ライフサイエンスコーパス: RFS

1 RFS and overall survival were measured using Kaplan-Meie

2 RFS remained superior in the imatinib arm (hazard ratio,

3 RFS was not significantly different between the groups (

4 ups in terms of overall survival (P<0.0001), RFS (P<0.0001), nonrelapse mortality (P=0.0043), and acu

5 dent predictor of non-progression (P<0.001), RFS (P<0.001), and DSS (P=0.024) in the test population.

6 9; [95% confidence interval [CI]: 3.1-11.2]; RFS: hazard ratio, 7.5 [95% CI: 3.4-16.5]).

7 tio, 0.79; 98.5% CI, 0.50 to 1.25; P = .21); RFS was 84% versus 66% at 3 years and 69% versus 63% at

8 ng a median follow-up time of 59 months, 214 RFS events occurred (local or distant recurrences or dea

9 (hazard ratio, 0.91; 95% CI, 0.59 to 1.41), RFS, or DF-free survival.

10 edian follow-up period of 6.1 years, and 437 RFS events, we achieved an HR of 1.26 (one sided 95% UCB

11 age III (OS: HR, 1.76; 95% CI, 1.26 to 2.46; RFS: HR, 1.34; 95% CI, 1.01 to 1.76; and DRFS: HR, 1.36;

12 (OS: P = .013; HR, 2.09; 95% CI, 1.16-3.77; RFS: P = .001; HR, 2.65; 95% CI, 1.48-4.89).

13 nfidence interval [CI], 0.56-1.72 [P = .94]; RFS: HR 0.7; 95% CI, 0.36-1.38 [P = .3]; CR: mutated 83%

14 However, a RFS and OS benefit is evident in the first 3 to 5 years,

15 The 5-year OS (75% vs 52%, P = 0.0008) and RFS (72% vs 20%, P < 0.0001) were better in group T; sim

16 27 vs 38 months, respectively; P = .009) and RFS (126 vs 18 months, respectively; P = .007).

17 R, 0.64; 95% CI, 0.44 to 0.95; P = .027) and RFS in women with triple-negative disease and in women w

18 OS (P = .003; HR, 1.82; 95% CI, 1.2-2.7) and RFS (P < .001; HR, 2.2; 95% CI, 1.4-3.3).

19 Female patients (n = 162) with FTV and RFS were included.

20 The 5-year MSS and RFS rates were 83% and 76%, respectively (median follow-

21 of invasive cancer in breast and nodes) and RFS, overall and within receptor subsets.

22 the effect of axillary pCR on 10-year OS and RFS among all women who received a diagnosis of breast c

23 l resection provides better long-term OS and RFS compared with RFA in patients with BCLC very early-s

24 significantly associated with better OS and RFS compared with RFA; the 5-year OS rates were 80% vers

25 .02), but no significant benefit for OS and RFS.

26 sion were poor prognostic factors for OS and RFS.

27 was associated with improved 10-year OS and RFS.

28 Rs) associated with alloHSCT for relapse and RFS were 0.30 (95% CI, 0.24 to 0.37; P < .001), and 0.52

29 months, cumulative incidence of relapse and RFS were 22% vs 54% (P < .001) and 73% vs 44% (P < .001)

30 The association between STILs and RFS was evaluated with Cox models.

31 on or insertion-deletion mutation had better RFS when allocated to the 3-year group compared with the

32 Younger patients had a significantly better RFS on HDC than did older patients.

33 AC and are included in the analyses of both RFS and OS.

34 on nucleotide binding, but not hydrolysis by RFS-1/RIP-1.

35 The lysosomal alterations induced by RFS-kappaLCs were reflected in increased cell proliferat

36 with high CCI than in patients with low CCI (RFS at 3 yrs 26% vs. 41%, P = 0.003; CSS at 5 yrs 46% vs

37 who received PV versus placebo was compared, RFS and OS were not significantly different.

