ライフサイエンスコーパス: relapse

1 une evasion mechanisms associated with tumor relapse.

2 cation was associated with increased risk of relapse.

3 k sufficient accuracy for predicting disease relapse.

4 ctivities and physical exercise can enable a relapse.

5 nt, and followed up for six months to assess relapse.

6 mistry that lead to increased probability of relapse.

7 downward spiral into persistent use and (ii) relapse.

8 se treatment intensity increases the risk of relapse.

9 onses, deplete AML cells and prevent disease relapse.

10 cles of compulsive drug use, abstinence, and relapse.

11 nitial high-risk disease are risk factors in relapse.

12 lates negative affective- and stress-induced relapse.

13 to have a greater correlation with addiction relapse.

14 erent VP cell types and their projections in relapse.

15 ssing, and is implicated in drug craving and relapse.

16 cover new candidate pathways associated with relapse.

17 se was the strongest predictor of subsequent relapse.

18 percent of patients experienced a subsequent relapse.

19 ed cancers, as tumors develop resistance and relapse.

20 fter remission, and risk factors for disease relapse.

21 amine binding during self-administration and relapse.

22 Three patients in the RMA group developed relapse.

23 le conditions such as chemotherapy and cause relapse.

24 ay fail to target self-renewal, allowing for relapse.

25 memories and reduce the propensity for drug relapse.

26 table DMTs for 3.7 person-years to prevent 1 relapse.

27 arded as the most common risk factor for the relapse.

28 ssociated memory traces that promote cocaine relapse.

29 significant reason for treatment failure and relapse.

30 sitive patients experienced early subsequent relapse.

31 cocaine-seeking behavior, an animal model of relapse.

32 d contributes to therapy resistance or tumor relapse.

33 free survival when compared to patients that relapsed.

34 at (18)F-FDG PET/CT was done in patients who relapsed.

35 dian of 9 avelumab cycles; none subsequently relapsed.

36 years, there were 8 major adverse events: 6 relapses, 1 treatment-related death (from septicemia) du

37 Rituximab was mainly used at relapses (11 [33%]).

38 of actionable mutations at diagnosis and at relapse; (2) deciding which drug to use among several th

39 Relapsed acute lymphoblastic leukemia (ALL) has remained

40 chemotherapy for acute myeloid leukemia and relapsed acute lymphoblastic leukemia (ALL).

41 able activity in patients with refractory or relapsed acute lymphocytic leukaemia.

42 re will be a dramatic rising tide of alcohol relapse, admissions for decompensated ALD, and an increa

43 Outcomes of patients with relapse after adjuvant BEP seem better compared with pat

44 ke receptors (KIRs) could reduce the risk of relapse after allogeneic hematopoietic cell transplantat

45 seline striatal K(i)(cer) values and time to relapse after antipsychotic discontinuation (R(2) = 0.51

46 40% of the patients showed psychotic relapse after antipsychotic discontinuation.

47 sociated cancer stem cells, as well as tumor relapse after cisplatin treatment.

48 We analyzed patients with relapse after ES-HL treated within the German Hodgkin St

49 acute lymphoblastic leukemia who experience relapse after or are resistant to CD19-targeted immunoth

50 We recently developed a rat model of drug relapse after palatable food choice-induced voluntary ab

51 ocular remission, incidence rate of disease relapse after remission, and risk factors for disease re

52 about the outcome of patients who experience relapse after such treatment.

53 Unfortunately, many patients relapse after the mentioned front-line treatment approac

54 The median time of relapse after the most recent infusion was 2.6 (0.6-5.8)

55 GBMs eventually relapse after treatment and the average survival of GBM

56 better compared with patients who experience relapse after treatment of metastatic disease but worse

57 nsible for viral persistence and virological relapse after treatment withdrawal.

58 , pneumonia and spiking fevers remitted, but relapsed after discontinuation.

59 arily successful but exhibits a high rate of relapse, after which, treatment options are few.

60 oved by the Food and Drug Administration for relapsed aggressive B-cell non-Hodgkin lymphoma in part

61 For early relapsed ALCL autologous SCT was not effective.

62 Exclusion criteria included: infant ALL, relapsed ALL, and stem cell transplant recipients.

63 29 patients went on to relapse and 38 remained well.

