ライフサイエンスコーパス: RFS

1 RFS of patients beyond Milan but within Metroticket 2.0

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

3 RFS remains significantly longer for patients treated wi

4 RFS significantly correlated with pCR and radiographic r

5 RFS was higher in patients with complete/extensive versu

6 ; 95.6% repeated CI, 0.61 to 0.99; P = .044; RFS: HR, 0.85; 99.4% CI, 0.66 to 1.09; P = .065).

7 dergoing upfront LDLT (5-y OS 65%, P = 0.06; RFS 66%, P = 0.33, respectively).

8 nths for patients who did not (OS: P = 0.06; RFS: P = 0.04).

9 .5 months (95% CI, 42.6 to 49.3 months), 126 RFS events and 82 deaths were recorded.

10 Pembrolizumab (190 RFS events) compared with placebo (283 RFS events) resul

11 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

12 (190 RFS events) compared with placebo (283 RFS events) resulted in prolonged RFS in the overall pop

13 f nCRT based on the formula cRFS3 = RFS(x+3)/RFS(x).

14 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;

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

16 In contrast, actuarial RFS rates for similar intervals were 79.1% (95% CI 72.5%

17 ystem would achieve more GHG savings than an RFS-compliant system: 10.7 TgCO(2) year(-1) in the non R

18 factors confirmed shorter OS (P < 0.001) and RFS (P < 0.001) in BRAF-mut.

19 27 vs 38 months, respectively; P = .009) and RFS (126 vs 18 months, respectively; P = .007).

20 78 (+/-0.03) vs 0.71 (+/-0.04), p < 0.05 and RFS (C-statistic = 0.76 ( +/- 0.05), vs 0.63 ( +/- 0.01)

21 In logrank analyses, CIR and RFS at 5 years were improved in recipients of four cours

22 s 4.9% and median overall survival, CSS, and RFS were 39, 42, and 15 months, respectively.

23 the latter in predicting long-term DRFI and RFS, especially in N0, ER/PR-positive, and HER2-negative

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

25 two clusters differ significantly for OS and RFS (p-value < 0.0001).

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

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

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

29 te were independently associated with OS and RFS on multivariate analysis.

30 Five-year post-LT OS and RFS was higher in MC (71.3% and 68.2%) compared with DS

31 e AUC increased by 5.7% and 13.0% for OS and RFS, respectively.

32 It had 2 coprimary end points: OS and RFS.

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

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

35 ncidental diagnosis as confounders on OS and RFS.

36 , 45 with RFS, and only 22 with both pCR and RFS (3.2%).

37 atures allowed for the prediction of pCR and RFS, both overall and within the residual disease group.

38 x regression were performed to model pCR and RFS, respectively.

39 S was analyzed as the primary end point, and RFS, OS, and recurrences in the regional lymph node basi

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

41 correlated with a higher pCR rate and better RFS.

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

43 ed extensive or complete necrosis had better RFS, supporting the practice of neoadjuvant treatment be

44 minus pre-LDLT) >2000 ng/mL predicted better RFS; Grade III/IV predicted worse OS in DS patients.

45 s of follow-up, THL had significantly better RFS and OS than did TH (RFS hazard ratio, 0.32; 95% CI,

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

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

48 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

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

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

51 pletion of nCRT based on the formula cRFS3 = RFS(x+3)/RFS(x).

52 l accounts for SOC losses, while the current RFS estimates do not include effects on SOC.

53 These results suggest that the current RFS GHG reduction threshold may not be the most efficien

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

55 ot superior to observation in terms of DMFS, RFS, or OS and support not recommending CLND in patients

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

57 Patients with POLEmut EC had an excellent RFS in both trial arms.

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

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

60 ysis with hazard ratios of 3.1 (1.6-6.0) for RFS (P = 0.0009) and 3.8 (1.6-9.0) for DRFI (P = 0.0028)

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

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

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

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

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

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

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

68 cancer-specific (CSS), and recurrence-free (RFS) survivals were analyzed along with independent risk

69 ion, was a strong predictor of relapse-free (RFS) and overall survival (OS) (p < 0.001, p < 0.001 res

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

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

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

73 of high-dose Ara-C reduced CIR and improved RFS, it did not result in a significant OS benefit.

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

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

76 of response significantly predicted improved RFS.

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

78 in high-risk EC, with significantly improved RFS with adjuvant CTRT for p53abn tumors, regardless of

79 t symptoms were not associated with improved RFS.

80 ith a statistically significant advantage in RFS with MAC.

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

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

83 There was no significant difference in RFS between the two arms (median, 30.4 months in arm A v

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

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

86 ned and clinically meaningful improvement in RFS at 3-year median follow-up.

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

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

89 229, and a reference ALV-E strain, RAV60, in RFS chickens.

90 t was pCR, and secondary end points included RFS, OS, and gene expression analyses.

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

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

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

94 toxicity and new perspectives on LC-induced RFS.