38 gated a heterodimeric Rad51 paralog complex, RFS-1/RIP-1, and uncovered the molecular basis by which

39 ears, the vaccination arm showed a decreased RFS rate of 1.2% (HR, 1.03; 95% CI, 0.84 to 1.25) and OS

40 HD5 expression was associated with decreased RFS (4.5 vs 16.3 months; P=0.001) and overall survival (

41 S), relapse-free survival (RFS), and distant RFS (DRFS) estimates were similar for the different TTC

42 hat a RAD51 paralog complex from C. elegans, RFS-1/RIP-1, functions predominantly downstream of filam

43 Achieving pCR predicted favorable RFS.

44 ion mutations were associated with favorable RFS, whereas KIT exon 9 mutations were associated with u

45 CA2, which nucleates RAD-51-ssDNA filaments, RFS-1/RIP-1 binds and remodels pre-synaptic filaments to

46 bsolute advantage of AC at 5 years is 3% for RFS (91 v 88%) and 1% for OS (95 v 94%).

47 y as indicated by the C statistics (0.74 for RFS and 0.70 for OS).

48 elated donor transplantation, especially for RFS (P=0.016) and acute GVHD (P=0.027).

49 monstrating that remodeling is essential for RFS-1/RIP-1 function.

50 The 10-year Kaplan-Meier estimates for RFS in arm A were 90.9% and 64.5% for patients with high

51 The 10-year estimates for RFS in arm C were 80.0% and 80.1% for patients with high

52 independent favorable prognostic factor for RFS and OS adjusted for age, gender, smoking, stage, and

53 The HR for RFS is 1.51 (95% CI, 1.25 to 1.83; P < .001).

54 A plateau for RFS was reached after approximately 18 months.

55 LT5 and FUT1 as an independent predictor for RFS (HR: 2.370, 95% CI: 1.505-3.731, P < 0.001) and OS (

56 ed without trastuzumab, the hazard ratio for RFS of pCR versus no pCR was 0.29 (95% CI, 0.07 to 0.82)

57 Relapse-free (RFS) and overall survival (OS) of AML+13 patients were i

58 ut) did not impact event-free, relapse-free (RFS), or overall survival (OS) in either the entire coho

59 associated with an unfavorable relapse-free (RFS, P = .0008) and overall survival (OS, P = .004); aft

60 Comparable 12-month HG RFS was noted for both doses.

61 imatinib therapy was associated with higher RFS in patients with a KIT exon 11 deletion of any type,

62 CI, 1.1 to 2.7; P = .03) but did not impact RFS (HR, 1.1; 95% CI, 0.7 to 1.9; P = .65).

63 nor baseline symptoms significantly impacted RFS (P > .10) in patients with or without baseline sympt

64 ubicin, and cyclophosphamide did not improve RFS significantly compared with a similar regimen withou

65 ned with bevacizumab resulted in an improved RFS for patients with hormone-sensitive prostate cancer.

66 ow-up of 7.2 years, biochemotherapy improved RFS (hazard ratio [HR], 0.75; 95% CI, 0.58 to 0.97; P =

67 or and/or joint symptoms would have improved RFS.

68 ant imatinib, 36 months of imatinib improved RFS and overall survival of GIST patients with a high ri

69 djuvant GM-CSF nor PV significantly improved RFS or OS in patients with high-risk resected melanoma.

70 t symptoms were not associated with improved RFS.

71 ith a statistically significant advantage in RFS with MAC.

72 ve plant vigor, and, if chronic, declines in RFS-dependent species abundance.

73 s did not reveal a significant difference in RFS between SCT and no-SCT cohorts.

74 There was no significant difference in RFS or overall survival between the groups (hazard ratio

75 Gain in RFS could be related to the lower cumulative incidence o

76 of 50 months, we observed no improvement in RFS between XT (87.5%; 95% CI, 82.7% to 91.1%) and WP (9

77 des statistically significant improvement in RFS but no difference in OS and more toxicity compared w

78 d a statistically significant improvement in RFS compared with patients treated with ADT alone (13.3

79 Walker box mutations in RFS-1, which abolish filament remodeling, fail to stimul

80 l ontology analyses suggested that increased RFS was linked to a subset of immune function genes.

81 mune gene enrichment was linked to increased RFS in arms B and C (HR, 0.35; 95% CI, 0.22 to 0.55; P <

82 signature was not associated with increased RFS in arm A (HR, 0.90; 95% CI, 0.60 to 1.37; P = .64).