64 se some treated lymphoma patients experience relapse and die, targeting B-cell lymphomas with a NMT i

65 The risk of clinical relapse and hepatic decompensation after cessation of NA

66 eatment recommendations and by high rates of relapse and increased risk of overdose after leaving tre

67 ity analyses with overall survival (OS) from relapse and Kaplan-Meier statistics.

68 have important roles in tumour development, relapse and metastasis; the intrinsic self-renewal chara

69 efined as absence of clinical and histologic relapse and no premature withdrawal for any reason.

70 he patient remained without evidence of CSCC relapse and received a kidney transplant from a living-u

71 metastases are closely associated with tumor relapse and reduced survival in colorectal cancer (CRC).

72 e minimal residual disease (MRD), leading to relapse and repeated treatments.

73 The bad prognosis, high rate of relapse and resistance against anticancer drugs have bee

74 We analyzed relapse and temporal daily corticosteroid dose with and

75 B-cell ALL (B-ALL) at very low risk (VLR) of relapse and treated them with a reduced-intensity treatm

76 otherapy in paediatric patients with heavily relapsed and refractory acute myeloid leukaemia suggests

77 romising clinical responses in patients with relapsed and refractory LCH treated with BRAF or MEK inh

78 ial results of CAR T cells for patients with relapsed and refractory mantle cell lymphoma following p

79 efficacy of melflufen plus dexamethasone in relapsed and refractory multiple myeloma (RRMM), a popul

80 eptor-T (CAR-T) cell therapies can eliminate relapsed and refractory tumors, but the durability of an

81 eloma and as a monotherapy for patients with relapsed and/or refractory diffuse large B cell lymphoma

82 Density curves, representing incidence of relapses and 6-month confirmed progression events, were

83 quantify the duration of therapeutic lag on relapses and disability progression in different therapi

84 ne point in time and, in most people, runs a relapsing and remitting course.

85 atic disease, 1 patient with suspected local relapse, and 6 treatment-naive patients.

86 with tumour regression and the prevention of relapse, and led to complete tumour eradication in about

87 here are few preclinical studies of fentanyl relapse, and these studies have used experimenter-impose

88 ncers, 63 untreated primary tumors, 29 local relapses, and 11 longitudinal pairs) using whole-genome

89 Overall survival from time of relapse at 1, 2, and 4 years were 100%, 73%, and 73%, re

90 d with all other treatments, the risk of MMP relapse at any site (HR = 0.17, P = .02) and of ocular M

91 ts with an anticipated high risk of leukemic relapse, because multiple studies strongly indicate that

92 Patients with relapsed BL/B-AL have a poor chance to survive after cur

93 with AAP who subsequently developed leukemic relapse, but neither AAP nor the asparaginase truncation

94 included assessment of treatment failure or relapse by day 14.

95 tion of IL33 in facilitating lung metastatic relapse by modulating the immune microenvironment.

96 of 37 patients in the azathioprine group had relapsed by the end of the study.

97 well as to cancer survivors could eliminate relapse causing dormant cells and offer a cure for cance

98 The cumulative incidence of relapse (CIR) in patients achieving a complete remission

99 NPM1mut TLs and the cumulative incidence of relapse (CIR) in patients with NPM1mut AML enrolled in t

100 antly reduced the risk of a subsequent NMOSD relapse compared with azathioprine.

101 was associated with a lower incidence of AAV relapse compared with standard maintenance therapy.

102 ignificantly fewer isolated and combined CNS relapses compared with patients who did not receive nela

103 Opioid use disorder (OUD) is a chronic, relapsing condition, often associated with legal, interp

104 g and withdrawal, often leading to a chronic relapsing course.

105 with different aspects of disease activity (relapses, disability, magnetic resonance imaging paramet

106 Overall survival in patients with relapsed disease remains poor, and thus novel therapeuti

107 nations for anti-PD-1 and anti-PD-L1 therapy-relapsed disease.

108 lus tremelimumab for anti-PD-1 or anti-PD-L1 relapsed disease.

109 h a positive predictive value for clinically relapsing disease of only 20%.

