ライフサイエンスコーパス: DFS

1 DFS and OS were analyzed using Kaplan-Meier curves and m

2 DFS and OS were significantly better for BR/LA PDAC pati

3 DFS at 2 years: Lap 80%; Open 82% (difference, 2.0%; 95%

4 DFS estimates for patients with ACC improved dramaticall

5 DFS events (n = 148) were much less than required (n = 4

6 DFS was 68.7% at 3 years (75 recurrences).

7 DFS was independently influenced by 3 factors: circumfer

8 DFS was longer in the (18)F-FMISO-negative patients (P =

9 DFS was not significantly prolonged with capecitabine ve

10 DFS was significantly better for the azacitidine treatme

11 DFS was similar for the combined group of stage I-III pa

12 roup LR (OS 73%/63% vs. 58%/35%, P = 0.0007; DFS 69%/61% vs. 27%/21%, P < 0.0001).

13 fidence interval [CI], 0.97-1.00; P = 0.013; DFS: HR, 0.99; CI, 0.98-1.00; P = 0.028).

14 CI: 98%, 100%), and 99% (95% CI: 98%, 100%); DFS of 94% (95% CI: 92%, 97%), 91% (95% CI: 88%, 96%), 8

15 erquartile range, 58-74 months), 157 and 156 DFS events were observed in arms 1 and 2, respectively (

16 ched liver resection patients (P >/= 0.176); DFS in this propensity matched cohort was greater after

17 median follow-up of 6.5 years, there were 23 DFS events.

18 were calculated as follows: CDFS3 = DFS(x+3)/DFS(x).

19 me of LT) (OS 54%/54% vs. 73%/63%, P = 0.35; DFS 48%/48% vs. 69%/61%, P = 0.18, respectively).

20 The final analysis was done at 709 DFS events (letrozole, 341 [16.5%]; anastrozole, 368 [17

21 ,140 men and 45% of 12,712 men experienced a DFS and MFS event, respectively.

22 fit from the addition of capecitabine with a DFS HR of 0.53 versus 0.94 in those with basal phenotype

23 rrhosis and (ii) single HCC lesion, although DFS was worse.

24 was 8.1 versus 20.0 months (P < 0.0001), and DFS 4.0 versus 10.5 months (P < 0.001).

25 ce interval (CI) = 0.50-0.94, P = 0.020] and DFS (HR = 0.73, 95% CI: 0.54-0.99, P = 0.040).

26 tio (HR) = 0.42 (0.17-0.99), P = 0.0498] and DFS [HR = 0.57 (0.37-0.88), P = 0.0116].

27 (HR 0.73 (95% CI 0.33-1.63), P = 0.442) and DFS (HR 0.68 (95% CI 0.34-1.34), P = 0.261) in the same

28 (HR 0.81 (95% CI 0.42-1.54), P = 0.512), and DFS (HR 1.01 (95% CI 0.56-1.81), P = 0.972).

29 rvival (HR, 0.91 [95% CI, 0.54 to 1.53]) and DFS in the clinical high and genomic high-risk subgroup

30 MAC is associated with better OS, EFS, and DFS.

31 End points included OS, MCCSS, and DFS.

32 of lower vitamin D with poorer OS, MSS, and DFS were independent of this association.

33 s independently associated with worse OS and DFS (OS: hazard ratio [HR], 0.98; confidence interval [C

34 OS and DFS analyses were performed using Kaplan-Meier curves an

35 OS and DFS did not differ significantly between the groups by p

36 used to control the effect of POC on OS and DFS for: 1) Method used to define postoperative complica

37 calculate pooled effect estimate for OS and DFS hazard ratios (HR), estimating between-study varianc

38 Both OS and DFS improved with up to 20 to 25 lymph nodes removed, re

39 D-positive category, AlloSCT prolongs OS and DFS to equal those of the FR category.

40 Two-year OS and DFS were 74% and 61% in the FR category, 42% and 45% in

41 (HR) between hospital volume and both OS and DFS.

42 from diagnosis associated with higher OS and DFS.

43 ant chemotherapy were correlated with OS and DFS.