83 toxicity and new perspectives on LC-induced RFS.

84 systems challenged by allelopathic invaders: RFS mutualism disruption drives carbon stress, subsequen

85 ng human control or RFS-associated kappaLCs (RFS-kappaLCs) and primary cultures of mouse PT cells exp

86 independently associated with improved liver RFS (HR = 0.34), overall RFS (HR = 0.65), and DSS (HR =

87 lung RFS (HR = 2.0, P = 0.01), but not liver RFS (P = 0.181).

88 .3%, P < 0.001) but not a lower 3-year liver RFS rate (43.8% vs 50.2%, P = 0.181).

89 to 1 year of adjuvant imatinib had a longer RFS.

90 ssigned for 36 months of imatinib had longer RFS compared with those assigned for 12 months (hazard r

91 ents assigned to the 3-year group had longer RFS than those assigned to the 1- year group; 5-year RFS

92 ars of planned adjuvant treatment had longer RFS.

93 However, SCT was associated with longer RFS in patients with postinduction minimal residual dise

94 In particular, CRLF2-d patients had a lower RFS compared with other patients (30%), whereas those wi

95 high mitotic rate were associated with lower RFS, whereas tumor genotype was not significantly associ

96 h RLI grade 2 or higher vs grade 1 or lower (RFS at 3 years, 6.4% [3 of 50] vs 39.2% [60 of 152]; P <

97 overall RFS (HR = 1.9, P = 0.005), and lung RFS (HR = 2.0, P = 0.01), but not liver RFS (P = 0.181).

98 ts with RAS mutation had a lower 3-year lung RFS rate (34.6% vs 59.3%, P < 0.001) but not a lower 3-y

99 Median RFS was 8.8 months (median follow-up, 28.9 months).

100 ELN Intermediate-II patients (n=855) (median RFS, 7.8 vs 14.1 months, P = .006; median OS 9.3 vs. 14.

101 % CI, 0.58 to 0.97; P = .015), with a median RFS of 4.0 years (95% CI, 1.9 years to not reached [NR])

102 9.8 months (95% CI, 8.5 to 14.9), and median RFS was 7.6 months (95% CI, 4.5 to 9.5).

103 The median RFS in the IFNalpha-2b and control arms were 42.2 (95% c

104 The median RFS times with GM-CSF versus placebo were 11.4 months (9

105 In stage III-N1 ulcerated melanoma, RFS (HR, 0.72; 99% CI, 0.46 to 1.13; P = .06), DMFS (HR,

106 After median follow-up of 39.5 months, RFS was 22.7 months (95% CI, 14.1 to 38.1 months) in arm

107 ement was associated with shorter neurologic RFS (HR, 2.35; 95% CI, 1.44-3.83; P < .001).

108 In a planned analysis of RFS rates at yearly intervals, group B showed better out

109 Association of RFS with FTV was assessed by Cox regression and compared

110 regression and compared with association of RFS with PCR and residual cancer burden (RCB), while con

111 Here, we investigate the consequences of RFS mutualism disruption on native plant fitness in a gl

112 Hazard ratio (HR) of RFS for the treatment group using tumor size categorizat

113 n a statistically significant improvement of RFS (hazard ratio [HR], 0.80; 95% CI, 0.63 to 1.01; P =

114 s, appear acceptable, given the magnitude of RFS and OS improvement.

115 ables were incorporated in the prediction of RFS: tumor size of at least 12 cm (hazard ratio [HR], 3.

116 pCR was more predictive of RFS by multivariate analysis when subtype was taken into

117 pCR is more highly predictive of RFS within every established receptor subset than overal

118 nsitive, specific, and accurate predictor of RFS and CSS than NLR.

119 sured by MR imaging is a strong predictor of RFS, even in the presence of PCR and RCB class.

120 ct of planned adjuvant treatment duration on RFS.

121 stage III melanoma had a positive impact on RFS, which was marginally significant and slightly dimin

122 hat adjuvant imatinib has an overt impact on RFS.

123 ite clinical effects-unfavorable for R882 on RFS (all: hazard ratio [HR], 1.29 [P = .026]; CN-AML: HR

124 motherapy regimen, ER/PgR, or HER2 status on RFS or OS.

