stabilization of Mcl1 mRNA in the absence of TTP.

124 nalysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated wi

125 K2, whereas retained RNA-binding capacity of TTP-AA to 3'UTRs caused profound changes in the transcri

126 ed C-terminal CNOT1 binding domain (CNBD) of TTP to the TTP deficiency phenotype in mice, we created

127 t count; a lower incidence of a composite of TTP-related death, recurrence of TTP, or a thromboemboli

128 y secondary outcomes included a composite of TTP-related death, recurrence of TTP, or a thromboemboli

129 ndent protein kinase (PKA) in the control of TTP family activity in mRNA decay remains largely unknow

130 vation may play a role in the development of TTP, which is caused by severe deficiency of plasma ADAM

131 d that both the N- and C-terminal domains of TTP are involved in an interaction with CNOT9.

132 approach, we examined whether knock-down of TTP can play a functional role on other RNABPs that comp

133 ion in vitro However, the in vivo effects of TTP mutation are uniformly anti-inflammatory despite the

134 The first acute episode of TTP usually occurs during adulthood, with a predominant

135 ating acute (first or recurrent) episodes of TTP.

136 ation suggested an effective inactivation of TTP by MK2, whereas retained RNA-binding capacity of TTP

137 S leads to phosphorylation and inhibition of TTP by the kinase MK2.

138 Conversely, inhibition of TTP phosphorylation by p38 MAPK inhibitors and non-phosp

139 othesis that increasing endogenous levels of TTP in an intact animal might be beneficial in the treat

140 ta suggest that increased systemic levels of TTP, secondary to increased stability of its mRNA throug

141 In light of TTP being a couple-dependent outcome, both partner and c

142 found that the intracellular localization of TTP in hepatocytes is dynamic and responds to the presen

143 placizumab show promise in the management of TTP.

144 Experimental modulation of TTP or HuR expression led to changes in the mitosis ARE-

145 shown that the gain-of-function mutation of TTP impairs IL-10-mediated negative feedback control of

146 ation leading to complete thiol oxidation of TTP mediated by H(2) S was observed by low-temperature E

147 However, knowledge of the pathophysiology of TTP has inspired new ways to prevent early deaths by tar

148 Persulfidation of TTP required O(2) , which reacts with H(2) S to form sup

149 Perturbation of TTP function may therefore have mixed effects on inflamm

150 esis is not restricted to phosphorylation of TTP at S52/S178 but includes independent processes, whic

151 3MAF of >60% was an independent predictor of TTP in multivariable analysis (hazard ratio 0.22, 95% CI

152 index of suspicion and prompt recognition of TTP are essential for achieving a good maternal and feta

153 Rapid recognition of TTP is crucial to initiate appropriate treatment.

154 rcentage of patients who had a recurrence of TTP at any time during the trial was 67% lower with capl

155 ng the trial treatment period; recurrence of TTP at any time during the trial; refractory TTP; and no

156 nt period; and a lower rate of recurrence of TTP during the trial than placebo.

157 omposite of TTP-related death, recurrence of TTP, or a thromboembolic event during the treatment peri

158 omposite of TTP-related death, recurrence of TTP, or a thromboembolic event during the trial treatmen

159 Regulation of TTP family function through phosphorylation by p38 MAP k

160 In vivo, restoration of TTP expression enhances anti-tumor immunity dependent on

161 Taken together, our study uncovers a role of TTP as a suppressor of feedback inhibitors of inflammati

162 The balancing role of TTP comes at the cost of an increased risk of bacterial

163 To explore the role of TTP in PD, an in vitro 1-methyl-4-phenylpyridinium (MPP(

164 only LPS-induced kinases for S52 and S178 of TTP and the role of MK2 and MK3 in the regulation of TNF

165 Silencing of TTP in endometriotic and endometrial epithelial cells re

166 we evaluated the potential binding sites of TTP to 3'-untranslated regions (3'-UTR) of NOX2 mRNA.

