ライフサイエンスコーパス: relapse risk

1 han did outpatients (10 vs 18 weeks to a 25% relapse risk).

2 t association between treatment duration and relapse risk.

3 p) retained their significance for effect on relapse risk.

4 Chronic GVHD was associated with lower relapse risk.

5 roups of patients with leukemia at differing relapse risk.

6 ceptably high and abrogated the reduction in relapse risk.

7 only be life threatening but may also affect relapse risk.

8 of treatment is associated with an increased relapse risk.

9 ears, type of induction also correlated with relapse risk.

10 to radiation therapy cost and breast cancer relapse risk.

11 mber of strategies can attempt to reduce the relapse risk.

12 erious posttransplant toxicities, may reduce relapse risk.

13 igh transplant-related mortality but a lower relapse risk.

14 explain the association between poverty and relapse risk.

15 eceptor or the C5 complement pathway reduces relapse risk.

16 ted mAHP, which can be ameliorated to reduce relapse risk.

17 preemptive treatment and potentially reduced relapse risk.

18 e who relapse point to a neural correlate of relapse risk.

19 ty of the antipsychotic drug may also affect relapse risk.

20 the association between extreme poverty and relapse risk.

21 o omit radiotherapy and accept the increased relapse risk.

22 es, matching or mismatching for G2 increased relapse risk.

23 is significantly associated with heightened relapse risk.

24 specificity in predicting lower SAM and MAM relapse risk.

25 could be considered for those with a higher relapse risk.

26 relapse and identify factors associated with relapse risk.

27 tients and was associated with increased ALL relapse risk.

28 d play a pivotal role in driving craving and relapse risk.

29 nomic landscape, and clinical and anatomical relapse risk.

30 uld be approached cautiously because of high relapse risk.

31 l help assess treatment response and predict relapse risk.

32 ipsychotics) is associated with an increased relapse risk.

33 thropometric indices to reduce postdischarge relapse risk.

34 ring the subsequent 2 study months; and (ii) relapse risk.

35 duced pulse frequency on overall survival or relapse risk.

36 mplementary predictive capacity for PIRA and relapse risk.

37 rly abstinence are associated with increased relapse risk.

38 imited CAR-T cell persistence, and increased relapse risk.

39 of melphalan were associated with a lowered relapse risk.

40 treatment identifies patients at the highest relapse risk.

41 y in chronic hepatitis C mediated by reduced relapse risk.

42 a hazards ratio greater than 8 for increased relapse risk.

43 g states significantly influence craving and relapse risk.

44 was reported to be associated with increased relapse risk.

45 amide (P = 0.005) were associated with lower relapse risk.

46 th lower, but not statistically significant, relapse risk.

47 on the basis of primarily differences in the relapse risk.

48 d the postpartum period to reduce peripartum relapse risk.

49 Lower adherence to oral MP increases relapse risk.

50 and alcohol cues contribute significantly to relapse risk.

51 full cessation and interventions to mitigate relapse risk?).

52 in a better CR (94% v 76%, P =.001), reduced relapse risk (13% v 35%, P =.04), and improved survival

53 was moderately associated with an increased relapse risk (18.4 vs. 10.3%; relative risk, 1.79, 95% c

54 Extended ATRA reduced relapse risk (20% v 36% at 4 years, P =.04) and resulted

55 Six patients relapsed (estimated 2-year relapse risk, 20%).

56 better CR (85% v 62%, P =.0001) and reduced relapse risk (22% v 42%, P =.002) and superior survival

57 nts treated on augmented therapy had a lower relapse risk (22.1%; 95% CI, 15.1 to 31.6) versus standa

58 T genotype, exposure to GO did not influence relapse risk (39% v 40%; P = .85).

59 sely, Q4 patients had a significantly higher relapse risk (53% v 39%, P < .001), lower event-free sur

60 ssociation between 6-MP ingestion habits and relapse risk (6-MP with food: hazard ratio [HR], 0.7; 95

61 ical changes and the effect of the latter on relapse risk (a critical variable in addiction treatment

62 Knowledge of the threshold relapse risks above which adjuvant treatment is worth pr

63 Here, we estimated relapse risks according to disease characteristics.

64 Use of MHT was associated with a 16% lower relapse risk (adjusted hazard ratio [aHR]=0.84, 95% CI=0

65 sease activity with a 54% reduction in first relapse risk (adjusted hazard ratio [HR], 0.46; 95% CI,

66 covariate) was not associated with a reduced relapse risk (adjusted HR, 0.90; 95% CI, 0.64-1.27).

