ライフサイエンスコーパス: relapse-free survival

1 9; 95% CI, 0.46-1.01; P = 0.06 for GvHD-free/relapse-free survival).

2 ted with a reduced prostate-specific antigen relapse-free survival.

3 sion, and IKZF1 lesions were associated with relapse-free survival.

4 expression is significantly correlated with relapse-free survival.

5 ot distinguish differences in probability of relapse-free survival.

6 ion increases the complete response rate and relapse-free survival.

7 cal association between ID1 upregulation and relapse-free survival.

8 The primary end point was relapse-free survival.

9 The primary end point was relapse-free survival.

10 d T cells at diagnosis correlated with worse relapse-free survival.

11 ppears to increase prostate-specific antigen relapse-free survival.

12 ffective therapy has resulted in an improved relapse-free survival.

13 e independent predictors of poor overall and relapse-free survival.

14 cific survival and showed a strong trend for relapse-free survival.

15 d carotidynia (P=0.003) were associated with relapse-free survival.

16 perioperative transfusion in their effect on relapse-free survival.

17 e marrow cells (BMCs) resulted in long-term, relapse-free survival.

18 was negatively correlated with prognosis and relapse-free survival.

19 ession of LRIG1 has been linked to decreased relapse-free survival.

20 ssociated with a worse 5-year probability of relapse-free survival.

21 tis prophylaxis was associated with improved relapse-free survival.

22 -OST3A in tumors was associated with reduced relapse-free survival.

23 ere has been a significant improvement in BC relapse-free survival.

24 ncer, which had different 5-year biochemical relapse-free survival.

25 gene expression is associated with decreased relapse-free survival.

26 hyperdiploidy (HeH) (HR = 0.29, P = .04) for relapse-free survival.

27 PSA relapse (median PSA relapse-free survival, 10.3 years for radiotherapy vs 3.

28 Patients with longer ITDs had a worse relapse-free survival (19% vs 51%, P = .035), while the

29 ethnicity (P < .001) had a very poor 4-year relapse-free survival (21.0% +/- 9.5%; P < .001).

30 o 5.38; P = .0008), with a reduction in both relapse-free survival (22% v 44%; HR = 2.16; 95% CI, 1.3

31 o, 0.90; 95% CI 0.70-1.15; P = .3) or 5-year relapse-free survival (40% vs 36%; hazard ratio, 0.88; 9

32 relapse (38% v 55%; P < .001) and improving relapse-free survival (45% v 34%; P = .01), overall and

33 v 3.3 months), response rate (23% v 21%), or relapse-free survival (5.1 v 3.7 months) between the ela

34 and was associated with significantly worse relapse-free survival (59% v 79%; P < .001) and overall

35 r relapse-free survival, 91% vs. 85%; 5-year relapse-free survival, 76% vs. 69%; 2-year overall survi

36 red with the 78 observation patients (5-year relapse-free survival, 83% v 59%; P =.0002).

37 groups than in the CMF-alone groups (2-year relapse-free survival, 91% vs. 85%; 5-year relapse-free

38 , 81.5% vs 89.2% (log-rank test, P = .429;); relapse-free survival, 96.6% vs 92.4% (P = .2); visual a

39 es (WT1-CTL) has been correlated with better relapse-free survival after allogeneic stem cell transpl

40 h PAT4 expression is associated with reduced relapse-free survival after colorectal cancer surgery.

41 independently associated with longer distant relapse-free survival after receiving taxane plus anthra

42 iate analyses were performed with respect to relapse-free survival after RP.

43 d independently predicts reduced overall and relapse-free survival after surgery.

44 ion of patients into subgroups with distinct relapse-free survival after therapy.

