ライフサイエンスコーパス: EFS

1 EFS (1-20 Hz) caused Ca(2+) transients in enteric motor

2 EFS increased force and phosphorylation of RLC, CPI-17 a

3 EFS responses were not corrected by the addition of a ne

4 EFS was defined as time from date of diagnosis to progre

5 EFS was higher with >/= 90% resection (45.9% +/- 4.3%) t

6 EFS was not associated with tumor grade (P= 0.98), histo

7 EFS was not significantly different in patients with vit

8 ing 5-year rates: FFS (52% vs 70%, P = .02), EFS (68% vs 86%, P = .02), TFS (76% vs 94%, P < .01), an

9 d patients was 76% (95% CI, 72% to 79%); 174 EFS events were reported (MAP, n = 93; MAP plus IFN-alph

10 Studies that addressed EFS or OS by MRD status in patients with ALL were includ

11 LN) 2010 intermediate I prognostic risk AML (EFS, 26% +/- 4 vs 40% +/- 5 at 4 years; Cox P = .002) an

12 GR group (n = 86) were an OS of 66.8% and an EFS of 62.5%.

13 -PR group (n = 43) had an OS of 74.8% and an EFS of 73.4%.

14 r with first pulmonary recurrence who had an EFS as well as biologic end point to determine the histo

15 l residual disease (>0.01%) at day 29 had an EFS in excess of 90%.

16 survival was 98% versus 86% ( P = .003), and EFS was 95% versus 83% ( P = .03), respectively.

17 0%; OS rate was 25% (95% CI, 16% to 36%) and EFS rate was 38% (95% CI, 28% to 49%) in the remaining c

18 -35) overall survival was 93% (52 of 56) and EFS was 89% (50 of 56).

19 cell, T cell, Philadelphia chromosome), and EFS and OS.

20 ith PEI did not significantly improve OS and EFS in patients at HR.

21 by risk group demonstrated decreased OS and EFS in the standard-risk group only (HR, 1.9; 95% CI, 1.

22 ER2 agents and chemotherapy for both pCR and EFS end points.

23 The optimal SUVmax for predicting pCR and EFS was, however, specific to the treatment regimen.

24 quency of pathological complete response and EFS (R(2)=0.03, 95% CI 0.00-0.25) and OS (R(2)=0.24, 0.0

25 n between pathological complete response and EFS and OS in various subgroups.

26 n between pathological complete response and EFS and OS, to establish the definition of pathological

27 otherapy can predict pathologic response and EFS in TNBC patients under different chemotherapy regime

28 (EFS), probabilities of overall survival and EFS at 2 years, incidence of acute and chronic GVHD, ach

29 veals no differences in overall survival and EFS between the control (EFS, 35% +/- 3 [standard error]

30 s, clofarabine improved overall survival and EFS for European Leukemia Net (ELN) 2010 intermediate I

31 s for ocular survival, patient survival, and EFS (related to target seeds) were 90.4% (95% confidence

32 resection (ie, anatomic v partial/wedge) and EFS ( P = .67).

33 We have now constructed baseline EFS outcomes that can be used as a comparison for future

34 A better EFS was associated with negative lymph node status ( P <

35 to chlorambucil led to significantly better EFS (hazard ratio, 0.54; 95% CI, 0.38 to 0.77).

36 90% was associated with significantly better EFS and lower CILP.

37 ed dose-dense group had significantly better EFS than the control group (HR, 0.79; 95% CI, 0.63-0.99;

38 haplotype B donor had a significantly better EFS than those transplanted from a KIR haplotype A donor

39 ed that earlier use of HD-araC led to better EFS and OS in AAML0431 than in past COG studies.

40 transients evoked in PDGFRalpha(+) cells by EFS and inhibitory junction potentials (IJPs) recorded w

41 Ca(2+) transients and IJPs elicited by EFS were blocked by MRS-2500, a P2Y1 antagonist, and abs

42 patients with triple-negative breast cancer (EFS: HR 0.24, 95% CI 0.18-0.33; OS: 0.16, 0.11-0.25) and

43 hat EFS24 has comparable power to continuous EFS when evaluating clinical trials in DLBCL.