67 The relapse risk after a subsequent pregnancy for women with

68 Local cancer relapse risk after breast conservation surgery followed

69 clones, aiding in patient stratification for relapse risk after chemotherapy.

70 Relapse risk after delivery is increased in women with a

71 oup analysis, we found a significantly lower relapse risk after double-unit transplantation in patien

72 ort demonstrates a modest reduction in early relapse risk after HCT associated with CMV reactivation

73 tional exploration confirmed that the higher relapse risks after transplantation of BM were limited t

74 iscontinuation or continuation on depressive relapse risk among bipolar subjects successfully treated

75 as associated with a significantly increased relapse risk and a shorter overall survival.

76 e first study to show an association between relapse risk and ADAMTS13 conformation when activity lev

77 ions could serve as useful neural markers of relapse risk and alcoholism treatment outcome.

78 Nonadherence to oral MP could increase relapse risk and also contribute to inferior outcome in

79 ve strategies are urgently needed to improve relapse risk and both short- and long-term mortality out

80 For example, reducing relapse risk and glucocorticoid toxicity.

81 3 mg/m(2)) to induction chemotherapy reduces relapse risk and improves survival with little increase

82 ve ALCL identifies patients with a very high relapse risk and inferior survival.

83 tolerable toxicity, and acceptable rates of relapse risk and overall survival.

84 with acute myeloid leukemia (AML) have high relapse risk and poor survival after allogeneic hematopo

85 s associated with a significantly higher CNS relapse risk and poorer outcome.

86 analysis were used to estimate the long-term relapse risk and rate.

87 Race affects overall relapse risk and response to rituximab in iTTP.

88 ould be considered when assessing subsequent relapse risk and that among patients experiencing relaps

89 This study examined relapse risk and time to relapse, within the first 18 mo

90 herapy with donor lymphocytes both to reduce relapse risk and to induce durable antitumor responses i

91 s) were significantly associated with higher relapse risk and worse event-free survival.

92 18 to 49 years between 2000 and 2013, 5-year relapse risks and 5-year restricted losses in expectatio

93 IT, and particularly mutKIT17, confer higher relapse risk, and both mutKIT17 and mutKIT8 appear to ad

94 ) subgroups showed similar overall survival, relapse risk, and leukemia-free survival, whereas high r

95 ycles of chemotherapy can accurately predict relapse risk, and most studied patients with abnormal po

96 he basis of response to induction treatment, relapse risk, and overall survival, three prognostic gro

97 ible, maladaptive coping; increased craving; relapse risk; and maintenance of drug intake are also pr

98 espectively (P <.001), while no gradation of relapse risk (approximately 18%) could be identified at

99 n the role of follow-up in patients with low relapse risk are missing.

100 Readily identified markers of tuberculosis relapse risk are needed, particularly in resource-limite

101 tive approaches to mitigating MRD-associated relapse risk are needed.

102 e imatinib was significantly associated with relapse risk, as was slower achievement of UMRD after sw

103 ogether with FLT3) is mandatory for accurate relapse-risk assessment.

104 The absolute increase in 30-day relapse risk associated with a second or third vaccine d

105 To further define the relapse risk associated with bcr-abl molecular detection

106 uli may be a critical factor in long-lasting relapse risk associated with cocaine addiction.

107 ceive myeloablative conditioning to mitigate relapse risk associated with high-risk genetics or measu

108 us the smartphone intervention stratified by relapse risk based on initial clinical status (low risk:

109 h-negative B-cell ALL; high VAF may increase relapse risk but is not independently associated with su

110 allografts was not associated with a higher relapse risk, but was associated with improved overall s

111 CT NGS positivity resulted in an increase in relapse risk by multivariate analysis (hazard ratio, 7.7

112 deactivating MTHFR allele would increase ALL relapse risk by potentially increasing 5,10-methylenetet

113 ery few studies have evaluated predictors of relapse risk, challenging clinical management.

114 [2.07-4.61]) vaping were linked to increased relapse risk compared to no vaping.

115 The final relapse risk did not significantly differ, but relapses

116 Ethnic difference in relapse risk differs by level of adherence-an observatio

117 linked to compulsive drug use and heightened relapse risk, drug omission cues suppressed three major

118 ving a closed conformation, highlighting the relapse risk even with undetectable anti-ADAMTS13 IgG an

119 l (OS) of 28%, driven primarily by increased relapse risk, even among patients treated with frontline

120 D123 expression quartiles (Q1-3) had similar relapse risk, event-free survival, and overall survival.

121 ned prognostic after adjusting for all known relapse risk factors, including minimal residual disease

122 We review the method of assessing CNS relapse risk, factors that increase the likelihood of re

123 We investigated relapse risk following suboptimal asparaginase exposure

124 ile maintaining excellent survival and a low relapse risk for both SR and HR patients with APL.