110 Patients were monitored for psychotic relapse during 12 weeks after antipsychotic discontinuat

111 In contrast, VP(PV) neurons contribute to relapse during both renewal and reacquisition via projec

112 tment failure (bacteriologic or clinical) or relapse during follow-up, which continued until 6 months

113 No patient with a pCR had tumor relapse during observation.

114 Concerns for IMD relapse during subsequent reinduction or consolidation c

115 One central driver for relapse events is the negative aversive symptoms experie

116 inst prostate cancer (PCa), but all patients relapse eventually.

117 However, overactive, relapsing fear behavior in the absence of danger is a ha

118 Tick-borne relapsing fever (TBRF) is a neglected zoonotic bacterial

119 Relapsing fever is a common clinical phenotype.

120 Relapsing fever pattern was reported in 52% of patients,

121 use disorder, there is still a high rate of relapse following detoxification.

122 Conversely, a single case of CLL relapse following spontaneous regression was associated

123 leotidase II (NT5C2) are considered to drive relapse formation in acute lymphoblastic leukemia (ALL)

124 rove prognosis for overall survival (OS) and relapse free survival (RFS) outcomes.

125 ted with CCR2 expression and correlated with relapse free survival.

126 95% CI, 3.37 to 12.10; P < .001), decreased relapse-free survival (HR, 2.94; 95% CI, 1.84 to 4.69; P

127 val (DRFI) (94.1% vs. 85.0%, P < 0.0001) and relapse-free survival (RFS) (90.0% vs. 80.5%, P = 0.0003

128 s have reported significant benefits in both relapse-free survival (RFS) and overall survival (OS) fo

129 ciles seem to derive a substantial long-term relapse-free survival benefit from targeted therapy (HR

130 To confirm the stability of the relapse-free survival benefit, longer-term data were nee

131 who achieved a complete response, the median relapse-free survival was 6.0 months (95% CI, 4.1 to 6.5

132 Four-year event-free survival, relapse-free survival, and overall survival rates were 6

133 il antigen, to be positively correlated with relapse-free, metastasis-free, or overall survival in br

134 ADM-treated sites displayed recession relapse from 1 to 9 years.

135 s: A TBR threshold of 1.95 differentiated BM relapse from treatment-related changes with an accuracy

136 mission of the parasite is driven largely by relapses from dormant liver stages, its timely eliminati

137 e NS relapse (< 2 years), and late viable NS relapse (> 2 years).

138 Patients aged > 60 years at relapse had shorter second PFS (hazard ratio [HR], 3.0;

139 was significantly associated with increased relapse (hazard ratio [HR], 6.38; 95% CI, 3.37 to 12.10;

140 ibody negativity was longer in patients with relapses (HR 0.18, 95% CI 0.05-0.59).

141 The 5-year cumulative incidence of relapse in 41 patients who underwent HSCT (17.8% [95% CI

142 adjunct pharmacological treatment to prevent relapse in male opioid users.

143 that can contribute to the high incidence of relapse in obesity management.

144 g the link between MCs and increased risk of relapse in patients with breast cancer.

145 interleukin-6 receptor, reduced the risk of relapse in patients with neuromyelitis optica spectrum d

146 ations in TNFAIP3 levels are associated with relapses in MOG-AAD patients, which may have clinical ut

147 emory B cells had reemerged in 2 of 10 (20%) relapses in patients with MOG antibodies and 12 of 13 (9

148 ther safe and effective treatment to prevent relapses in patients with NMOSD.

149 IQR 22-67), 33 (28%) of the 116 patients had relapses, including 17 (17%) of 100 diagnosed at first e

150 Crohn's disease (CD) is a chronic relapsing inflammatory bowel disease (IBD) that may be m

151 Hidradenitis suppurativa (HS) is a chronic, relapsing, inflammatory skin disease.

152 Relapse is caused by leukemia stem cells (LSC), the cell

153 reverse vitiligo in humans; however, disease relapse is common after stopping treatments.

154 cumulative incidence of isolated bone marrow relapse, isolated CNS relapse, or combined bone marrow a

155 The most striking findings were relapsing, large, contrast-enhancing focal lesions in th

156 who had a tonsillectomy at 10 years old and relapsed later.

