ライフサイエンスコーパス: DFS

1 DFS estimates for patients with ACC improved dramaticall

2 DFS estimates for patients with ovarian cancer improved

3 DFS in the ER-negative cohort, whole population, and ove

4 DFS in this study was compared with that in the chemorad

5 DFS was calculated using the Kaplan-Meier method.

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

7 DFS/PFS in both groups were 8 to 10 months.

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

9 ficantly reduced MSS (HR = 2.10; P < 0.001), DFS (P < 0.001), RNRFS (P < 0.001), and DRFS (P = 0.010)

10 S: HR, 0.56; 95% CI, 0.38 to 0.81; P = .002; DFS: HR, 0.59; 95% CI, 0.42 to 0.83; P = .002; SDFS: HR,

11 OS: HR, 0.45; 95% CI, 0.23 to 0.85; P = .01; DFS: HR, 0.44; 95% CI, 0.24 to 0.78; P = .005; SDFS: HR,

12 lyses confirmed these results (CR, P = 0.03; DFS, P = 0.009; OS, P = 0.009).

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

14 ; 95% CI, 0.51 to 0.99; interaction P = .18; DFS: HR, 0.60; 95% CI, 0.44 to 0.82; interaction P = < .

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

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

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

18 mpared with ymrEMVI-negative tumors (79.8%); DFS for was 36.9% versus 65.9% positive and negative ypE

19 analysis was planned to take place after 940 DFS events.

20 ,140 men and 45% of 12,712 men experienced a DFS and MFS event, respectively.

21 istical evidence of a reduction in risk of a DFS event with bisphosphonate therapy.

22 there was a 66% reduction in the hazard of a DFS event with letrozole for LB (hazard ratio [HR], 0.34

23 significant 35% reduction in the hazard of a DFS event with letrozole for the LB subtype (HR, 0.65; 9

24 Additional DFS experiments support this assumption and allow identi

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

26 In multivariate analysis, DFS did not differ between CBT and BMT recipients.

27 LPFS (56% vs 45% after 5 years, P=0.044) and DFS (34% vs 27% after 5 years, P=0.040).

28 t 3 and 5 years, respectively (P = 0.72) and DFS rates of 40% and 32% vs 52% and 36% at 3 and 5 years

29 gnificantly improved local tumor control and DFS without increasing surgical complications.

30 OS, EFS, and DFS for SR and HR patients were 83%, 63%, and 66% and 64

31 LPFS and DFS as well as overall survival were determined.

32 End points included OS, MCCSS, and DFS.

33 mulative incidence of distant metastasis and DFS were 10.5% and 89.5% for patients with TRG 4 (comple

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

35 This update presents 10-year OS and OS and DFS by mismatch repair (MMR) status and BRAF mutation.

36 alysis (156 matched patients), median OS and DFS did not differ significantly between patients in 1-

37 as a highly prognostic biomarker for OS and DFS in Klatskin tumor patients.

38 ith historical controls, resulting in OS and DFS similar to those reported in developed countries.

39 ap-corrected Harrell C statistics for OS and DFS were 0.74 and 0.71 in the developing set and 0.68 an

40 atients with bCRLM achieve comparable OS and DFS, despite the high dropout of the 2-stage strategy.

41 were poor prognostic factors for both OS and DFS, presence of satellite tumor nodules additionally pr

42 the absence of impact of strategy on OS and DFS.

43 These nomograms accurately predict OS and DFS.

44 is (P < .001 and P = .035, respectively) and DFS (P < .001 and P = .039, respectively), whereas local

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

46 were independently correlated with a better DFS.

47 l residual disease (MRD) had markedly better DFS (80%) and OS (80%) than patients in CR with MRD or w

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

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

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

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

52 In the PET group, both DFS and DSS were higher in patients with negative findin

53 eradiotherapy/CCRT PET/CT scan improves both DFS and DSS in patients with advanced oral cavity squamo

54 pread and lymphatic invasion) predicted both DFS (P = 0.001 and P < 0.001, respectively) and DSS (P =

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

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

57 Conditional DFS accounts for elapsed time since achieving remission

58 Conditional DFS estimates were calculated.

59 Conditional DFS estimates were computed using cumulative DFS estimat

60 Conditional DFS improves over time following resection of GISTs.

61 Conditional DFS is a more relevant measure of prognosis for patients

62 This study aimed to estimate conditional DFS among patients with ovarian cancer and to evaluate t

63 Using conditional DFS, the probability of remaining disease free for an ad

64 Multivariable analyses for CR, DFS, and OS identified the lncRNA score as an independen

65 nts) and benefit with anthracycline-only CT (DFS, interaction P = .042; OS, P = .018).