44 verall survival and EFS between the control (EFS, 35% +/- 3 [standard error] at 4 years) and clofarab

45 e/FLT3 without internal-tandem duplications (EFS, 18% +/- 5 vs 40% +/- 7; Cox P < .001).

46 lasmic calcium concentration in hASCs during EFS, our findings also suggest that primary cilia may po

47 cial calcium-signaling nexus in hASCs during EFS.

48 recommendations for developing an efficient EFS process to meet the goal of improving access to earl

49 Pediatric LPHL has excellent EFS with chemotherapy that is less intensive than standa

50 ratio, 1.97) were independent risk factors (EFS).

51 astic (n = 5) medulloblastoma ( P < .001 for EFS; P = .001 for OS).

52 5), and ETV6-RUNX1 (HR = 0.14, P = .006) for EFS and age (HR = 0.48, P < .001), ETV6-RUNX1 (HR = 0.1,

53 th a hazard ratio (HR) of 2.1 (P = .008) for EFS and 1.9 (P = .040) for OS.

54 Rs of 2.7 (95% CI, 1.3 to 5.9; P = .011) for EFS, 4.4 (95% CI, 1.8 to 10.6; P = .001) for PFS, and 4.

55 en odds ratios for pCR and HRs were 0.63 for EFS and 0.29 for OS.

56 se could be used as a surrogate endpoint for EFS or OS.

57 Summary risk estimates for EFS, OS, and CIR (ALL only) were calculated with random-

58 Positive predictive factors for EFS were age younger than 10 years and tumor size less t

59 ease were independent prognostic factors for EFS.

60 pCR and the corresponding treatment HRs for EFS and OS.

61 improvements in pCR rate, predicted HRs for EFS for RCTs were concordant with observed HRs.

62 alysis of the four studies, the top loci for EFS were marked by rs7712513 at 5q23.2 (near SNX2 and SN

63 Factors predictive for EFS by multivariable analysis were baseline MTV (bMTV) (

64 tional benefit to imatinib (hazard ratio for EFS = 0.64, 95% confidence interval 0.44-0.93, P = .02),

65 were evaluated by HTS and FC for event-free (EFS) and overall survival (OS).

66 after the onset of stimulation (latency from EFS was 280 ms at 10 Hz).

67 n Most patients with stage III FHWT had good EFS/overall survival with DD4A and radiation therapy.

68 tuximab maintenance therapy does not improve EFS, which was the primary end point of this trial, or O

69 tentially addressable risk factor to improve EFS and morbidity in pediatric ALL.

70 (GO 32% v No-GO 49%, P < .001) and improved EFS (GO 53% v No-GO 41%, P = .005).

71 GO added to chemotherapy improved EFS through a reduction in RR for children and adolescen

72 esponse as a surrogate endpoint for improved EFS and OS.

73 e between treatment groups predicts improved EFS and OS.

74 GO significantly improved EFS (3 years: 53.1% v. 46.9%; hazard ratio [HzR], 0.83;

75 stology-based postoperative therapy improved EFS and OS and preservation of renal parenchyma compared

76 ades 1-3 aGVHD were associated with improved EFS (P = .02), whereas grade 4 aGVHD and extramedullary

77 is ypN0) was better associated with improved EFS (ypT0 ypN0: hazard ratio [HR] 0.44, 95% CI 0.39-0.51

78 on but significantly reduces RR and improves EFS in patients with high CD33 expression, which suggest

79 we investigate the role of primary cilia in EFS-enhanced osteogenic response of human adipose-derive

80 There was no significant difference in EFS across trials according to number of prior treatment

81 Differences in EFS and OS were not statistically significant.

82 Overall, the improvement in EFS for pCR vs non-pCR was substantial: HR, 0.37 (95% pr

83 We found no improvement in EFS with more extensive or serial resections.

84 id tissue lymphoma; however, improvements in EFS and progression-free survival did not translate into

85 of maintenance therapy resulted in inferior EFS (hazard ratios, 1.43 and 2.30, respectively; global

86 ls was consistently correlated with inferior EFS (P < .003).