44 to identify independent predictors of OS and DFS.

45 gery were associated with higher overall and DFS.

46 to establish the association between TD and DFS.

47 ed for these seconday outcomes, OS, TTP, and DFS did not differ between groups at a minimum follow-up

48 ary outcomes analyzed here were OS, TTP, and DFS.

49 estate the difficulties inherent to applying DFS to polymer-linked adhesion and present an approach t

50 tcomes were similar in the EC-T and TC arms (DFS, 89.6% [95% CI, 87.9% to 91.5%] v 89.9% [95% CI, 88.

51 isk STS, HT was not associated with a better DFS or OS, suggesting that A+I should remain the regimen

52 were independently correlated with a better DFS.

53 tage III patients was associated with better DFS (p = 0.006).

54 ge II colon cancer patients, and with better DFS in stage III colon cancer patients treated with adju

55 Differences between DFS in a four-arm comparison were significant (P = .01),

56 re used to evaluate the relationship between DFS and treatment adherence (persistence [duration] and

57 Biochemical DFS, the primary end point, was defined from entry until

58 geneity P = .79 and P = .66, for biochemical DFS and progression-free survival, respectively).

59 T plus AS significantly improved biochemical DFS (HR, 0.52; 95% CI, 0.41 to 0.66; P < .001, with 319

60 surgery were calculated as follows: CDFS3 = DFS(x+3)/DFS(x).

61 djuvant AS improves biochemical and clinical DFS of intermediate- and high-risk cT1b-c to cT2a (with

62 The cumulative DFS rates in the first, second, and third years were 75.

63 to 2 tumors derived most benefit from EC-D (DFS: interaction P = .02; and OS: interaction P = .03).

64 A total of 736 iDFS and 548 D-DFS events and 533 deaths were observed.

65 chi(2), 48.9 iDFS; P < .001; chi(2), 55.8 D-DFS; P < .001; chi(2), 48.5 OS; P < .001).

66 3-year iDFS was 92% (95% CI, 89% to 98%), D-DFS was 97% (95% CI, 95% to 99%), and OS was 99% (95% CI

67 for iDFS, 0.83 (95% CI, 0.79 to 0.88) for D-DFS, and 0.84 (95% CI, 0.79 to 0.89) for OS.

68 end point), distant disease-free survival (D-DFS), and overall survival (OS), fitting sTILs as a cont

69 y non-responders in regard of all endpoints (DFS p < 0.001, LC p = 0.003, OS p = 0.001).

70 The 5-year estimated DFS rate was 84.9% for letrozole versus 82.9% for anastr

71 To evaluate DFS and overall survival (OS) in ccRCC high-risk patient

72 For DFS and MFS, 61% and 90% of the patients, respectively,

73 0.004 for OS, 0.60 (0.40-0.90)p = 0.014 for DFS).

74 5% CI, 1.00 to 1.04; P = .048), and 1.02 for DFS (95% CI, 1.00 to 1.04; P = .0427).

75 In cohort 1, for DFS and OS, a significant treatment effect was found for

76 r OS, 0.63 (95% CI: 0.26, 1.52; P = .30) for DFS, and 0.83 (95% CI: 0.26, 2.74; P = .77) for LPFS.

77 .36 (1.54-3.61) for OS, 2.37 (1.47-3.80) for DFS (both p < 0.001), superseding T and N categories.

78 ated ( R(2), 0.73 [95% CI, 0.53 to 0.82] for DFS and 0.92 [95% CI, 0.81 to 0.95] for MFS).

79 au correlation with OS was 0.85 and 0.91 for DFS and MFS, respectively.

80 values generated by the training cohort for DFS (p = 0.025) and OS (p = 0.002), external validation

81 R status on treatment effect was evident for DFS (adjusted P = .06) and OS (adjusted P = .04).

82 TDs is an independent prognostic factor for DFS in patients with stage III CC.

83 9], P = .94) and BRAF V600E mutation (HR for DFS: 1.22 [95% CI, 0.81-1.85], P = .34; HR for OS: 1.13

84 tellite-stable tumors that both KRAS (HR for DFS: 1.64 [95% CI, 1.29-2.08], P < .001; HR for OS: 1.71

85 ], P = .002) and BRAF V600E mutation (HR for DFS: 1.74 [95% CI, 1.14-2.69], P = .01; HR for OS: 1.84

86 variate analysis, MSI (hazard ratio [HR] for DFS: 1.10 [95% CI, 0.73-1.64], P = .67; HR for OS: 1.02

87 status and treatment group was observed for DFS ( P = .04) but not for OS ( P = .07).