167 ompetitively bind to inflammatory targets of TTP in both endometriotic and endometrial epithelial cel

168 he close similarity of the transcriptomes of TTP-deficient and TTP-expressing macrophages upon short

169 a 136-base instability motif in the 3'UTR of TTP mRNA was deleted in the endogenous genetic locus.

170 ttonseed extracts exhibited modest effect on TTP family gene expression in macrophages but glandless

171 not powered for these seconday outcomes, OS, TTP, and DFS did not differ between groups at a minimum

172 he secondary outcomes analyzed here were OS, TTP, and DFS.

173 pendent processes, which could involve other TTP phosphorylations (such as S316) or other substrates

174 Median overall TTP was 11.1 months (95% CI: 8.8 months, 25.6 months) in

175 Time to peak (TTP) was employed to detect hypoperfusion.

176 d-type TTP and by a non-MK2-phosphorylatable TTP mutant (TTP-AA) in 1 h LPS-stimulated macrophages an

177 p38 MAPK inhibitors and non-phosphorylatable TTP mutant decreases ARE-bearing TNFalpha and DUSP1 mRNA

178 Mean placental TTP negatively correlated with fetal liver and brain vol

179 Mean placental TTP positively correlated with placental pathology.

180 Maps of oxygen Time-To-Plateau (TTP) were obtained in the placentas by voxel-wise fittin

181 change in time to sputum culture positivity (TTP) in liquid medium over days 0-56 in the drug-suscept

182 h a secondary outcome of time to positivity (TTP) of blood culture.

183 milliliter (CFU/mL) and time to positivity (TTP).

184 hich contains two highly conserved potential TTP binding sites, was significantly upregulated relativ

185 n imaging-based risk score system to predict TTP and CLOVAR profiles.

186 Additionally, epitype predicted TTP and OS with 2 common CLL therapies: chemoimmunothera

187 C was not effective in resolving preexisting TTP signs; thrombocytopenia, hemolytic anemia, and organ

188 of fecundity, measured as time to pregnancy (TTP).

189 ar elastic model with total tissue pressure (TTP) increasing above interstitial fluid pressure (IFP)

190 sociations with time-to-disease progression (TTP) and HGSOC transcriptomic profiles (Classification o

191 inical variables, time to first progression (TTP), and 2-year overall survival (OS) were correlated w

192 t prognostic factor for time to progression (TTP) (hazard ratio [HR], 2.7; P = .007) and overall surv

193 first treatment (TTFT), time to progression (TTP) after treatment, and overall survival (OS).

194 ss the relation between time to progression (TTP) and individual gene expression adjusting for clinic

195 The 5-year time to progression (TTP) and overall survival (OS) for the entire cohort wer

196 We hypothesize time to progression (TTP) could be increased by integrating evolutionary dyna

197 isk group with a median time to progression (TTP) of 1.8 years, an intermediate-risk group with a med

198 vels, imaging response, time to progression (TTP), 90-day mortality, and survival.

199 lume measurements (CT), time to progression (TTP), and survival.

200 The primary outcome was time to progression (TTP), evaluated by intention-to-treat analysis.

201 edictor of response and time to progression (TTP).

202 SMA RNT or anti-PD-1 alone tended to prolong TTP (isotype control, 25 d; anti-PD-1, 33.5 d [P = 0.015

203 e hepatic alpha-tocopherol transfer protein (TTP) preferentially selects dietary alpha-tocopherol and

204 cquired thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are appropriate

205 to rule thrombotic thrombocytopenic purpura (TTP) in or out, with urgency, using ADAMTS13 activity te

206 ediated thrombotic thrombocytopenic purpura (TTP) is a life-threatening disorder caused by antibodies

207 cquired thrombotic thrombocytopenic purpura (TTP) is a life-threatening disorder resulting from the d

208 Thrombotic thrombocytopenic purpura (TTP) is a life-threatening hematological condition assoc

209 Thrombotic thrombocytopenic purpura (TTP) is a microangiopathic disorder diagnosed by thrombo

210 Thrombotic thrombocytopenic purpura (TTP) is a rare and life-threatening thrombotic microangi

211 Thrombotic thrombocytopenic purpura (TTP) is an acute, life-threatening thrombotic microangio

212 cquired thrombotic thrombocytopenic purpura (TTP) is caused by aggregation of platelets on ultralarge

213 ts with thrombotic thrombocytopenic purpura (TTP) survive the acute TTP episode.