157 after cocaine withdrawal negatively impacts relapse-like behaviors in rats.

158 Twelve patients experienced relapse-local (n= 6), distant (n = 3), and combined (n =

159 ent outcomes: pure teratoma, early viable NS relapse (< 2 years), and late viable NS relapse (> 2 yea

160 after rituximab therapy and none of them had relapse (median follow-up after remission = 3.6 years).

161 ntext-induced reinstatement procedure, a rat relapse model.

162 with cocaine use disorder and in preclinical relapse models.

163 unately, imatinib-treated patients typically relapse, most often due to clonal emergence of the resis

164 In AQP4 antibody-associated disorder, relapse mostly occurs when the biological effect of RTX

165 selective B-cell depletion in patients with relapsing multiple sclerosis (MS) and primary progressiv

166 phase 3 trial is underway, in patients with relapsing multiple sclerosis.

167 with fingolimod were tested in patients with relapsing multiple sclerosis.

168 ivity in two phase 3 trials of patients with relapsing multiple sclerosis.

169 gression in a phase 3 trial of patients with relapsing multiple sclerosis.

170 r with temozolomide, a reference therapy for relapsed neuroblastoma, caused long-term suppression of

171 nce of disease activity (NEDA; occurrence of relapses, new white matter lesions, and Expanded Disabil

172 efractory acute GVHD, disease-free survival, relapse, nonrelapse mortality, or overall survival.

173 king-typified by chronic substance abuse and relapse-observed after drug use.

174 retreatment viral load <2000 IU/mL, clinical relapse occurred in 10 (19.6 %) and hepatic decompensati

175 CNS relapse occurred in only 4 patients.

176 Under RTX, 10 relapses occurred in 6 of 16 (37.5%) patients with MOG a

177 In < 18months, relapses occurred independent of segmental chromosome ab

178 the effectiveness of this treatment, disease relapse occurs in a subset of patients; thus, focus has

179 rd ratio [HR], 0.66 [95% CI, 0.48 to 0.89]), relapse of cancer (HR, 0.76 [CI, 0.61 to 0.94]), relapse

180 Methods: Patients suspected of relapse of lung cancer after definitive radiotherapy (co

181 Relapse of ME was defined as increase in macular thickne

182 analyses, OS and the cumulative incidence of relapse of patients with a KIR-advantageous donor were c

183 ischarged on the 7(th) day, but her symptoms relapsed on the 8(th) day.

184 ted in a longer duration of survival without relapse or distant metastasis than placebo with no appar

185 Patients were eligible at first relapse or first designation of refractory disease.

186 (5.0 months vs. 1.0 month; hazard ratio for relapse or progression of hematologic disease, non-relap

187 profile in patients with treatment-naive, or relapse or refractory Waldenstrom macroglobulinemia.

188 tatus and conditioning regimen intensity for relapse or survival.

189 confirmed diffuse large B-cell lymphoma, who relapsed or had refractory disease after previous treatm

190 Outcomes for children with relapsed or refractory acute myeloid leukaemia remain po

191 nosed AML and molecularly defined subsets of relapsed or refractory AML.

192 l and single-agent activity in patients with relapsed or refractory B-cell malignancies.

193 derived from cord blood to 11 patients with relapsed or refractory CD19-positive cancers (non-Hodgki

194 mustine plus rituximab (BR) in patients with relapsed or refractory chronic lymphocytic leukemia (CLL

195 Patients with relapsed or refractory diffuse large B-cell lymphoma who

196 nhibitor of nuclear export, in patients with relapsed or refractory DLBCL who had no therapeutic opti

197 able adverse events profile in patients with relapsed or refractory DLBCL who received at least two l

198 olerated in heavily pretreated patients with relapsed or refractory follicular lymphoma.

199 independent centers involving patients with relapsed or refractory HL and administered CD30.CAR-Ts a

200 nivolumab exhibit activity in patients with relapsed or refractory Hodgkin lymphoma.

201 rolled adult patients (aged >=18 years) with relapsed or refractory large B-cell lymphomas.

202 le remissions in a majority of patients with relapsed or refractory mantle-cell lymphoma.