88 lated with a significantly worse outcome for DFS in the 10/10 HLA match group (HR, 1.77; CI, 1.26-2.5

89 = 0.009) were both positively prognostic for DFS, remaining upon multivariate analysis.

90 Adjusted hazard ratios for DFS and OS were, respectively, 1.12 (95% CI, 0.98 to 1.5

91 which precluded statistical significance for DFS in a joint model.

92 ation using these cutoffs was successful for DFS (p = 0.002) but not for the other investigated endpo

93 e primary outcomes were 5-year disease-free (DFS) and overall survival (OS).

94 outcomes were overall (OS) and disease-free (DFS) survival in SNB only vs SNB + AD patients, assessed

95 tive/HER2 low FISH ratio (>/=2 to <5) group (DFS: 3-way ITT Pvalue for interaction = .07; censored =

96 , whereas a statistically significant higher DFS was achieved in treated patients (P = 0.036).

97 078; HR RR, GO 40% v No-GO 73%, P = .016; HR DFS, GO 47% v No-GO 28%, P = .135).

98 Node positivity negatively impacted DFS (p = 0.04).

99 GemErlo for 24 weeks did not improve DFS or overall survival over Gem.

100 abilitation independently predicted improved DFS (hazard ratio 0.45; 95% confidence interval, 0.21-0.

101 ition of nelarabine to ABFM therapy improved DFS for children and young adults with newly diagnosed T

102 prehabilitation was associated with improved DFS (73.4% vs 50.9%, P = 0.044).

103 ture positivity was associated with improved DFS (hazard ratio [HR], 0.67; 95% CI, 0.48 to 0.92; P =

104 of patients and was associated with improved DFS (HR, 0.70; 95% CI, 0.51 to 0.96; P = .026 for sTILs

105 erapy is feasible and significantly improves DFS.

106 Although there was no difference in DFS between anatomical and nonanatomical resections in p

107 There was no difference in DFS observed between the HR and standard-risk groups (P

108 There was no difference in DFS or OS according to BMI in the non-docetaxel group, w

109 of therapy altered the lack of difference in DFS or OS in this population of patients with high-risk

110 ose without MD (95% CI for the difference in DFS, 0.17-0.23; P = .004).

111 No differences in DFS (adjusted hazard ratio [HR], 0.87; 95% CI, 0.61 to 1

112 is, there were no significant differences in DFS (hazard ratio, 0.82; P = .45) or OS (hazard ratio, 1

113 d not demonstrate significant differences in DFS or OS in Protocol A or Protocol B.

114 We observed no differences in DFS or overall survival in all randomly assigned patient

115 show a statistically significant increase in DFS by adding extended capecitabine to standard chemothe

116 e did not produce a significant reduction in DFS events in hormone receptor-negative early breast can

117 ing all prescribed ASNase doses had inferior DFS (hazard ratio [HR], 1.5; 95% CI, 1.2 to 1.9; P = .00

118 ize <= 2 cm on final pathology, had inferior DFS but not overall survival in the entire cohort.

119 of ASNase doses is associated with inferior DFS in higher-risk patients.

120 CYP2C19*2 or *19 alleles did not influence DFS.

121 007; IR RR, GO 44% v No-GO 57%, P = .044; IR DFS, GO 51% v No-GO 40%, P = .078; HR RR, GO 40% v No-GO

122 The surprisingly long DFS and OS in these patients represent a challenge to ad

123 ion was associated with significantly longer DFS (HR, 0.23 [95% CI, 0.06-0.92]; P = .04) but not OS (

124 heir tumors experienced significantly longer DFS.