87 stage, 1q gain was associated with inferior EFS (stage I, 85% v 95%; P = .0052; stage II, 81% v 87%;

88 eradication from the breast alone (ypT0/is; EFS: HR 0.60, 95% CI 0.55-0.66; OS 0.51, 0.45-0.58).

89 Five-year LC, EFS, and OS rates were similar to those observed in comp

90 >/= 90% resection was associated with longer EFS after adjustment for MYCN amplification or diploidy

91 nd 4/6 matched UCB was associated with lower EFS.

92 an follow-up period of 6.4 years, the median EFS was 3.4 years (95% CI, 2.1 to 5.3) in the short-term

93 The 12-month EFS for the 42 evaluable patients enrolled in AOST0221 w

94 of the cholinesterase inhibitor neostigmine, EFS led to an additional increase in phosphorylation of

95 comparator model specified that the observed EFS rate should not be significantly < 92%.

96 survival was 96% (95% CI 86.46-99.09) and of EFS was 91% (79.78-96.17).

97 Upon cessation of EFS, several fast Ca(2+) transients were noted in SMCs (

98 The chance of EFS was higher in patients with successful CD4(+) IR (HR

99 lia seem to functionally modulate effects of EFS-induced cellular calcium oscillations.

100 d lymph nodes, with a secondary end point of EFS.

101 morphism risk score was highly predictive of EFS (P = 1.78 x 10(-12)) and was independent of treatmen

102 node and LOH status was highly predictive of EFS and should be considered as a potential prognostic m

103 7.6% vs 31.6%, P = .06), and prolongation of EFS (hazard ratio [HR] = 0.59, P = .08) and OS (HR = 0.4

104 Influence of weight extremes on EFS and TRT is not set at diagnosis as previously report

105 ver treatment, we hypothesized its impact on EFS is instead determined by cumulative time spent at an

106 In hierarchical order, EFS was 45.9% (4.4) in 132 MRD-HR patients, 41.2% (11.9)

107 OS, EFS, and DFS for SR and HR patients were 83%, 63%, and 6

108 tients had viable tumor and a worse outcome (EFS: 50%; P = 0.01).

109 Overall EFS (+/- SE) was 72.6 +/- 5.4% at 1 year, 57.6 +/- 6.2%

110 Inferior PFS, EFS, and OS were predicted by positron emission tomograp

111 .042, and .0012) were associated with a poor EFS.

112 sk for positive end-induction MRD and poorer EFS.

113 In ALL, we observed poorer EFS in children with a higher BMI (RR: 1.35; 95% CI: 1.2

114 is, and monosomal karyotype predicted poorer EFS.

115 analysis, 1q gain was associated with poorer EFS (P < .001; hazard ratio, 2.33) and OS (P = .01; haza

116 BMI was significantly associated with poorer EFS and OS (RR: 1.36; 95% CI: 1.16, 1.60 and RR: 1.56; 9

117 Gain of 1q remained associated with poorer EFS in tumor subsets limited to either intermediate-risk

118 r notable aberrations associated with poorer EFS included MYCN gain and TP53 loss.

119 y and overweight were associated with poorer EFS irrespective of end-induction MRD (P = .012).

120 The association of 1q gain with poorer EFS retained significance in multivariable analysis adju

121 and iAMP21 were associated with the poorest EFS and OS; absence of both was associated with the best

122 tly associated with decreasing postoperative EFS ( P < .01).

123 .5% for the 3-year event-free survival rate (EFS), equivalent to 1.43 in terms of the hazard ratio of

124 ble data for pathological complete response, EFS, and OS; and have a median follow-up of at least 3 y

125 ors review the current landscape of the U.S. EFS and make recommendations for developing an efficient

126 , .048, .004, and .0005) predicted a shorter EFS.

127 Vmax at baseline was associated with shorter EFS (P < 0.001).

128 ABVD8 and BEACOPP4+4 resulted in similar EFS and OS in patients with high-risk advanced-stage HL.

129 ntation for HS are encouraging, with similar EFS rates after MSD, 6/6 matched UCB, 5/6 UCB, and 10/10

130 rostimulation by electric field stimulation (EFS) in bovine tracheal smooth muscle.