203 ion-free survival versus Kd in patients with relapsed or refractory multiple myeloma and was associat

204 ubstantial efficacy with tolerable safety in relapsed or refractory multiple myeloma in a phase 1 stu

205 th America, Europe, Australia, and Asia with relapsed or refractory multiple myeloma were randomly as

206 an improved safety profile in patients with relapsed or refractory multiple myeloma.

207 1 study in heavily pre-treated patients with relapsed or refractory multiple myeloma.

208 need for novel treatments for patients with relapsed or refractory multiple myeloma.

209 n anti-CD20 antibodies in heavily pretreated relapsed or refractory non-Hodgkin lymphoma warrants fur

210 ) had histologically confirmed CD20-positive relapsed or refractory non-Hodgkin lymphoma, had an East

211 , 67% of treatment-naive patients and 50% of relapsed or refractory patients had undetectable minimal

212 treatment-naive patients and 21.5 months in relapsed or refractory patients, the median progression-

213 ma or a centrally confirmed, PD-L1-positive, relapsed or refractory solid tumour or lymphoma, and a L

214 ormance status score of 2 or lower, and were relapsed or refractory to, or ineligible for, standard t

215 Patients had disease that had relapsed or was refractory after the receipt of up to fi

216 igible patients had multiple myeloma and had relapsed or were refractory to 2 or more previous lines

217 f isolated bone marrow relapse, isolated CNS relapse, or combined bone marrow and CNS relapse rates,

218 ementation was not associated with toxicity, relapse, or survival.

219 coccal beta-lactam on mortality, bacteremia, relapse, or treatment failure in patients with MRSA bact

220 In relapsed patients, a significant correlation was found b

221 p was in patients residing in areas of short relapse periodicity (adjusted hazard ratio [AHR] = 6.2,

222 Effective surveillance to detect IFD relapse post-HSCT and careful drug selection for antifun

223 ly be seen as potential players not only for relapse prevention but also as candidate drugs for a fas

224 critical to allow better recovery and ensure relapse prevention in addicted subjects.

225 dministered epigenetic enzyme inhibitors for relapse prevention in human drug users.

226 pment as analgesics, should be considered as relapse prevention maintenance treatment for opioid addi

227 epresents a true challenge for treatment and relapse prevention.

228 r CB1R as a potential therapeutic target for relapse prevention.

229 notypes of poor prognosis included ADEM-like relapses progressing to leukodystrophy-like features, an

230 ed PET agent, in patients with biochemically relapsed prostate cancer after primary local therapy.

231 Outcomes were recurrence/relapse rate of any mood episode (RR-any, primary), depr

232 ed analysis, those on newer DMTs had a lower relapse rate than those on injectables (rate ratio = 0.4

233 Post-hoc analyses revealed a reduced annual relapse rate, disability stabilization, and reduced brai

234 osed early because of a higher than expected relapse rate.

235 e that also targets S1PR1 and S1PR5, reduced relapse rates and MRI activity in two phase 3 trials of

236 Symptoms improved and relapse rates decreased with psychological therapies (24

237 tic leukemia (Ph-like B-ALL) experience high relapse rates despite best-available conventional chemot

238 Even in this setting, relapse rates remain high.

239 CNS relapse, or combined bone marrow and CNS relapse rates, or in toxicities observed for patients re

240 th emergency, with fatal overdoses following relapse reaching epidemic proportions and disease-associ

241 fy clonally and serve as reservoirs to drive relapse, recurrence or progression to more aggressive fo

242 Treatment options for relapsed/refractory (R/R) diffuse large B-cell lymphoma

243 In this phase 1b/2 study, 134 patients with relapsed/refractory CLL or SLL (median age, 66 years [ra

244 In relapsed/refractory Hodgkin lymphoma (R/R HL), immunothe

245 lecule AMG 420 was assessed in patients with relapsed/refractory multiple myeloma.

246 nificant antitumor activity in patients with relapsed/refractory neuroblastoma.

247 tiple myeloma cells from newly diagnosed and relapsed/refractory patients, including plasma cells bea

248 No established treatments exist for relapsed/refractory systemic light-chain (AL) amyloidosi

249 g a strategy for the prevention of psychotic relapse related to antipsychotic discontinuation.