125 ore was significantly associated with longer DFS (HR = 0.17; P = 0.015).

126 ore was significantly associated with longer DFS (HR = 0.19; P = 0.011) independent of clinical stage

127 sis, lung primary was associated with longer DFS [hazard ratio (HR): 0.49, P = 0.008).

128 ion (LR RR, GO 13% v No-GO 35%, P = .001; LR DFS, GO 79% v No-GO 59%, P = .007; IR RR, GO 44% v No-GO

129 ollowed for a minimum 2 years to assess LRR, DFS, and overall survival (OS).

130 Median DFS and overall survival have not been reached; 5-year D

131 Median DFS was 71.4 months (interquartile range, 3 months to no

132 Median DFS was not reached for 3 years of sorafenib or for plac

133 had worse DFS at univariate analysis (median DFS: 20 vs 15 months, P < 0.01).

134 There was no difference in median DFS (GemErlo 11.4 months; Gem 11.4 months) or median ove

135 The median DFS for pCR patients was 29 months and OS 76 months.

136 Post-adrenalectomy, the median DFS was 18 months (1-year DFS: 54%, 5-year DFS: 31%).

137 The 12-month DFS was estimated at 64% for the azacitidine group and 4

138 mpared with those without an SF3B1 mutation (DFS, 132.8 vs. 174.4 months; P = 0.008).

139 gene for both end points was also observed (DFS Pvalue for interaction = .06; OS = .02), indicating

140 information about the changing likelihood of DFS over time.

141 on of rectal cancer based on the outcomes of DFS and recurrence.

142 val), serving as an independent predictor of DFS and OS in PHC patients with surgical resection.

143 PNI was the only independent predictor of DFS in R0/N0 tumors (hazard ratio [HR]: 2.2) and in PDAC

144 N-stage was the only predictor of DFS.

145 was no significant difference in the risk of DFS events (hazard ratio [HR], 1.00; 95% CI, 0.78 to 1.2

146 We evaluated the surrogacy of DFS and MFS for OS by using a two-stage meta-analytic va

147 POC had also a negative impact on DFS.

148 dentify two SNPs associated with early-onset DFS, rs715212 (P meta = 3.54 x 10(-5)) and rs10963755 (P

149 d no impact on the 3-year OS (P = 0.8868) or DFS (P = 0.9409).

150 tal number of nodes removed and 5-year OS or DFS was plotted using restricted cubic spline functions.

151 y status beforehand, without affecting OS or DFS.

152 n surgery in effects on 2-year recurrence or DFS and OS.

153 ltivariate models for overall survival (OS), DFS and a competing risk analysis for HCC recurrence.

154 5% in the longer interval group, and the OS, DFS, R0 resection rates, sphincter preservation, and com

155 =3 months, benefited most with regard to OS, DFS, and HCC-recurrence (HR: 0.49-0.59, P = 0.0079-0.024

156 tion between POC after CRLM resection and OS/DFS were sought using the PubMed and Web of Science data

157 e were no significant differences in overall DFS (P = .069) or OS (P = .77) across the three randomiz

158 metastatic risk and rapid decline in patient DFS.

159 ions of 33 laboratory variables with patient DFS.

160 NOX compared with upfront resected patients (DFS: 29.1 vs 13.7, P < 0.001; OS: 37.7 vs 25.1 months fr

161 ndent prognostic factor associated with poor DFS in stage II colon cancer patients, and with better D

162 The 5-year postinduction DFS and overall survival rates (+/- SE) of children rand

163 median follow-up of 52 months, the projected DFS and OS probabilities were 0.55 and 0.47 (log-rank P

164 somatic mutation carriers had more prolonged DFS and OS.

165 relapse after surgery (p = 0.05) and reduced DFS in multivariable analysis (p = 0.02).