131 High-frequency electrical field stimulation (EFS) of distal colon segments produced up to a 10-fold g

132 ous purines or electrical field stimulation (EFS) of enteric neurons.

133 ination of the electrical field stimulation (EFS) with data acquisition in spatially separated areas

134 Electrical field stimulation (EFS), which releases ACh from nerves, increased force an

135 ial sensor for electrical field stimulation (EFS)-enhanced osteogenic response in osteoprogenitor cel

136 induced-, (ii) electrical field stimulation (EFS)-induced force, (iii) pCa-force, (iv) slack-tests an

137 ntly introduced the Early Feasibility Study (EFS) Program for facilitating the conduct of these studi

138 sulting in lower 8-year event-free survival (EFS) (64% +/- 2% vs 81% +/- 2%, P < .0001) and overall s

139 significantly improved event-free survival (EFS) (94%) compared with patients with a PR genetic prof

140 ry objective was 1-year event-free survival (EFS) after HLA allele-matched (at HLA-A, -B, -C, and -DR

141 Survivor functions for event-free survival (EFS) and OS were estimated using the Kaplan-Meier method

142 primary end point, with event-free survival (EFS) and overall survival (OS) as secondary end points.

143 gly predicted for worse event-free survival (EFS) and overall survival (OS) in a cohort of 290 childr

144 d chemotherapy improved event-free survival (EFS) and overall survival (OS) in children with newly di

145 s (HRs) and 95% CIs for event-free survival (EFS) and overall survival (OS) using a log-additive gene

146 At 2 years, event free survival (EFS) and overall survival (OS) were 56% vs 46%, and 65%

147 up, 5.38 years), 5-year event-free survival (EFS) and overall survival (OS) were 62% (95% CI, 52 to 7

148 EN0534 aimed to improve event-free survival (EFS) and overall survival (OS) while preserving renal ti

149 e relationships between event-free survival (EFS) and overall survival (OS) with MRD status in pediat

150 lms tumors (FHWTs) with event-free survival (EFS) and overall survival (OS) within each tumor stage a

151 Four-year event-free survival (EFS) and overall survival estimates were 88% (95% CI, 85

152 influence of weight on event-free survival (EFS) and treatment-related toxicity (TRT) in childhood a

153 e previously shown that event-free survival (EFS) at 24 months (EFS24) is a clinically useful end poi

154 Overall survival and event-free survival (EFS) at 5 years were 74% and 63%, respectively.

155 To investigate whether event-free survival (EFS) can be maintained among children and adolescents wi

156 The median event-free survival (EFS) for the entire study population was 8.4 months; 1-y

157 ective of the trial was event-free survival (EFS) from randomization.

158 and the probability of event-free survival (EFS) in children with acute lymphoblastic leukemia who r

159 associated with poorer event-free survival (EFS) in pediatric acute lymphoblastic leukemia (ALL).

160 ion failure with 5-year event-free survival (EFS) of 50.7% (95% CI, 37.4 to 64.0) and 5-year overall

161 R patients had a 5-year event-free survival (EFS) of 58.9% (standard error [SE] = 2.8) and an overall

162 th rituximab had 3-year event-free survival (EFS) of 59% and 79% and 3-year overall survival (OS) of

163 thotrexate had a 5-year event-free survival (EFS) of 82% versus 75.4% (P = .006).

164 MRD <0.01% had a 5-year event-free survival (EFS) of 87% +/- 1% vs 74% +/- 4% for those with MRD 0.01

165 patients), had a 6-year event-free survival (EFS) of 89.0% (standard error [SE] = 1.5%) and a 6-year

166 an estimated long-term event-free survival (EFS) of less than 20%.

167 s and age (> 70 years), event-free survival (EFS) of patients with bulky disease was inferior without

168 determine the effect on event-free survival (EFS) of staging variables, extent of resection, and repe

169 sk patients, the 5-year event-free survival (EFS) rate was 93% (SE 2%), the 5-year survival rate was

170 erall survival (OS) and event-free survival (EFS) rates at 10 years were, respectively, 90% and 88.6%

171 or DL (P = .78); 4 year event-free survival (EFS) was 27% for TRIL and 27% for DL (P = .83).