250 e or progression of hematologic disease, non-relapse-related death, or addition of new systemic thera

251 This model could provide local relapse-related information and could be helpful in clin

252 pse of cancer (HR, 0.76 [CI, 0.61 to 0.94]), relapse-related mortality (HR, 0.69 [CI, 0.54 to 0.87]),

253 ular and circuit-level mechanisms to promote relapse remains largely unknown.

254 Relapse remains the most common cause of treatment failu

255 Moreover, its role as a driver of relapse remains unproven.

256 the lateral funiculi and gray matter (GM) in relapsing-remitting MS and GM atrophy in patients with p

257 cting fingolimod (FTY) treatment response in relapsing-remitting multiple sclerosis (RRMS) are lackin

258 The transition from relapsing-remitting multiple sclerosis (RRMS) to seconda

259 m safety and effectiveness of natalizumab in relapsing-remitting multiple sclerosis patients.

260 Subjects with relapsing-remitting multiple sclerosis showed a greater

261 Fingolimod is an effective treatment for relapsing-remitting multiple sclerosis.

262 We prospectively recruited 20 relapsing-remitting, 15 secondary progressive multiple s

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

264 t association between treatment duration and relapse risk.

265 ssion, progression-free survival (PFS) after relapse (second PFS) treated with either ASCT or CTx and

266 ferent pediatric cancers with a high risk of relapse share a common generic pattern of extensively br

267 Salvage patterns after melanoma relapse showed significantly higher rates of ipilimumab

268 n of patients in the tocilizumab group had a relapse than in the azathioprine group (five [20%] of 25

269 ay more important roles in opioid reward and relapse than MORs on VTA GABA neurons.SIGNIFICANCE STATE

270 EE presents higher rates of relapse than NEE.

271 breast cancers (TNBCs) have a higher risk of relapse than non-TNBCs with standard therapy.

272 The resistance and relapse that follows is driven by tumor heterogeneity an

273 ore knowledge is gained about the biology of relapse through comprehensive genomic profiling, incorpo

274 ons, and DNA methylation) that contribute to relapse to cocaine, amphetamine, methamphetamine, morphi

275 ons between the Pir and OFC are critical for relapse to fentanyl seeking.

276 a new motivation-related pathway critical to relapse to opioid seeking after voluntary abstinence.SIG

277 However, many patients eventually relapse to the original conditioned fear response.

278 a 10-year follow-up showed a lower degree of relapse using the mandibular irregularity index when com

279 may be critical to balancing propensity for relapse versus abstinence.

280 brafenib plus trametinib reduced the risk of relapse versus placebo in patients with resected, BRAF(V

281 Relapse was associated with an increased number of B cel

282 Relapse was defined as new or reappearing symptoms or wo

283 Treatment upon relapse was diverse: the majority of patients received a

284 full analysis set, median time to the first relapse was longer in the tocilizumab group than the aza

285 However, microbiologic relapse was observed after 11/12 treatment courses, nota

286 Relapse was observed in 41% patients, even though final

287 Shorter time to relapse was the strongest predictor of subsequent relaps

288 Using an instrumental model of cocaine relapse, we evaluated whether systemic CB1R antagonism (

289 Mean days to relapse were 296.0 +/- 22.1 in the 4-week group, and 182

290 Late relapses were associated with a significantly higher ris

291 Relapses were not observed among those patients treated

292 ation of alloreactivity will lead to disease relapse, whereas untamed allo-immune responses will lead

293 E STATEMENT Drug-associated cues precipitate relapse, which is correlated with transient synaptic enl

294 Despite impressive outcomes, relapse with CD19(-) disease remains a challenge.

295 There seem to be three patterns of relapse with different outcomes: pure teratoma, early vi

296 to FLT3 inhibitors, most patients eventually relapse with drug resistance.

297 th RMA after ATT may experience tuberculosis relapse within 6 mo of completing ATT.

298 ith resolved ME, the cumulative percent with relapse within 7 years was 43% (95% CI, 32-51).

299 e of treatment for advanced breast cancer or relapsed within 12 months of neoadjuvant or adjuvant che

300 dual decrease in parasite load; however, 25% relapsed within 18 months of follow-up.