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

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

97 <50%; OS: 42.3 vs 24.3 months, P < 0.001; L-RFS-27.3 vs 14.1 months, P = 0.042; MFS-29.3 vs 13 month

98 ed (NR) vs 40.3 vs 26.1 months, P < 0.001; L-RFS-NR vs 24.5 vs 21.4 months, P = 0.044; MFS-NR vs 23.7

99 There was no difference in L-RFS, MFS, or OS between patients who received FLX or GNP

100 with NAC FLX or GNP result in improved OS, L-RFS, and MFS in PDAC.

101 OS, L-RFS, and MFS were superior in patients with marked bioch

102 ival (OS), local recurrence-free survival (L-RFS), and metastasis-free survival (MFS) associated with

103 Local RFS and DSS were both significantly shorter in the trans

104 the route of biopsy did not influence local RFS (P = 0.128) or DSS (P = 0.096).

105 ) and significantly associated with a longer RFS (hazard ratio 0.55, 95% confidence interval 0.29-0.9

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

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

108 ars of planned adjuvant treatment had longer RFS.

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

110 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 <

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

112 patients developed recurrence, with a median RFS of 120 (95% confidence interval, 69-150) months.

113 % 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])

114 9.8 months (95% CI, 8.5 to 14.9), and median RFS was 7.6 months (95% CI, 4.5 to 9.5).

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

116 The median RFS was 18.4 months (95% CI, 13.5 to 24.8 months).

117 The 24-month RFS probability was 53.3% (95% CI, 0.36 to 0.68) with pl

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

119 Neck node RFS was 89.6% (95% CI, 0.83% to 0.94%) at 2 years in the

120 Secondary outcomes were 5-year neck node RFS, 2- and 5-year disease-specific survival (DSS), and

121 ant system: 10.7 TgCO(2) year(-1) in the non RFS-compliant system compared with 4.4 TgCO(2) year(-1)

122 Thus, taken as a whole, the non RFS-compliant system would achieve more GHG savings than

123 biofuel will be produced compared to the non RFS-compliant system.

124 and 46.30 +/- 10.05 gCO(2) MJ(-1) in the non RFS-compliant system.

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

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

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

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

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

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

131 d CD8 infiltration was a strong predictor of RFS and OS and associated strongly with disease stage (A

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

133 >10 cm remained independently prognostic of RFS [hazard ratio (HR) 3.85, 95% confidence interval (CI

134 ct of planned adjuvant treatment duration on RFS.

135 hat adjuvant imatinib has an overt impact on RFS.

136 The impact of pembrolizumab on RFS was similar in subgroups, in particular according to

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

138 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)

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

140 tations were not associated with worse OS or RFS.

141 There were no differences in OS/RFS for patients who were bridged or downstaged.

142 in DS+LDLT versus non-DS LDLT group (5-y OS/RFS-48%/40%).

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

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

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

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

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

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

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

150 AJCC 8 significantly predicted RFS and OS.

151 were selected to create nomograms predicting RFS and OS.

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

153 acebo (283 RFS events) resulted in prolonged RFS in the overall population (3-year RFS rate, 63.7% v

154 ar median follow-up, pembrolizumab prolonged RFS (hazard ratio [HR], 0.57; P < .0001) compared with p

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

156 st FRalpha is also associated with prolonged RFS.

157 f the samples were obtained using a FT-Raman RFS/100 spectrometer in the spectral range of 3500-400 c

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

159 her pCR rate, showed a significantly shorter RFS.

160 dual HER2-targeting resulted in significant RFS and OS benefits.

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

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

163 The Renewable Fuel Standard (RFS) program specifies a greenhouse gas (GHG) reduction

164 DS patients had superior RFS (60% vs. 54%, P = 0.043) and lower 5-year HCC-R (18%

165 5.0%, P < 0.0001) and relapse-free survival (RFS) (90.0% vs. 80.5%, P = 0.0003).

166 2-year, and 3-year recurrence-free survival (RFS) [overall survival (OS)] rates were 23.5 (58.8) mont

167 response (pCR) and recurrence-free survival (RFS) after neoadjuvant chemotherapy (NAC).

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

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

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

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

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

173 cant benefits in both relapse-free survival (RFS) and overall survival (OS) for high-dose interferon

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

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

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

177 nt improvements in recurrence-free survival (RFS) and overall survival compared with capecitabine.

178 0.3 months, median recurrence-free survival (RFS) and overall survival were not reached.

179 endpoint was local recurrence free survival (RFS) and the secondary endpoint was DSS.

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

181 come was neck node recurrence-free survival (RFS) at 2 years.

182 erall survival and recurrence-free survival (RFS) at 5 years were 81.9% (95% CI 74.0%-87.6%) and 60.4

183 n the basis of 351 recurrence-free survival (RFS) events at a 1.25-year median follow-up, pembrolizum

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

185 survival (OS) and recurrence free survival (RFS) for patients who received postoperative therapy wer

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

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

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

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

190 not predictive of recurrence-free survival (RFS) or overall survival (OS).