172 s (IPI, 3 to 5); 3-year event-free survival (EFS) was 71%, 75%, and 67%, respectively; and 3-year ove

173 Five-year event-free survival (EFS) was 75.0% in patients with 1q gain (95% CI, 68.5% t

174 of 11.5 months; 5-year event-free survival (EFS) was 77% (range, 62% to 87%).

175 igible patients, 4-year event-free survival (EFS) was 85.0%: 86.9% for RERs and 77.4% for SERs (P < .

176 s 95.5%, and the 5-year event-free survival (EFS) was 89.8%.

177 l survival was 94%, and event-free survival (EFS) was 91%.

178 f 62 months, the 5-year event-free survival (EFS) was significantly better for the patients treated i

179 ar overall survival and event-free survival (EFS) were 95% and 82%, respectively.

180 , patient survival, and event-free survival (EFS) were calculated and then compared using the Mantel-

181 abolic change, pCR, and event-free survival (EFS) were examined (log-rank test).

182 n to cancer occurrence, event-free survival (EFS), and overall survival (OS).

183 disease-free survival, event-free survival (EFS), and overall survival (OS).

184 Overall survival (OS), event-free survival (EFS), and progression-free survival (PFS) at 4 years wer

185 overall survival (OS), event-free survival (EFS), and relapse risk from the end of induction 1 (haza

186 (ML-DS) have favorable event-free survival (EFS), but experience significant treatment-related morbi

187 points included 5-year event-free survival (EFS), distant disease-free survival (DDFS), overall surv

188 and imatinib cohorts in event-free survival (EFS), OS, and relapse-free survival (RFS) seen in univar

189 tment outcomes included event-free survival (EFS), overall survival (OS), and cumulative incidence of

190 s associated with worse event-free survival (EFS), overall survival (OS), and cumulative incidence of

191 Five-year event-free survival (EFS), overall survival (OS), and local control (LC) were

192 re overall survival and event-free survival (EFS), probabilities of overall survival and EFS at 2 yea

193 re-free survival (FFS), event-free survival (EFS), transformation-free survival (TFS), and overall su

194 Primary end points were event-free survival (EFS), treatment discontinuation, no complete response (C

195 orts of both pCR and an event-free survival (EFS)-type outcome.

196 es of interest included event-free survival (EFS).

197 ted for their impact on event-free survival (EFS).

198 l lesion glycolysis, on event-free survival (EFS).

199 sequencing with pCR and event-free survival (EFS).

200 ng associated with poor event-free survival (EFS).

201 The main end point was event-free survival (EFS).

202 e primary end point was event-free survival (EFS).

203 y/surgery alone [5-year event-free survival (EFS): 85.7%].

204 % vs 28%; P < .001) and event-free survival (EFS, 36% vs 21%; P < .001) at 5 years, independent of cy

205 Event-free survival (EFS, primary endpoint) and other clinical endpoints and

206 nostic significance for event-free survival (EFS, the main endpoint of the IELSG-19 trial) were age >

207 26%; P = .07) and lower event-free survival (EFS; 4-year EFS, 31% vs 43%; P < .01), but progression-f

208 - 4%; Plog-rank = .64), event-free survival (EFS; 87% +/- 3% vs 89% +/- 4%; Plog-rank = .71), and cum

209 ed with superior 5-year event-free survival (EFS; 90% v 81% for prednisone; P = .01) but higher rates

210 versely correlated with event-free survival (EFS; P < .004) and positively correlated with the cumula

211 al (OS; P = 0.0441) and event-free survival (EFS; P = 0.0114) compared with low MAP7 expression (MAP7

212 Outcome measures were event-free survival (EFS; primary) and overall survival and toxicity (seconda

213 e cell infiltration and event-free-survival (EFS).

214 v No-GO 34%, P = .731; event-free survival [EFS]: GO 53% v No-GO 58%, P = .456).