125 uent effects of new or worsening symptoms on RFS were examined with landmark analyses and stratified

126 B-CTx were associated with shorter bone-only RFS (both P = .02) when added to a model with factors si

127 x was also associated with shorter bone-only RFS (P = .02) when added to a model with factors signifi

128 tio, 0.94; 95% repeated CI, 0.77 to 1.15) or RFS (P = .131; hazard ratio, 0.88; 95% CI, 0.74 to 1.04)

129 nsgenic mice overexpressing human control or RFS-associated kappaLCs (RFS-kappaLCs) and primary cultu

130 No association for OS, DFS or RFS was observed in rectal cancer patients.

131 was found between neuropathy and DFS, OS, or RFS.

132 hazard ratio (HR) = 2.3, P = 0.002), overall RFS (HR = 1.9, P = 0.005), and lung RFS (HR = 2.0, P = 0

133 with improved liver RFS (HR = 0.34), overall RFS (HR = 0.65), and DSS (HR = 0.39), P < 0.01.

134 onset of renal failure, mice overexpressing RFS-kappaLCs showed PT dysfunction related to loss of ap

135 soil resources, invaders that disrupt plant-RFS mutualisms can significantly depress native plant fi

136 Moreover, high NLR was associated with poor RFS as well.

137 pTrp557_Lys558del were associated with poor RFS in the 1-year group but not in the 3-year group.

138 hat high expression of both genes had poorer RFS and OS than the others (P < 0.001).

139 Nomograms to predict RFS and OS after surgical resection of ACC were proposed

140 and calibration of the nomograms to predict RFS and OS were tested using C statistics, calibration p

141 were selected to create nomograms predicting RFS and OS.

142 n cancer in first remission does not prolong RFS or OS.

143 ubicin, and cyclophosphamide did not prolong RFS or survival compared with a regimen that contained o

144 ogeneic SCT led to a significantly prolonged RFS in patients with NPM1(mut) AML.

145 gh status remained associated with prolonged RFS (P = .007), OS (P = .01), and EFS (P = .003).

146 roved in patients with a high allelic ratio (RFS, P = .02; OS, P = .03), whereas no benefit was seen

147 s seen in patients with a low allelic ratio (RFS, P = .38; OS, P = .64).

148 d ratio (HR) of six to four cycles regarding RFS was 1.03 (95% CI, 0.84 to 1.28; P=.77).

149 cond interim analysis for futility regarding RFS (hazard ratio [HR], 1.00; P = .99) and detrimental o

150 is, KLH was less effective than MM regarding RFS (all P < .001).

151 enomic data to evaluate pathologic response, RFS, and their relationship and predictability based on

152 y did not occur with control LCs or the same RFS-kappaLC carrying a single substitution (Ala30-->Ser)

153 ies at CR (n = 71) had significantly shorter RFS (P = .001) and OS (P < .001) compared with patients

154 es was significantly associated with shorter RFS in stage I NSCLC: HIST1H4F, PCDHGB6, NPBWR1, ALX1, a

155 cess rate of the rigidifying flexible sites (RFS) strategy is still low due to a limited understandin

156 l production in the Renewable Fuel Standard (RFS) and reducing hypoxia in the northern Gulf of Mexico

157 The Renewable Fuel Standard (RFS) is among the cornerstone policies created to increa

158 ated by the current Renewable Fuel Standard (RFS).

159 IC were found to be associated with superior RFS after alloSCT in multivariate analysis.

160 (DSS P<0.001) and recurrence-free survival (RFS P<0.001).

161 arm did not influence relapse-free survival (RFS) (64% in both arms; P = .91).

162 CI: 1.15-1.84) and recurrence-free survival (RFS) (HR: 1.32, 95% CI: 0.98-1.76) in colon cancer patie

163 imatinib prolonged recurrence-free survival (RFS) after resection of primary GI stromal tumor (GIST).