166 The HR for reduced DFS was 1.38 [95% CI 1.27, 1.49], P < 0.0001.

167 MI in the non-docetaxel group, while reduced DFS and OS were observed with increasing BMI category in

168 score of < 90%) were associated with reduced DFS (multivariable model hazard ratio, 1.45; 95% CI, 1.0

169 endent negative prognostic factors regarding DFS and OS, and the occurrence of both is associated wit

170 RNA expression level is related to a shorter DFS (disease free survival) and OS (overall survival), s

171 on was significantly associated with shorter DFS (HR, 1.55 [95% CI, 1.23-1.95]; P < .001) and OS (HR,

172 s were significantly associated with shorter DFS and OS in patients with microsatellite-stable tumors

173 .95, P = 0.009) were associated with shorter DFS.

174 irentuximab had no statistically significant DFS (hazard ratio, 0.97; 95% CI, 0.79-1.18) or OS advant

175 aving pN2 disease (n = 35, 2.3%) had similar DFS as patients initially classified as pN2.

176 Exploratory analysis showed similar DFS with letrozole and anastrozole in all evaluated subg

177 e pN1a/b and pN1c populations showed similar DFS.

178 ere disease-free survival (DFS) and specific DFS (SDFS).

179 ening licensed origin-a "double fork stall" (DFS)-replication cannot be completed by conventional mea

180 sion had a significantly decreased survival (DFS, 69.0 vs. 147.9 months; P < 0.001).

181 r of overall (OS) and disease free survival (DFS) (p = 0.00001; p = 0.01, respectively).

182 hanging likelihood of disease-free survival (DFS) according to time elapsed after surgery.

183 all survival (OS) and disease-free survival (DFS) according to whether or not patients received adjuv

184 primary end point was disease-free survival (DFS) after a median of 5 years of follow-up.

185 new model to predict disease free survival (DFS) after surgical removal of primary breast cancer.

186 maintenance compared disease-free survival (DFS) among those receiving all prescribed PEG-ASNase dos

187 Disease-free survival (DFS) and metastasis-free survival (MFS) were determined

188 clinical outcomes by disease-free survival (DFS) and overall survival (OS) and benefit from trastuzu

189 s uncovered the worse disease-free survival (DFS) and overall survival (OS) associated with altered c

190 uvant girentuximab on disease-free survival (DFS) and overall survival (OS) in patients with localize

191 prognostic value for disease-free survival (DFS) and overall survival (OS) using Cox regression mode

192 these biomarkers and disease-free survival (DFS) and overall survival (OS) were analyzed with Cox pr

193 Disease-free survival (DFS) and overall survival (OS) were the primary and seco

194 ndary end points were disease-free survival (DFS) and overall survival (OS), estimated using the Kapl

195 rol, distant control, disease-free survival (DFS) and overall survival (OS).

196 primary outcomes were disease free survival (DFS) and overall survival (OS).

197 prognostic effect on disease-free survival (DFS) and overall survival (OS).

198 imary end points were disease-free survival (DFS) and overall survival (OS).

199 ndary end points were disease-free survival (DFS) and specific DFS (SDFS).

200 recurrence (LRR) and disease-free survival (DFS) at 2 years.

201 ective was to compare disease-free survival (DFS) between both arms.

202 e pregnancy rate, and disease-free survival (DFS) between patients with and without a pregnancy after

203 postinduction 5-year disease-free survival (DFS) compared with intrathecal methotrexate (IT MTX), wh

204 investigator-reported disease-free survival (DFS) comparing 3 years of sorafenib versus placebo.

205 nt decrease in RR and disease-free survival (DFS) for patients with higher CD33 expression (LR RR, GO

206 study was to improve disease-free survival (DFS) from 14 to 18 months by adding erlotinib to gemcita

207 The 4-year disease-free survival (DFS) from end-induction was 85.9% +/- 2.6%.

208 ation of neoadjuvant, disease-free survival (DFS) from the date of surgery, and post-recurrence survi

209 y end point of 2-year disease-free survival (DFS) greater than 85%, improving on historic data of 76%

210 all survival (OS) and disease-free survival (DFS) in 6042 patients from four cohorts.

211 capecitabine improves disease-free survival (DFS) in locally advanced rectal cancer.

212 Median disease-free survival (DFS) in the entire cohort was 21.3 months, whereas 1-, 3

213 associated with poor disease free survival (DFS) in univariate analysis (p = 0.056).