191 all survival (OS) and relapse free survival (RFS) outcomes.

192 Median recurrence-free survival (RFS) was 22 and 10 months for BRAF-wt and BRAF-mut patie

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

194 Relapse-free survival (RFS) was the primary endpoint of this trial.

195 survival (OS) and recurrence-free survival (RFS) were 82%, 57%, and 77%, 51%, respectively, comparab

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

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

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

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

200 GEMOX) would increase relapse-free survival (RFS) while maintaining health-related quality of life (H

201 all survival (OS), recurrence-free survival (RFS), and HCC recurrence (HCC-R) were compared between p

202 all survival (OS), recurrence-free survival (RFS), and overall recurrence rates using the random-effe

203 nce of relapse (CIR), relapse-free survival (RFS), and overall survival (OS).

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

205 all survival (OS), recurrence-free survival (RFS), disease-specific mortality (DSM), and time-to-recu

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

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

208 Here, we report relapse-free survival (RFS), overall survival (OS), and gene expression signatu

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

210 Recurrence-free survival (RFS), the primary outcome measure, was evaluated accordi

211 fier in predicting recurrence-free survival (RFS).

212 survival (OS) and recurrence-free survival (RFS).

213 as to evaluate median relapse-free survival (RFS).

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

215 Recurrence-free survival (RFS).

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

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

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

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

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

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

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

223 48], p = 0.0004), and relapse-free survival (RFS; HR 1.92 [1.34-2.76], p = 0.0004).

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

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

226 y known as the rapid feathering-susceptible (RFS) line, of chickens lacks all endogenous ALV and is f

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

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

229 significantly better RFS and OS than did TH (RFS hazard ratio, 0.32; 95% CI, 0.14 to 0.71; P = .005;

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

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

232 The RFS rate at 36 months was 35.4% (95% CI, 22.5% to 47.9%)

233 andard chemotherapy versus capecitabine, the RFS rates were 56% and 50%, respectively (hazard ratio [

234 43% by AF227 in combination with SB-1 in the RFS chickens under controlled conditions.

235 e spontaneous LL-like tumor incidence in the RFS chickens.

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

237 ethanol: 34.39 +/- 4.92 gCO(2) MJ(-1) in the RFS-compliant system and 46.30 +/- 10.05 gCO(2) MJ(-1) i

238 em compared with 4.4 TgCO(2) year(-1) in the RFS-compliant system.

239 phomas and nonmalignant bursa tissues of the RFS line of birds identified hundreds of differentially

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

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

242 e the effects of the GHG threshold under the RFS on projected GHG savings from two corn stover-based

243 er-based cellulosic biofuel system under the RFS program.

244 tical biorefinery systems complying with the RFS will not process the more GHG-intensive corn stover,

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

246 to identify key biologic processes linked to RFS.

247 atients were well stratified with respect to RFS by Milan criteria, Metroticket 2.0 criteria, and AFP

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 With longer follow-up, RFS remains superior for standard adjuvant chemotherapy

252 Here, we report an updated RFS analysis at the 3.05-year median follow-up.

253 The main outcome was RFS.

254 Primary end points were RFS and HRQOL.

255 The two coprimary end points were RFS in the overall population and in those with programm

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

257 ciations were found in 215 with pCR, 45 with RFS, and only 22 with both pCR and RFS (3.2%).

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

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

260 objectives were risk factors associated with RFS, relapse, and death and treatment modalities after r

261 Cirrhosis was positively associated with RFS, while incidental diagnosis was not.

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

263 ating lymphocytes and their association with RFS.

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

265 nd TNR were significant predictors for worse RFS.

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

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

268 Factors associated with worse RFS were node-positive primary tumor, >=4 CRLM, and posi

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

270 57% (95% CI, 54%-61%) (P < .001) and 10-year RFS rates 79% (95% CI, 74%-83%) and 50% (95% CI, 46%-53%

271 57% (95% CI, 20%-82%) (P = .003) and 10-year RFS rates 89% (95% CI, 81%-94%) and 44% (95% CI, 18%-68%

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

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

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

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

276 longed RFS in the overall population (3-year RFS rate, 63.7% v 44.1% for pembrolizumab v placebo, res

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

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

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

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

281 2 cm) iCCA exhibited superior pooled 5-year RFS (67%, 95%CI: 47%-86%) versus advanced iCCA (34%, 95%

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

283 The 5-year RFS and OS also showed no difference (HR, 1.01 and 0.99,

284 The 5-year RFS and the 2- and 5-year DSS and OS were not significan

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

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

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

288 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%

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 The pooled 1-, 3-, and 5-year RFS rates were 70% (95%CI: 63%-75%), 49% (95%CI: 41%-57%

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

293 The 5-year RFS with CTRT versus RT for p53abn EC was 59% versus 36%

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

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

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

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

298 Five-year RFS was 48% for patients with p53abn EC, 98% for POLEmut

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