214 ause of thrombotic thrombocytopenic purpura (TTP) whereas overwhelming activation of complement via a

215 cquired thrombotic thrombocytopenic purpura (TTP), an immune-mediated deficiency of the von Willebran

216 oach to thrombotic thrombocytopenic purpura (TTP).

217 cquired thrombotic thrombocytopenic purpura (TTP).

218 In cell-free experiments, recombinant TTP lacking its CNBD could still activate target mRNA de

219 TTP at any time during the trial; refractory TTP; and normalization of organ-damage markers.

220 In addition to the risk of relapse, TTP survivors have higher all-cause mortality than the g

221 in inducing responses in refractory/relapsed TTP and increasing relapse-free survival; caplacizumab t

222 ital and acquired cases of pregnancy-related TTP is mandatory for safe subsequent pregnancy planning.

223 py, is effective in preventing and resolving TTP signs, using well-established murine and baboon mode

224 Our results suggest that RNABPs TTP and HuR are dysregulated in endometriotic lesions co

225 exchange, was effective in preventing severe TTP signs in mice, but NAC was not effective in resolvin

226 on of NAC was effective in preventing severe TTP signs.

227 FABP3 and CD36 were associated with shorter TTP (p = 0.045 and p = 0.08) as was low expression of RA

228 T1E) was found to be associated with shorter TTP and may help classify a group of patients with MPBC-

229 ass (P = .0037) were associated with shorter TTP.

230 of chemotherapy was associated with shorter TTP.

231 Transfection of small interfering (si)-TTP RNA upregulated pro-oxidative NOX2 expression and RO

232 lated anti-oxidative GSH and SOD activity;si-TTP upregulated pro-apoptotic cleaved-caspase-3 expressi

233 ioxidant N-acetyl cysteine (NAC) reversed si-TTP-induced cell apoptosis.

234 In doing so, TTP regulates body-wide levels of alpha-tocopherol.

235 glandless cottonseed coat extract stimulates TTP gene expression.

236 Together, these results demonstrate that TTP in IECs targets Nos2 expression and aggravates acute

237 ing proteins in cancer, and demonstrate that TTP induces an antimitotic pathway that is diminished in

238 We demonstrate that TTP interacts with AU-rich elements in the Nos2 3' UTR a

239 These results reveal that TTP plays an important role in inhibiting TNFalpha/JNK-i

240 Here the authors show that TTP, encoded by Zfp36, degrades p28 to inhibit IL-27 pro

241 Our results suggest that TTP deficiency has profound effects on the splenic trans

242 he MPP(+) /MPTP model of PD, suggesting that TTP could be a potential therapeutic target for regulati

243 The TTP was comparable regardless of bottle type.

244 results reveal new molecular details for the TTP-CNOT interaction that shape an emerging mechanism wh

245 excludes regulatory elements, including the TTP- and miRNA-223-binding sites.

246 al CNOT1 binding domain (CNBD) of TTP to the TTP deficiency phenotype in mice, we created a mouse mod

247 Thus, TTP lacking its CNBD can still act to promote target mRN

248 sk stratification remains similar over time, TTP and OS have changed dramatically with the introducti

249 , triclosan and triclorcarban in relation to TTP; chemical concentrations were modeled both continuou

250 H(2) S was unreactive towards TTP when the protein was bound to RNA, thus suggesting a

251 Tristetraprolin (TTP) acts by binding to AU-rich elements in certain mRNA

252 Tristetraprolin (TTP) is an anti-inflammatory protein that modulates the

253 Tristetraprolin (TTP) is an inducible, tandem zinc-finger mRNA binding pr

254 Tristetraprolin (TTP) is an RNA-binding protein and an essential factor o

255 Tristetraprolin (TTP), an RNA-binding protein encoded by the ZFP36 gene,

256 Tristetraprolin (TTP), encoded by the Zfp36 gene, is a zinc-finger protei

257 Human antigen R (HuR) and Tristetraprolin (TTP) are RNA binding proteins that competitively bind to

258 S with a ZF protein called tristetraprolin (TTP).

259 e mRNA-destabilizing factor tristetraprolin (TTP) binds in a sequence-specific manner to the 3' untra

260 ation of mRNA decay factor, Tristetraprolin (TTP) in G0.