125 and confirm that the intervention decreases relapse risk for individuals in asymptomatic recovery.

126 Relapse risk for patients in AAML0631 from end consolida

127 Relapse risk for patients treated with six to eight cour

128 otective variables in reducing the recurrent relapse risk for the AQP4-IgG NMOSD group.

129 clinical trial did not detect a reduction in relapse risk for the smartphone intervention (hazard rat

130 on: HR 2.28, 95% CI, 1.08 to 4.82, P = .032, relapse risk from complete remission: HR 3.03, 95% CI 1.

131 urvival (OS), event-free survival (EFS), and relapse risk from the end of induction 1 (hazard ratio [

132 attempt, we defined 3 groups with differing relapse risk: granulocyte-positive group (100%), granulo

133 ter associated with heavy smoking and higher relapse risk has led to the identification of the midbra

134 c differences in dexamethasone contribute to relapse risk has never been studied.

135 rly alcohol recovery, but their influence on relapse risk has not been well studied.

136 a first vaccine dose was not associated with relapse risk (hazard ratio [HR]=0.67; 95% confidence int

137 rate below 90% was associated with increased relapse risk (hazard ratio, 3.9; P = .01).

138 ility in TGN levels contributed to increased relapse risk (hazard ratio, 4.4; 95% CI, 1.2-15.7; P = .

139 alized stigma are domains highly relevant to relapse risk, health outcomes, and quality of life.

140 oids were associated with a higher estimated relapse risk (HR 1.76, 95% CI 0.90 to 3.45, p=0.097).

141 Similarly, standard relapse risk (HR, 1.67 [95% CI, 1.10-2.54]) and high rel

142 tients treated with cladribine showed higher relapse risk (HR, 1.81; 95% CI, 1.02-3.20; P = .04) and

143 0.5), but this was offset by an increase in relapse risk (HR, 2.0), and the conditioning intensity d

144 risk (HR, 1.67 [95% CI, 1.10-2.54]) and high relapse risk (HR, 2.22 [95% CI, 1.43-3.43]) were associa

145 ached genome-wide significance in predicting relapse risk (HR=2.18, p=3.30x10(-8)).

146 ionships between ARID5B SNP genotype and ALL relapse risk in 1,605 children treated on the Children's

147 levant level of adherence needed to minimize relapse risk in a multiracial cohort of children with AL

148 inactivation (SI) is common and may increase relapse risk in acute lymphoblastic leukemia (ALL).

149 T correlates are associated with prospective relapse risk in AD.

150 ntation in CR1 was associated with a reduced relapse risk in all molecular subgroups with the excepti

151 is associated with chemoresistance and high relapse risk in children and adults.

152 Multivariate analysis showed increased relapse risk in children with >/=0.1% minimal residual d

153 the most sensitive and specific predictor of relapse risk in children with acute lymphoblastic leukae

154 d disease (MDD) at diagnosis correlates with relapse risk in children with anaplastic lymphoma kinase

155 CNS relapse risk in DZsig+ (2 year: 6.4%) was independent of

156 iable models identified significantly higher relapse risk in G1G2 and G2G2 compared with G1G1 HLA-mat

157 Altogether, the CNS relapse risk in HGBCL-DH-BCL2 is lower than previously r

158 The 2-year CNS relapse risk in HGBCL-DH-BCL2 was 6.8%.

159 lvement were associated with an elevated CNS relapse risk in HGBCL-DH-BCL2.

160 than tapering speed in predicting psychotic relapse risk in individuals remitted from a first psycho

161 nts of health contribute to the disparity in relapse risk in iTTP deserves further study.

162 ctors that are prospectively associated with relapse risk in late-life depression.

163 Moderate-high-efficacy DMTs reduced relapse risk in LOMS.

164 Pregnancy has a well documented effect on relapse risk in multiple sclerosis (MS).

165 r impact of pretransplant VitD deficiency on relapse risk in myeloid diseases was also observed in an

166 Ravulizumab significantly reduced relapse risk in patients with AQP4+ NMOSD, with a safety

167 of long-term eculizumab treatment to reduce relapse risk in patients with AQP4-IgG+ NMOSD.

168 whether early relapses increase longer-term relapse risk in patients with MOGAD.

169 al Cortex (VmPFC) alcohol cue reactivity and relapse risk in severe Alcohol Use Disorders (AUDs), but

170 also confirm the adverse impact of mutKIT on relapse risk in t(8;21) AML.