164 S) are prognostic for relapse-free survival (RFS) after surgical resection.

165 Recurrence-free survival (RFS) and cancer-specific survival (CSS) after hepatic re

166 Recurrence-free survival (RFS) and cancer-specific survival (CSS) rates after hepa

167 Recurrence-free survival (RFS) and overall survival (OS) after hepatectomy were wo

168 Recurrence-free survival (RFS) and overall survival (OS) after hepatic resection w

169 We compared relapse-free survival (RFS) and overall survival (OS) depending on the availabi

170 e vaccination (PV) on relapse-free survival (RFS) and overall survival (OS) in patients with resected

171 Results Relapse-free survival (RFS) and overall survival (OS) rates at 3 years were 80%

172 ted with increased recurrence-free survival (RFS) and overall survival (OS), in univariate and multiv

173 imary end points were relapse-free survival (RFS) and overall survival (OS).

174 m B) and observed for relapse-free survival (RFS) and overall survival.

175 overall survival and relapse-free survival (RFS) and the cumulative incidences of relapse and nonrel

176 y end points included relapse-free survival (RFS) and TRM.

177 Relapse-free survival (RFS) at 5 years was 17% versus 7% (P = .003).

178 survival (OS), and recurrence-free survival (RFS) by treating neuropathy status as a time dependent c

179 all survival (OS) and relapse-free survival (RFS) data demonstrate continued strong benefit from post

180 ion of each gene with relapse-free survival (RFS) for 433 patients who received chemotherapy alone (a

181 significantly shorter relapse-free survival (RFS) for those with high expression of either FUT1 or B3

182 all survival (OS) and relapse-free survival (RFS) in a phase 2 study of the bispecific T-cell engager

183 d with an unfavorable relapse-free survival (RFS) in breast cancer patients (HR = 1.93, 95%CI: 1.33-2

184 by FEC would improve relapse-free survival (RFS) in operable breast cancer.

185 DGFRA mutations on recurrence-free survival (RFS) in patients with gastrointestinal stromal tumors (G

186 his for predicting recurrence-free survival (RFS) is not established.

187 ssion had a median recurrence-free survival (RFS) of 5.3 vs 15.4 months for patients with high CHD5 e

188 rgery has improved recurrence-free survival (RFS) of patients with operable gastrointestinal stromal

189 all survival (OS) and relapse-free survival (RFS) only in the NPM1+ subgroup (OS: hazard ratio, 5.9;

190 P = 0.002); 3-year recurrence-free survival (RFS) rates were 33.5% with wild-type versus 13.5% with m

191 1-, 3-, and 5-year recurrence-free survival (RFS) rates were 96%, 60%, and 40%.

192 rvival (EFS), OS, and relapse-free survival (RFS) seen in univariate analysis was even greater in the

193 Relapse-free survival (RFS) was 52% in the alloSCT group compared with 33% in t

194 overall survival, and relapse-free survival (RFS) were assessed.

195 survival (OS) and recurrence-free survival (RFS) were compared.

196 survival (OS) and recurrence free survival (RFS) were determined by Cox proportional hazards models

197 elapse mortality, and relapse-free survival (RFS) were estimated at 19.5%, 15.5%, and 64.7%, respecti

198 heir association with relapse-free survival (RFS) were evaluated using microarray data from 148 patie

199 es of on-treatment recurrence-free survival (RFS) were performed, and exploratory survival end points

200 verall survival (OS), relapse-free survival (RFS), and complete remission rates (CR) were not influen

201 verall survival (OS), relapse-free survival (RFS), and distant RFS (DRFS) estimates were similar for

202 s with SLN status, recurrence-free survival (RFS), and melanoma-specific survival (MSS) were analyzed

203 event-free survival, relapse-free survival (RFS), and overall survival (OS) rates for the whole coho

204 mary objective was recurrence-free survival (RFS), and the secondary objectives included survival.

205 Recurrence-free survival (RFS), disease-specific survival (DSS), and overall survi

206 Recurrence-free survival (RFS), distant metastasis (DM), and local recurrence (LR)

207 redictors of worse recurrence-free survival (RFS), namely, an NLR >/= 5 (P < 0.0001, hazard ratio, HR

208 n), overall survival, relapse-free survival (RFS), nonrelapse mortality, and acute or chronic GVHD we

209 n (HSCT) realization, relapse-free survival (RFS), overall survival (OS), and incidence of adverse ev

210 was overall survival; relapse-free survival (RFS), relapse-free interval, and toxicity were secondary

211 an impact on their recurrence-free survival (RFS).