66 DFS estimates were computed using cumulative DFS estimates.

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

68 MIP/SOL patients (but not ACN/PAP) derived DFS and SDFS but not OS benefit from ACT (OS: HR, 0.71;

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

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

71 loped between the two randomization factors (DFS P = .024; OS P = .010) in the 2,716 patients randoml

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

73 rates were 24.0% versus 33.4% (P < .001) for DFS and 12.4% versus 21.2% (P < .001) for OS, respective

74 zumab were 17.3% versus 24.3% (P < .001) for DFS and 7.8% versus 11.6% (P = .005) for OS, respectivel

75 sults were 12.7% versus 19.4% (P = .005) for DFS and 5.3% versus 7.4% (P = .12) for OS, respectively.

76 5% CI, 1.00 to 1.04; P = .048), and 1.02 for DFS (95% CI, 1.00 to 1.04; P = .0427).

77 esults were 20.4% versus 26.3% (P = .05) for DFS and 8.2% versus 12.2% (P = .084) for OS, respectivel

78 eatment arm and age (P interaction = .09 for DFS, .05 for OS, and .36 for TTR), although the stratifi

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

80 was 1.34 (95% CI, 0.93 to 1.91; P = .14) for DFS and 1.19 (95% CI, 0.73 to 1.93; P = .51) for OS.

81 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).

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

83 s no significant difference between arms for DFS (5-year rate: 87.9% v 89.7%; log-rank P = .62) or OS

84 clearance was the only prognostic factor for DFS and OS.

85 olidation) as the only prognostic factor for DFS and OS.

86 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

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

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

89 ta, the regression of either the log(HR) for DFS or the log(HR) for OS on the log(OR) for pCR demonst

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

91 HRs for DFS and OS benefit in the FOLFOX4 arm were 0.48 (95% CI,

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

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

94 the use of pCR as a surrogate end point for DFS and OS in patients with breast cancer.

95 ictor value of the VDR-FokI polymorphism for DFS.

96 = 0.009) were both positively prognostic for DFS, remaining upon multivariate analysis.

97 nostic and predictive factors, disease-free (DFS) and overall survival (OS) hazard ratios (HRs) were

98 tes (TILs) are associated with disease-free (DFS) and overall survival (OS) in operable triple-negati

99 enced similar overall (OS) and disease-free (DFS) survival rates [OS rates of 88% and 78% vs 84% and

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

101 of treatment assignment (observation group: DFS HR age </= 40 v > 40 years, 1.18; 95% CI, 0.90 to 1.

102 01; 95% CI, 0.60 to 1.69; trastuzumab group: DFS HR age </= 40 v > 40 years, 1.11; 95% CI, 0.81 to 1.

103 In the experimental and control groups, DFS was similar in the intention-to-treat population (ha

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

105 078; HR RR, GO 40% v No-GO 73%, P = .016; HR DFS, GO 47% v No-GO 28%, P = .135).

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

107 tion of cetuximab to FOLFOX4 did not improve DFS compared with FOLFOX4 alone in patients with KRAS ex

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

109 Weekly paclitaxel improved DFS and OS (HR, 0.69; P = .010 and HR, 0.69; P = .019, r

110 egimen shows favorable outcome with improved DFS and OS relative to historical controls and has comme

111 ill associated with a significant benefit in DFS and OS.

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

113 s no statistically significant difference in DFS for women assigned to triptorelin and those assigned

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

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

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

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

118 esults were accompanied by an improvement in DFS of 40% (HR, 0.60; 95% CI, 0.53 to 0.68; P < .001) an

119 result in an overall significant increase in DFS (hazard ratio [HR], 0.93; 95% CI, 0.81 to 1.08; P =

120 icant difference in OS (P = .040) but not in DFS (P = .11), with all treatments given once every 2 we

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

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

123 Secondary endpoints were invasive DFS (IDFS), overall survival, time to bone metastases, t

124 007; 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

125 opyrimidine dehydrogenase expression levels, DFS HR was 2.45 (95% CI, 1.55 to 3.86; P < .001), and OS

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

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

128 n did not correlate significantly with lower DFS because these patients received intensive therapy.