215 The EFS difference reflected a significant difference in the

216 The EFS for 96 patients with osteosarcoma and measurable dis

217 The EFS for SR patients in AAML0631 was noninferior to that

218 The EFS hazard ratio (HR) for achieving MRD negativity is 0.

219 The EFS was 5.7 months for patients with prior bortezomib ex

220 The EFS was uniformly poor for children with recurrent/refra

221 Conclusion The EFS rate for children with IR MGCT observed after three

222 in 15 of 147 patients with no impact on the EFS (87.5%; P = 0.666).

223 y LN sampling seems to have no impact on the EFS and should not be recommended.

224 oc analysis, we also compared results to the EFS rate of comparable patients treated with four cycles

225 on the frequency-maximal force responses to EFS in isolated ileal tissues.

226 r-negative tumours who received trastuzumab (EFS: 0.15, 0.09-0.27; OS: 0.08, 0.03, 0.22).

227 iations between loci at 5q23.2 and 6q21 with EFS and OS in patients with diffuse large B-cell lymphom

228 pCR was associated with EFS (log-rank, P= 0.001).

229 the evaluated variables was associated with EFS after correction for multiple testing, but this anal

230 UVmax was also significantly associated with EFS both in patients receiving SIM (P= 0.028) and in tho

231 ic indicator and is strongly associated with EFS.

232 pN0, and ypT0/is--for their association with EFS and OS in a responder analysis.

233 Associations with EFS (ie, freedom from disease progression or recurrence)

234 ilar to that seen in MRD-negative ones, with EFS/OS curves for patients with 0.1% to 1% MRD crossing

235 A total of 36 studies with EFS by pCR status representing 5768 patients with HER2-p

236 endent prognostic factors predicting a worse EFS.

237 , high levels of these mRNAs predicted worse EFS and OS in BM but not in PB.

238 ad a tumor SUVmax of 10 or greater and a 3-y EFS of 49% (vs. 92% in patients with baseline SUVmax < 1

239 ated with a significantly worse outcome (3-y EFS: 11.8% +/- 7.8% vs. 49.6% +/- 7.7%, respectively; P

240 ing associated with an inferior outcome (5-y EFS, 39.2% +/- 4.7% [CS </= 2] vs. 16.4% +/- 4.2% [CS >

241 nificant outcome difference by CS noted (5-y EFS, 43.0% +/- 5.7% [CS </= 12] vs. 21.4% +/- 3.6% [CS >

242 Although the 1-year EFS met the prespecified target of >/=75%, this regimen

243 The 1- and 2-year EFS rates were 76% and 69%, respectively.

244 al review and the Deauville criteria, 2-year EFS was 41% versus 76% (P < .001) for patients who had i

245 t was event-free survival at 2 years (2-year EFS).

246 RICOVER-60 was associated with better 3-year EFS (67% v 54%) and OS (80% v 67%) in poor-prognosis pat

247 re 75.4% and 78.2%, respectively, the 3-year EFS difference was -2.8% (91.4% CI, -7.8 to 2.2%), the H

248 With median follow-up of 44 months, 3-year EFS for all 716 randomly assigned patients was 76% (95%

249 p of surviving patients of 3.8 years (3-year EFS for all patients, 38% [95% CI, 29% to 48%]; survival

250 CT PET were independently prognostic; 3-year EFS for pre-ASCT PET-positive patients with low bMTV was

251 s with two or more risk factors had a 3-year EFS of 20% (95% CI, 11% to 30%).

252 one or bone marrow involvement) had a 3-year EFS of 69% (95% CI, 52% to 82%); high-risk patients with

253 o Oberlin risk factor had an improved 3-year EFS of 69% on ARST0431 compared with an historical cohor

254 disease identified a favorable group (3-year EFS, 100%).

255 patients enrolled from 2003 to 2011, 4-year EFS (EFS4) rate was 89% (95% confidence interval, 83% to

256 ed prolonged chemotherapy; on NWTS-5, 4-year EFS for all children with BWT was 56%.

257 was powered to detect a reduction in 4-year EFS from 87% to 75% and overall survival from 95% to 88%

258 Post-ASCT, 4-year EFS was 45% for TRIL and 46% for DL.

259 At median follow-up of 4.1 years, 4-year EFS was 91% for exemestane and 91.2% for anastrozole (st

260 In contrast, the 4-year EFS was only 74% in patients with combined positive lymp

261 ) and lower event-free survival (EFS; 4-year EFS, 31% vs 43%; P < .01), but progression-free survival

262 e of persistent or recurrent disease (4-year EFS, 52%; 95% CI, 31% to 69%).