214 sessed if biochemical disease-free survival (DFS) is improved by adding 6 months of androgen suppress

215 demonstrated a 3-year disease-free survival (DFS) of 98.7%.

216 The disease-free survival (DFS) of patients with MDM2rs2279744 TT or MDM2rs937283 A

217 year overall (OS) and disease-free survival (DFS) of the whole series was 56% and 54%, respectively.

218 cator (p = 0.0006) of disease free survival (DFS) on our OSCC test cohort.

219 The mean disease-free survival (DFS) rate was 24.1 +/- 2.5 months.

220 The 5-year disease-free survival (DFS) rates for patients with T-ALL randomly assigned to

221 -RT results in 5-year disease-free survival (DFS) that is not worse than C-RT by more than 7.65% (H-R

222 all survival (OS) and disease-free survival (DFS) using data obtained from the international CRITICS

223 Disease-free survival (DFS) was the primary endpoint, and overall survival (OS)

224 all survival (OS) and disease-free survival (DFS) was worse for all categories of CLRT combined, than

225 e survival (EFS), and disease-free survival (DFS) were 78.2%, 58.1%, and 72.3% 5 years after HSCT.

226 ly, 5-yr/10-yr OS and disease-free survival (DFS) were better in group PLT versus group LR (OS 73%/63

227 001).Overall (OS) and disease-free survival (DFS) were both greater after tumor downstaging and trans

228 ic survival (CSS) and disease-free survival (DFS) were calculated by log-rank and Cox regression.

229 all survival (OS) and disease-free survival (DFS) were estimated using Kaplan-Meier methods, and a mu

230 all survival (OS) and disease-free survival (DFS) were evaluated among a 52-week of follow-up.

231 endpoint of improved disease-free survival (DFS) with sirolimus was not met, outcomes were improved

232 recurrence (LR), (iv) disease free survival (DFS), (v) overall survival (OS).

233 S), imaging-confirmed disease-free survival (DFS), and local progression-free survival (LPFS) were ca

234 points were toxicity, disease-free survival (DFS), and overall survival at 1 y.

235 3-year overall (OS), disease-free survival (DFS), and recurrence rates.

236 end point was 5-year disease-free survival (DFS), and the key secondary end points were overall surv

237 all survival (OS) and disease-free survival (DFS), in patients who underwent resection of an ampullar

238 verall survival (OS), disease-free survival (DFS), nonrelapse mortality (NRM), relapse-incidence (RI)

239 verall survival (OS), disease-free survival (DFS), R0 resection rates, sphincter preservations, and w

240 atio) had a prolonged disease-free survival (DFS), regardless of the influence of clinical factors.

241 all survival (OS) and disease-free survival (DFS), respectively.

242 Primary endpoint was disease-free survival (DFS), secondary endpoints were overall survival (OS) and

243 rial showing improved disease-free survival (DFS), the appropriate strategy for treating high-risk pa

244 primary end point was disease-free survival (DFS), which included invasive recurrences, second (breas

245 prognostic effect on disease-free survival (DFS).

246 e primary outcome was disease-free survival (DFS).

247 ostic impact of TD on disease-free survival (DFS).

248 experience long-term disease-free survival (DFS).

249 shorter postoperative disease-free survival (DFS); Charlson comorbidity index >1, preoperative CA 19-

250 primary end point was disease-free survival (DFS); secondary end points were overall survival (OS) an

251 overall had a longer disease-free survival (DFS; 190.1 vs. 100.2 months; P < 0.001).

252 erapy with respect to disease-free survival (DFS; primary end point) and overall survival (OS; second

253 rd of recurrence (ie, disease-free survival [DFS]) stratified by anti-HER2 Th1 responsivity.

254 erall survival(OS) and disease free survival(DFS) between the two approaches.

255 noninferiority criterion that required that DFS outcomes be consistent with HR < 1.52 was met (P < .