212 ated with superior recurrence-free survival (RFS).

213 primary end point was relapse-free survival (RFS).

214 ilure pattern, and recurrence-free survival (RFS).

215 primary end point of relapse-free survival (RFS).

216 Primary end point was relapse-free survival (RFS).

217 mary end point was recurrence-free survival (RFS).

218 fficacy end point was relapse-free survival (RFS).

219 Recurrence-free survival (RFS).

220 me measurement was recurrence-free survival (RFS).

221 all survival (OS) and relapse-free survival (RFS).

222 nt was 12-month HG recurrence-free survival (RFS).

223 ary end point was PSA relapse-free survival (RFS).

224 imary endpoint was recurrence-free survival (RFS); intention-to-treat (ITT) analysis was conducted af

225 predicted a lower recurrence-free survival (RFS; all P < .01).

226 NSCLC who had shorter relapse-free survival (RFS; hazard ratio [HR], 2.35; 95% CI, 1.29 to 4.28; P =

227 significantly better relapse-free survival (RFS; P < .001), overall survival (OS; P < .001), and eve

228 al (OS; P = .005) and relapse-free survival (RFS; P = .002) than did MRD status at CR (P = .11 and P

229 [CI], 1.04-1.81), and relapse-free survival (RFS; P = .005; HR, 1.52; 95% CI, 1.13-2.05) than DNMT3A(

230 d the other regarding relapse-free survival (RFS; PINARFS), were derived from data of 572 patients wi

231 Recurrence-free survival (RFS; primary end point), distant metastasis-free surviva

232 ics, and outcomes (recurrence-free survival [RFS] and overall survival [OS]), were studied.

233 Recurrence-free survivals (RFS) were calculated using the Kaplan-Meier method.

234 (PT) dysfunction and renal Fanconi syndrome (RFS).

235 cipients with HCC does not improve long-term RFS beyond 5 years.

236 Here, we demonstrate that RFS-1/RIP-1 acts by shutting down RAD-51 dissociation fr

237 Using stopped-flow experiments, we show that RFS-1/RIP-1 confers this dramatic stabilization by cappi

238 On multivariable analysis, the RFS rate was lower with increasing tumor size, small bow

239 cirr of size smaller than 3 cm; however, the RFS still remains lower than that in patients of group T

240 meeting the cellulosic biofuel target in the RFS using Miscanthus x giganteus reduces system profits

241 stinguishable: we observed inhibition of the RFS soil hyphal network and significant reductions in M.

242 a result of using corn stover to satisfy the RFS.

243 emissions have played a role in shaping the RFS, water implications are less understood.

244 otprint of six scenarios are compared to the RFS, including shale oil, coal-to-liquids, shale gas-to-

245 These changes were specific to the RFS-kappaLC variable (V) sequence, because they did not

246 Exposure of PT cells to RFS-kappaLCs resulted in kappaLC accumulation within enl

247 to identify key biologic processes linked to RFS.

248 atients with stage I disease with respect to RFS, DSS, and OS.

249 worse in patients with midgut origin tumors (RFS rate at 3 years: 15% vs 27%, P < 0.001; OS rate at 3

250 otic counts were associated with unfavorable RFS in the 1-year group but not in the 3-year group.

251 The main outcome was RFS.

252 The primary end point was RFS; secondary end points were OS and immunologic respon

253 The primary end point was RFS; the secondary end points included overall survival

254 The primary endpoint of this study was RFS.

255 When RFS and survival of the patients were compared within th

256 tatus remained significantly associated with RFS in arm A and not significantly associated in arm C (

257 of STILs was prognostically associated with RFS in patients treated with chemotherapy alone but not

258 bly, CHD7 expression was not associated with RFS or OS for patients not receiving gemcitabine.

259 Seven genes associated with RFS were further examined by quantitative reverse transc

260 notype was not significantly associated with RFS.

261 d DeltaFTV4 had significant association with RFS, as did HR/HER2 status and RCB class.

262 ating lymphocytes and their association with RFS.

263 (TNR >/= 2) was a strong predictor for worse RFS (hazard ratio, 13.52; 95% confidence interval, 4.77-

264 nd TNR were significant predictors for worse RFS.