129 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

130 TNM-based criteria for assessing risk of LR, DFS, and OS.

131 Median DFS was 19.2 months.

132 Median DFS was 2.54 years (range, 0.03-9.96 years) and 3-year D

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

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

135 ly reduced melanoma-specific survival (MSS), DFS, regional node recurrence-free survival (RNRFS) and

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

137 Donor relatedness did not affect NRM, DFS, or OS.

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

139 information about the changing likelihood of DFS over time.

140 Ls to be an independent prognostic marker of DFS, DRFI, and OS.

141 The number of DFS events did not differ between groups: 493 in the con

142 For the primary end point of DFS, association with TIL scores was determined by fitti

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

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

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

146 The effects of zoledronic acid on DFS were not affected by oestrogen-receptor status.

147 Treatment effects on DFS and OS were expressed as hazard ratios (HRs), and tr

148 For R0 resections only, DFS in LAP cancer was 76% and 57% in RRC (P = 0.212).

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

150 parameter that remained significant for OS, DFS, and LR on multivariate analysis.

151 5% in the longer interval group, and the OS, DFS, R0 resection rates, sphincter preservation, and com

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

153 Updated analyses of overall DFS and related subgroups were also performed.

154 metastatic risk and rapid decline in patient DFS.

155 ions of 33 laboratory variables with patient DFS.

156 addition of oxaliplatin in elderly patients (DFS hazard ratio [HR], 0.94; 95% CI, 0.78 to 1.13; OS HR

157 PFS/DFS and OS were estimated by the Kaplan-Meier method.

158 system, higher stages correlated with poorer DFS.

159 splant significantly improved posttransplant DFS and OS without excess of treatment-related mortality

160 ion of CXCR4 was associated with a prolonged DFS, MFS, and OS (multivariate hazard ratio MFS=0.76 [95

161 .022) were significant predictors of reduced DFS.

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

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

164 chemotherapy versus standard-dose regimens (DFS: R(2) = 0.79; 95% CI, 0.26 to 0.95; P = .003; and OS

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

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

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

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

169 Patients achieved a similar DFS with any of these regimens.

170 r the large difference in OS despite similar DFS/PFS is likely different metastatic patterns at relap

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

172 es of the structural segments, dynamic SMFS (DFS) probes their stability over a wide range of loading

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

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

175 oscopy (FCS) and dynamic force spectroscopy (DFS).

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

177 mized trastuzumab trials derived substantial DFS and OS benefit from adjuvant trastuzumab.

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

179 0.54; P = 0.008] and disease-free survival (DFS) (HR = 0.59; P = 0.001) compared with a less than 8-

180 demonstrated improved disease-free survival (DFS) (P < 0.001) and regional recurrence-free survival (

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

182 54% vs. 89%], shorter disease-free survival (DFS) [P < 0.001, hazard ratio (HR) = 2.88] and overall s

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

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 s demonstrated 3-year disease-free survival (DFS) and 6-year overall survival (OS) benefit of adjuvan

187 ningfully improve 2-y disease-free survival (DFS) and disease-specific survival (DSS) rates.

188 endpoints were 3-year disease-free survival (DFS) and local recurrence-free survival (LRFS).

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

190 Disease-free survival (DFS) and OS of patients included in the SECA study were

191 We investigated disease-free survival (DFS) and overall survival (OS) after response-guided neo

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

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

194 Five-year disease-free survival (DFS) and overall survival (OS) probabilities were 37% an

195 2.2 years, the 2-year disease-free survival (DFS) and overall survival (OS) rates were 62% and 67%, r

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

197 Disease-free survival (DFS) and overall survival (OS) were estimated by the Kap

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

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

200 icacy end points were disease-free survival (DFS) and overall survival (OS).

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

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

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

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

205 Traditional disease-free survival (DFS) does not reflect changes in prognosis over time.

206 g with updates on the disease-free survival (DFS) end point.

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

208 e primary endpoint of disease-free survival (DFS) for ymrEMVI and ypEMVI was calculated using the Kap

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

210 ith 3,250 patients, a disease-free survival (DFS) hazard ratio of 0.82 for each randomization could b

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

212 of zoledronic acid on disease-free survival (DFS) in high-risk patients with early breast cancer.

213 e survival (LPFS) and disease-free survival (DFS) in patients with abdominal and extremity sarcomas.

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

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

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

217 However, disease-free survival (DFS) over time is dynamic and changes based on disease-f

218 survival (MCCSS), and disease-free survival (DFS) relationships in a cohort of patients with MCC.