261 ied the RNA-binding protein Tristetraprolin (TTP) as a negative regulator of NLRP3 in human macrophag

262 The zinc-finger protein tristetraprolin (TTP) binds to AU-rich elements present in the 3' untrans

263 mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated in

264 ich element-binding protein tristetraprolin (TTP).

265 by the RNA-binding protein tristetraprolin (TTP, encoded by the Zfp36 gene).

266 of the RNA-binding proteins tristetraprolin (TTP, ZFP36) and HuR (ELAVL1).

267 The RBP tristetraprolin (TTP/Zfp36) is a signal-induced phosphorylated anti-infla

268 sac-specific member of the tristetraprolin (TTP) family of CCCH tandem zinc finger proteins.

269 TIS11b/BRF1) belongs to the tristetraprolin (TTP) family of zinc-finger proteins, which bind to mRNAs

270 fission yeast homologues of Tristetraprolin/TTP and Pumilio/Puf (Zfs1 and Puf3) interact with Ccr4-N

271 lation of anti-inflammatory tristrataprolin (TTP) family gene expression in mouse cells.

272 and highlights the importance of fine-tuned TTP activity-regulation by MK2 in order to control the p

273 ied numerous mRNA targets bound by wild-type TTP and by a non-MK2-phosphorylatable TTP mutant (TTP-AA

274 In refractory or unresponsive TTP, more intensive therapies including twice-daily plas

275 In the absence of the vitamin, TTP is localized to perinuclear vesicles that harbor CD7

276 ion that shape an emerging mechanism whereby TTP targets inflammatory mRNAs for deadenylation and dec

277 The mechanisms by which TTP facilitates alpha-tocopherol trafficking in hepatocy

278 e in mice, we created a mouse model in which TTP lacked its CNBD.

279 While TTP is expressed abundantly in the intestines, its funct

280 While TTP was largely dispensable for establishment and mainte

281 model of the 10th percentile of the ADC with TTP yielded accurate results in discriminating cancers w

282 model of the 10th percentile of the ADC with TTP yielded the highest AUC in both data sets.

283 For all patients, RS was associated with TTP (P = .01) and 2-year OS (P = .04).

284 Ocular manifestations associated with TTP are uncommon.

285 d RAETE1; were significantly associated with TTP.

286 tration, but not CA-125, was associated with TTP.

287 nivariate and multivariate associations with TTP and CLOVAR mesenchymal profile (worst prognosis).

288 with poor response and identified cases with TTP < 6 mo with 71% sensitivity (95% CI 42%-92%) and 88%

289 er one cycle of treatment were compared with TTP.

290 PBK, TOP2A) that negatively correlated with TTP/HuR mRNA ratios and was involved in the mitotic cell

291 ied CCR4-NOT subunits shown to interact with TTP.

292 phages and correlated their interaction with TTP to changes at the level of mRNA abundance and transl

293 trated the association of the ARE-mRNAs with TTP and HuR.

294 Also, long-term follow-up of patients with TTP is crucial to identify the occurrence of other autoi

295 rial, we randomly assigned 145 patients with TTP to receive caplacizumab (10-mg intravenous loading b

296 Among patients with TTP, treatment with caplacizumab was associated with fas

297 e association of these genetic variants with TTP and OS in patients receiving ADT.

298 with inferior outcomes for D5 vs D4 (5-year TTP 33% vs 87%, P = .0002).

299 e (D)-scored PET scans (n = 103), the 5-year TTP for PET-negative cases by Deauville criteria (D1-D3,

300 63% negative and 37% positive with a 5-year TTP of 90% vs 71% and 5-year OS of 97% vs 88%, respectiv