263 histology had a significantly better 5-year EFS (87.5%) than patients with alveolar histology (39.1%

264 ny detectable level who had excellent 5-year EFS (98.1%) and OS (100%).

265 1 (66%) patients with tumor material, 5-year EFS and OS differed between low-risk (wingless [WNT], n

266 HTS and FC showed similar 5-year EFS and OS for MRD-positive and -negative patients using

267 % of children as ultrahigh risk, with 5-year EFS and OS rates of 0%; OS rate was 25% (95% CI, 16% to

268 The 5-year EFS and OS were both 89% (95% CI, 67 to 100) for desmopl

269 The difference in 5-year EFS between the two groups was 1.1% (95% CI -5.6 to 2.5)

270 and a low EOI MRD level (< 0.01%) had 5-year EFS of 100%.

271 1 of 2,633) had high MRD (>/= 5%) and 5-year EFS of 47.0% (95% CI, 32.9 to 61.1), which was similar t

272 33 patients) of the trial cohort with 5-year EFS of 48.0% (95% CI, 39.3 to 58.6).

273 with MRD >0.1% did not improve either 5-year EFS or overall survival (OS).

274 ts resulted in a significantly better 5-year EFS rate (78%, SE 8% v 16%, SE 8% in controls).

275 k patients had a significantly higher 5-year EFS rate (88%, SE 2%) with therapy intensification (incl

276 erall outcome improved significantly (5-year EFS rate 87%, 5-year survival rate 92%, and 5-year cumul

277 The 5-year EFS rates in the low-, intermediate-, and high-risk grou

278 Mature final data showed 5-year EFS rates of 79.6% for high-dose methotrexate and 75.2%

279 For 204 eligible patients, 5-year EFS was 89.9% and overall survival (OS) was 93.0%.

280 with a median follow-up of 64 months, 5-year EFS was not statistically significantly different betwee

281 Poor early treatment response (5-year EFS, 58% +/- 16% vs 88% +/- 3%; Plog rank = .0008) and g

282 16% +/- 7% vs 3% +/- 2%, PGray = .02; 5-year EFS, 73% +/- 8% vs 91% +/- 4%, Plog rank = .018) were id

283 HR, 0.79; 95% CI, 0.63-0.99; P = .04; 5-year EFS, 86.7% vs 82.1%).

284 ho received the other three regimens (5-year EFS, 91.2% v 83.2%, 80.8%, and 82.1%; P = .015).

285 ents received only radiochemotherapy (5-year EFS: 27.3%).

286 rapy/surgery was used in 12 patients (5-year EFS: 63.6%).

287 Eight-year EFS was 77% for those with 1q gain and 90% for those lac

288 Eight-year EFS was 86% (95% CI, 84% to 88%) for the entire cohort.

289 Five-year EFS did not differ significantly whether, after surgery,

290 Five-year EFS for the entire cohort was 85.5% (95% CI, 79.2% to 90

291 Five-year EFS was 66.0% in the CT1 arm and 70.0% in the RT1 arm (P

292 Five-year EFS was 88.8% (95% CI, 81.8% to 93.2%).

293 Five-year EFS, OS, and CILP (+/- SE) were 43.5% +/- 3.7%, 54.9% +/

294 Four-year EFS was 79.3% versus 75.2% (P = .11) for SERs who were r

295 Four-year EFS was 87.9% versus 84.3% (P = .11) for RERs with CR wh

296 Two-year EFS was significantly shorter for PET-positive compared

297 a median follow-up of 5.9 years, the 3-year EFSs were 75.4% and 78.2%, respectively, the 3-year EFS

298 gnificantly associated with poorer five-year-EFS (25.0%. vs. 69.4%, p = 0.014).

299 0.031) were associated with worse five-year-EFS.

300 At 4 years, EFS was 63.7% for ABVD8 versus 69.3% for BEACOPP4+4 (haz