265 High CCI is a potent predictor of worse RFS and CSS after resection of CLM.

266 ly available independent predictors of worse RFS, grade 4 HCC's (P < 0.0001, HR: 5.6), vascular invas

267 The estimated 10-year RFS rate was 14% (95% CI, 9%-22%) for all relapses and 2

268 57% (95% CI, 54%-61%) (P < .001) and 10-year RFS rates 79% (95% CI, 74%-83%) and 50% (95% CI, 46%-53%

269 57% (95% CI, 20%-82%) (P = .003) and 10-year RFS rates 89% (95% CI, 81%-94%) and 44% (95% CI, 18%-68%

270 age IA and stage IB disease in 5- or 10-year RFS, DSS, or OS.

271 remission were censored at SCT time, 2-year RFS was 53.3% (95% CI, 39% to 66%) in the CLARA arm and

272 ated with R-CHOP experienced inferior 3-year RFS compared with those who received intensive front-lin

273 oSCT was not associated with improved 3-year RFS or OS.

274 The 3-year RFS rates in the donor and no-donor groups were 71% and

275 nal tandem duplication (n = 148), the 3-year RFS rates in the donor and no-donor groups were 83% and

276 normal cytogenetics at CR (n = 183); 3-year RFS was 15% and 45%, and 3-year OS was 15% and 56%, resp

277 us non-autoSCT patients (n = 97), but 3-year RFS was inferior in patients who received R-CHOP compare

278 rse in patients with double mutation (3-year RFS, 3.1% vs 20% [P < 0.001]; 3-year OS, 44% vs 84% [P <

279 a median follow-up of 5.3 years, the 4-year RFS was 90.9% and 91.8% for six and four cycles, respect

280 athologic response (cPR) had superior 5-year RFS (72%) and lower post-LT recurrence (HR 0.52, P < 0.0

281 ermediate v poor) was associated with 5-year RFS (90.5% v 78.7% v 58.5%; P < .001), 5-year DM rates (

282 The estimated 5-year RFS in these groups were 85.5%, 83.9%, and 29.6% accordi

283 risk patients in the Pre-MORAL had a 5-year RFS of 17.9% compared with 98.6% for the low risk group

284 HDI (95% CI, 1.2 to 2.8 years) and a 5-year RFS of 48% versus 39%.

285 ths (95% CI, 7.5 to 11.2 months); the 5-year RFS probability rates were 31.2% (95% CI, 26.7% to 35.9%

286 When using the AJCC classification, 5-year RFS rates for stages I through III were 78%, 53%, and 33

287 Using the ENETS classification, 5-year RFS rates for stages I to III were 100%, 70%, and 53% (P

288 fter their metastatic recurrence, the 5-year RFS rates for stages I to III were 90%, 73%, and 66% acc

289 were 80% versus 66% (P = 0.034), and 5-year RFS rates were 48% versus 18% (P < 0.001) for SR and RFA

290 e 81% versus 76% (P = 0.136), whereas 5-year RFS rates were 49% versus 24% (P < 0.001) for SR and RFA

291 those assigned to the 1- year group; 5-year RFS was 71.1% versus 52.3%, respectively (hazard ratio [

292 mediate-risk disease (5-year OS, 28%; 5-year RFS, 27%), and 15% of all patients and 29% of responding

293 had high-risk disease (5-year OS, 3%; 5-year RFS, 5%), respectively.

294 had low-risk disease (5-year OS, 74%; 5-year RFS, 55%); 56% of all patients and 39% of responding pat

295 ], 0.46; 95% CI, 0.32-0.65; P < .001; 5-year RFS, 65.6% vs 47.9%, respectively) and longer overall su

296 group compared with the 1-year group (5-year RFS, 71.0% vs 41.3%; P < .001), whereas no significant b

297 0.79; 95% CI, 0.60 to 1.04; P = .087; 5-year RFS, 86.6% for TX/CEX v 84.1% for T/CEF).

298 .87; 95% CI, 0.76 to 1.00; P = .055); 7-year RFS rate was 39.1% versus 34.6%.

299 Three-year RFS and OS did not differ significantly for patients in

300 Three-year RFS and OS rates did not differ significantly for autoSC