256 The DFS and OS at 10 years postactivation were calculated fo

257 The DFS and recurrence were not powered, and are being asses

258 The DFS difference was within the noninferiority margin of t

259 The DFS HR was 0.85 (95% CI, 0.64 to 1.14), and the predefin

260 Thus, the DFS was worse with CLRT-SLT (OR, 0.31; 95% CI, 0.2-0.6)

261 ignificant benefit from trastuzumab therapy (DFS HR, 0.71; 95% CI, 0.60 to 0.83; P < .0001; OS HR, 0.

262 At 5 years of median follow-up, DFS was not different between DC (n = 652) and control (

263 After a median of 6.9 years of follow-up, DFS was not significantly better for patients assigned t

264 Co-primary end points were DFS and OS, based on imaging studies assessed by indepen

265 ors of OS in multivariable analysis, whereas DFS was only adversely predicted by N-stage (HR = 2.65 [

266 nd normalized ADC95 remained associated with DFS (hazard ratio, 0.90-0.98; P < .05).

267 he radiotherapy dose was not associated with DFS when adjusting for the (18)F-FMISO status.

268 ere used to evaluate factors associated with DFS.

269 rsistence and compliance are associated with DFS.

270 The association of PNI with DFS and OS was analyzed using Cox proportional-hazards m

271 ameters and relevant clinical variables with DFS.

272 (OS) rates were not different as well, with DFS of 66.1% v 65.5% (HR, 1.02) and OS of 73.5% v 73.7%

273 ysis (P = 0.07), patients with PNI had worse DFS at univariate analysis (median DFS: 20 vs 15 months,

274 the 2 polymorphisms had significantly worse DFS and a higher recurrence risk than patients with fewe

275 was not associated with significantly worse DFS or OS compared with group 5.

276 ring hepatectomies are associated with worse DFS in patients with KRAS-mutated tumors.

277 ectomy, the median DFS was 18 months (1-year DFS: 54%, 5-year DFS: 31%).

278 95%CI: 78-95%) in SNB + AD patients; 10-year DFS 79% (95%CI: 68-92%) vs 69% (95%CI: 58-81%).

279 The 2-year DFS and recurrence were secondary endpoints of Z6051.

280 th adjuvant erlotinib had an improved 2-year DFS compared with historic genotype-matched controls.

281 e median follow-up was 5.2 years, and 2-year DFS was 88% (96% stage I, 78% stage II, 91% stage III).

282 The 2-year DFS was LAP 79.5% (95% confidence interval [CI] 74.4-84.

283 primary end point was improvement of 3-year DFS by oxaliplatin from 65% to 72% (hazard ratio [HR], 0

284 Children with MD had a 3-year DFS of 0.78 compared with 0.98 in those without MD (95%

285 pared with TD-negative patients, with 3-year DFS rates of 65.6% (95% CI, 58.0% to 72.1%) and 74.7% (9

286 regression of 8-year OS rates versus 5-year DFS and MFS rates, respectively.

287 prophylaxis with ITT did not improve 5-year DFS for children with HR B-ALL.

288 ilitation is associated with improved 5-year DFS in stage III colorectal cancer.

289 ing arm, C-MTX plus nelarabine, had a 5-year DFS of 91% (n = 147).

290 erall survival have not been reached; 5-year DFS was 56% (95% CI, 45% to 66%), 5-year overall surviva

291 Overall 1-, 3-, and 5-year DFS was 59%, 34%, and 22%, respectively.

292 was 21.3 months, whereas 1-, 3-, and 5-year DFS was 67.3%, 34.9%, and 31.5% respectively.

293 The estimated 5-year DFS was 85.3% (95% CI, 81.9 to 88.1) in the C-RT arm and

294 ted potential follow-up of 69 months, 5-year DFS was 87.9% (95% CI, 85.6% to 89.8%) in the EC-D arm a

295 n DFS was 18 months (1-year DFS: 54%, 5-year DFS: 31%).

296 The 7-year DFS and overall survival (OS) rates were not different a

297 The 7-year DFS was 93% (95% CI, 90.4 to 96.2) with four (1.0%) dist

298 Five-year DFS was only 14.4% in the nonanatomically resected group

299 Three-year DFS and OS in a subgroup of patients with DDIR positivit

300 Three-year DFS rate was not different, with 76.5% (95% CI, 72.7% to