171 with the CC genotype had significantly lower relapse risk in the GO arm than in the No-GO arm (26% v

172 Covariates that putatively influence relapse risk included demographic factors, clinical char

173 Assessment of expected locoregional relapse risk informs the magnitude and timeframe of expe

174 Relapse risk is high after successful MAM/SAM treatment.

175 he relevance of early relapse on longer-term relapse risk is unknown.

176 S) could distinguish 2 groups with differing relapse risks: low (4-year RFS, 81%, n = 109) versus hig

177 and intermediate-risk groups and have a CNS relapse risk < 5%; they may be spared any diagnostic and

178 Thus, AML relapse risk might be more effectively reduced with T ce

179 As a result of this 3-fold increase in relapse risk, newly diagnosed patients with iAMP21 recru

180 n showed that the mutations most influencing relapse risk occur at initiation of clonal expansion in

181 diagnosis was significantly associated with relapse risk (odds ratio, 2.4; p = 0.03).

182 years or older was a risk factor for greater relapse risk (odds ratio, 4.9; P =.006) and worse surviv

183 nd cerebral events, with an overall relative relapse risk of 0.681 (P = 0.001) compared to Caucasians

184 elihood of cerebral attacks, with a relative relapse risk of 3.309 (P = 0.009) compared to Caucasians

185 testicular primary identified a group with a relapse risk of 50%.

186 with and without RD at the EOI1 had a 3-year relapse risk of 60% and 29%, respectively (P < .001); th

187 It was previously reported that the relapse risk of bcr-abl detection 6 to 12 months after t

188 ar invasion positivity, or estimated distant relapse risk of greater than 15% at 10 years based on On

189 or Oncotype DX RS with an estimated distant relapse risk of less than 15% at 10 years.

190 expression of which can thus predict higher relapse risk of PTC.

191 The effect on relapse risk of this variability is unknown.

192 ere the most useful prognostic variables for relapse risk on multivariate analysis.

193 favored over surveillance for patients with relapse risk on surveillance greater than 33% and 37% by

194 before or after HCT, may reduce the post-HCT relapse risk or delay relapse.

195 For patients with PEPI = 0 disease, the relapse risk over 5 years was only 3.6% without chemothe

196 This study aimed to quantify the relapse risk over time in patients with schizophrenia fo

197 ciated with worse survival compared with low relapse risk (P < .001 overall).

198 h NQ exceeding 10(-5) had 4.1-fold increased relapse risk (P =.008); however, 73% of patients who exp

199 Early puberty and perimenopause increase relapse risk; pediatric cases show more severe anterior

200 d to identify reliable biomarkers for better relapse risk prediction and novel druggable targets for

201 a (AML) is associated with poor outcomes and relapse risk prediction approaches have not changed sign

202 duction toxicity (randomization 1 [R1]), CNS relapse risk (randomization 2 [R2]-interim maintenance [

203 to sulfur dioxide (SO(2)) and schizophrenia relapse (risk ratio, RR=1.005 and 1.004 per 1 mug/m(3) i

204 group of PREVENT (during 46.9 patient-years; relapse risk reduction = 98.6%, 95% confidence interval

205 ernally controlled analyses presented show a relapse risk reduction in patients with HRNB treated wit

206 ssociated with longer times to relapse and a relapse risk reduction of 41.1% (hazard ratio, 0.59; 95%

207 between these states and alcohol craving and relapse risk remain unclear.

208 reshold RR10 for an absolute 1% reduction in relapse risk remained fairly low (5% to 6% for tamoxifen

209 Relapse risk remains higher than for B-lineage ALL and o

210 10(-6) had 17.5-fold and 7.6-fold increased relapse risk, respectively (P <.001), while no gradation

211 to the RR10 for an absolute 1% reduction in relapse risk, rose sharply.

212 a highly significant trend for worsening in relapse risk (RR) and overall survival (OS) with increas

213 ion randomizations except for a reduction in relapse risk (RR) on the mitoxantrone arm, which was off

214 88% v. 85%; P = .15), posthoc analyses found relapse risk (RR) was significantly reduced among GO rec

215 ival (EFS), disease-free survival (DFS), and relapse risk (RR) were determined overall and for higher

216 (P =.04), and was associated with increased relapse risk (RR), adverse disease-free survival (DFS),

217 addition of GO to conventional chemotherapy (relapse risk [RR]: GO 36% v No-GO 34%, P = .731; event-f

218 justed for the white blood cell count or the relapse risk score, none of these outcomes were signific