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

220 the estimated 5-year disease-free survival (DFS) was 50% and 5-year overall survival (OS) was 51%.

221 docetaxel arm; 2-year disease-free survival (DFS) was 57% and 66%, respectively.

222 N, and 5- and 10-year disease-free survival (DFS) was 82% and 78%, respectively.

223 The 6-year disease-free survival (DFS) was 86% and 80% in TM patients after BMT and CBT, r

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

225 all survival (OS) and disease-free survival (DFS) were 72% and 56%.

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 ty and morbidity, and disease-free survival (DFS) were calculated.

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

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

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

232 verall survival (OS), disease-free survival (DFS), and time to local recurrence (LR).

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

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

235 ts included toxicity, disease-free survival (DFS), radiologic response (RaR), and biomarker correlate

236 tivariable models for disease-free survival (DFS), significant interactions between treatment and his

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

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

239 primary end point was disease-free survival (DFS).

240 le), pregnancies, and disease-free survival (DFS).

241 stant metastasis, and disease-free survival (DFS).

242 all survival (OS) and disease-free survival (DFS).

243 colon cancer improved disease-free survival (DFS).

244 primary endpoint was disease-free survival (DFS).

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

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

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

248 (MSS; P = .0025), and disease-free survival (DFS; P = .0466).

249 rter overall (OS) and disease-free survival (DFS; P = 0.001 and P < 0.001, respectively).

250 astasis-free survival, and overall survival (DFS, MFS, and OS, respectively).

251 type patients (4-year disease-free survival [DFS] of 30.0 +/- 6.8% vs 57.5 +/- 9.4%; P = .01).

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

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

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

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

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

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

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

259 tive disease at the time of transplantation (DFS, P = .0005; OS, P = .019).

260 etween histologic subgroups, but univariable DFS and SDFS were worse for MIP/SOL compared with LEP or

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

262 The primary endpoint was DFS.

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

264 nts after BMT and CBT, respectively, whereas DFS in SCD patients was 92% and 90%, respectively.

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

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

267 ere used to evaluate factors associated with DFS.

268 rsistence and compliance are associated with DFS.

269 ameters and relevant clinical variables with DFS.

270 -nonresponsive patients demonstrated a worse DFS (median, 47 vs 113 months; P < .001) compared with T

271 e tumor nodules additionally predicted worse DFS.

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

273 t ymrEMVI-positivity had significantly worse DFS at 3 years (42.7%) compared with ymrEMVI-negative tu

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

275 versus 79% (P=0.0954), a significantly worse DFS: 41% versus 65% (P=0.0267).

276 ent oral HPV16 DNA was associated with worse DFS (hazard ratio, 29.7 [95% CI, 9.0-98.2]) and OS (haza

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

278 3 to 0.68; P < .001) and increase in 10-year DFS rate from 62.2% to 73.7%.

279 ), reflecting absolute improvement in 2-year DFS of 2.5% and 11.1%, respectively.

280 Initial differences in 3-year DFS at time of remission between age, stage, histology,

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

282 54 years (range, 0.03-9.96 years) and 3-year DFS was 48.2%.

283 arm based on early clinical response (4-year DFS of 51.9 +/- 8.8% for IKZF1-deleted vs 78.6 +/- 13.9%

284 03), even when treated with imatinib (4-year DFS of 55.5 +/- 9.5% for IKZF1-deleted vs 75.0 +/- 21.7%

285 lar CR2 rate but significantly higher 5-year DFS (68% vs 42%; P = .05) and OS (65% vs 44%; P = .02).

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

287 Overall 1-year, 3-year, and 5-year DFS following resection of GISTs was 95%, 83%, and 74%,

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

289 The 5-year DFS was 67.2% (95% CI, 61.4% to 73%) for MRI-clear CRM c

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

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

292 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

293 Five-year DFS was 80.5% (95% CI, 73.1%-86.1%) in the LHRHa group a

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

295 One-year DFS was 89% versus 67% for patients who achieved PaR com

296 Seven-year DFS rates were 63% and 56% in the XELOX and FU/FA groups

297 Three-year DFS for R0, R1, and R2 resections was 67%, 49%, and 0%,

298 Two-year DFS (80% vs. 70%, P = 0.033) and DSS (84% vs. 75%, P = 0

299 Two-year DFS and OS were 92% (95% CI, 94%-100%) and 98% (95% CI,

300 arm, after a median follow-up of 12.1 years, DFS significantly improved and overall survival (OS) mar