219 All patients were assigned relapse risk scores based on their respective clinicopat

220 atterns of deregulation that correspond with relapse risk scores to refine prognosis with the clinico

221 increased impulsivity that may contribute to relapse risk.SIGNIFICANCE STATEMENT Persons with alcohol

222 The FLT3ITD mRNA level contributes to relapse risk stratification and might help to guide post

223 tive of an earlier return to alcohol use and relapse risk, suggesting a significant role for gray mat

224 erapy combined with pharmacotherapy improves relapse risk, symptom burden, and quality of life, but p

225 IFX was associated with less relapse risk than ADA (hazard ratio [HR] = 0.52, 95% CI

226 h risk of relapse and was more predictive of relapse risk than c-KIT mutations.

227 and acute lymphocytic leukaemia had a higher relapse risk than did matched controls in the IKZF1 dele

228 a higher AUC in predicting lower SAM and MAM relapse risk than MUAC or WAZ at discharge.

229 autografts had a two-fold (P =.0009) greater relapse risk than patients who received purged autograft

230 ted to identify genetic factors that predict relapse risk (the primary endpoint of many pivotal clini

231 hemotherapy alone; among those with a higher relapse risk, the corresponding values were 94.1+/-2.5%

232 solidation therapies are to be determined by relapse risk, then NPM1(MUT) cases with low-level FLT3(I

233 ation in CR1 and CR2 is associated with less relapse risk, this analysis reveals an enhanced graft-ve

234 rimary cortex (M1), is crucial in regulating relapse risk, though the mechanisms are unclear.

235 red with TAU, produced significantly reduced relapse risk to drug use and heavy drinking.

236 ality therapy did not mitigate the continued relapse risk, underscoring the value of prolonged clinic

237 to identify genetic variants that predict MS relapse risk, using a three-stage approach.

238 t disease, transplant-related mortality, and relapse risk vary by donor source.

239 T01892345), eculizumab significantly reduced relapse risk versus placebo in patients with aquaporin-4

240 no evidence that EOT delivery increases CNS relapse risk vs i-HD-MTX.

241 Without risk factors, the relapse risk was 12%.

242 Although relapse risk was 26%, this was significantly reduced whe

243 estimated nonrelapse mortality was 32%, and relapse risk was 33%.

244 The overall postpartum relapse risk was 35% (95% CI=29, 41).

245 The relapse risk was 57% if the RT-PCR was positive versus 2

246 free survival among patients with an average relapse risk was 97.5+/-1.3% with blinatumomab and chemo

247 Recurrent relapse risk was assessed using an Andersen-Gill model a

248 rate higher relapse, whereas at rates < 90%, relapse risk was comparable to that of non-Hispanic whit

249 tterns of pathway deregulation in predicting relapse risk was established using related but not ident

250 on of SET index and ESR1 levels with distant relapse risk was evaluated from microarrays of ER-positi

251 sant-antipsychotic combinations, a decreased relapse risk was found for amitriptyline-olanzapine (aHR

252 Relapse risk was high among persons who were underweight

253 The relapse risk was high within 6 months of discontinuing o

254 The very early relapse risk was highest in no-DMT-no-exclusive-breastfe

255 Relapse risk was highest within 2 years of an index epis

256 However, a significant decrease in relapse risk was observed for individuals in asymptomati

257 Relapse risk was reduced by both C-CT and fluoxetine in

258 ut antithymocyte globulin (ATG), whereas the relapse risk was similar in the group treated with busul

259 NGS)-MRD better identifies pre- and post-HCT relapse risk, we performed immunoglobulin heavy chain (I

260 iteria as a strategy to reduce postdischarge relapse risk, weighing the operational and financial tra

261 Ancestry-related differences in relapse risk were abrogated by the addition of a single

262 Improved OS and lower relapse risk were observed following TBI plus etoposide

263 apse mortality risks (HR, 0.92; P = .74) but relapse risks were higher after transplantation of BM (H

264 ed by age, MHT was associated with decreased relapse risks when used between ages 40-49 (aHR=0.86, 95

265 cantly higher among patients with an average relapse risk who had been assigned to receive blinatumom

266 ts with AML, and integration of toxicity and relapse risks will determine the best approach for allog

267 ysis, this functional connectivity predicted relapse risk with a balanced accuracy of 0.86.

268 showed lower nonrelapse mortality but higher relapse risk with RIC; however, overall survivals were s

269 ted with significant reductions in recurrent relapse risk, with notably greater protection conferred

270 y was associated with a significantly higher relapse risk within both complete metabolic response (CM