45 rd ratio [aHR], 0.43; P = .009) and improved relapse-free survival (aHR, 0.50; P = .006) and overall

46 sociated with worse overall, event-free, and relapse-free survival among patients with either normal

47 Finally, the relapse-free survival analysis showed a statistically si

48 Identification of CSS sets to predict relapse-free survival and identify a subset of patients

49 All arms provide similar relapse-free survival and OS, with different toxicity pr

50 OGG1-expressing patients had a worse relapse-free survival and overall survival and an increa

51 At a median follow-up of 40.4 months, relapse-free survival and overall survival are 64% and 7

52 We compared relapse-free survival and overall survival between rofec

53 Associations of relapse-free survival and overall survival of 92 primary

54 ode metastasis but inversely correlated with relapse-free survival and overall survival of breast can

55 of TBX5, HOXD10, and DYRK1A correlates with relapse-free survival and overall survival outcomes in p

56 dence that RIC resulted in at least a 2-year relapse-free survival and overall survival similar to MA

57 Median relapse-free survival and overall survival were 6.7 and

58 ut not VGLL1-3, correlated with both shorter relapse-free survival and shorter disease-specific survi

59 PO gene expression correlated with shortened relapse-free survival and that pharmacologic JAK2 inhibi

60 LAR subtype includes patients with decreased relapse-free survival and was characterized by androgen

61 survival, distant metastasis free survival, relapse free survival, and post-progression survival.

62 survival, 44.8% (95% CI, 37.0% to 52.2%) for relapse-free survival, and 31.5% (95% CI, 25.7% to 37.4%

63 tumor stage and metastasis, reduced time of relapse-free survival, and decreased time of tumor-assoc

64 67 months, the 5-year local control, distant relapse-free survival, and disease-specific survival rat

65 parameters, prostate-specific antigen (PSA) relapse-free survival, and hormone receptor expression i

66 Factors associated with event-free survival, relapse-free survival, and incidences of vascular compli

67 CI, 0.33 to 4.49) for the overall survival, relapse-free survival, and local recurrence, respectivel

68 9%; relapse, nonrelapse mortality, GVHD-free relapse-free survival, and overall survival at 1 year we

69 Chronic GVHD, relapse-free survival, and overall survival at 2 years w

70 city, dose modification, therapy completion, relapse-free survival, and overall survival.

71 59% in CHD, respectively, and the estimated relapse-free survival at 2 years was 81% and 40% for the

72 composite end point of chronic GVHD-free and relapse-free survival at 2 years was significantly highe

73 without CRLF2 rearrangements (35.3% vs 71.3% relapse-free survival at 4 years; P < .001).

74 Kaplan-Meier relapse-free survival at 5 years was 89%, compared with

75 enes that were significantly associated with relapse-free survival at a stringent significance level

76 reatment of Cancer trial 18991 and has shown relapse-free survival benefits in patients with microsco

77 e aimed to estimate the difference in opioid relapse-free survival between XR-NTX and BUP-NX.

78 Overall Kaplan-Meier biochemical relapse-free survival (bRFS) was 85% at 59 months.

79 elapse-free survival (cRFS), and biochemical relapse-free survival (bRFS)-in patients treated with he

80 The outcome of interest was biochemical relapse-free survival (bRFS).

81 irst remission produced a trend for improved relapse-free survival but did not improve overall surviv

82 ival outcomes-overall survival, locoregional relapse-free survival, clinical relapse-free survival (c

83 f its ability to confer superior overall and relapse-free survival compared with matched marrow stem

84 locoregional relapse-free survival, clinical relapse-free survival (cRFS), and biochemical relapse-fr

85 The 2-y overall survival, locoregional relapse-free survival, cRFS, and bRFS were 87%, 91%, 51%

86 There was no significant difference in relapse-free survival curves between the treatment and c

87 The percentage of clinical relapse-free survival defined as the percent free of res

88 random assignment to death (any cause), and relapse-free survival, defined as time from random assig

89 variate Cox proportional hazards analysis of relapse-free survival demonstrated the prognostic value

90 The 4-year actuarial PSA relapse-free survival, distant metastasis-free survival,

91 nodes with respect to disease-free survival, relapse-free survival, distant-disease-free survival, or

92 e rate (in advanced disease), progression or relapse-free survival, dose-intensity, and overall survi

93 ssigned a Mammostrat risk score, and distant relapse-free survival (DRFS) and disease-free survival (

94 by subtype and size, but the 5-year distant relapse-free survival (DRFS) did not exceed 10% in any s

95 Distant relapse-free survival (DRFS) if predicted treatment sens

96 (number and size) for prediction of distant relapse-free survival (DRFS) in multivariate Cox regress

97 o identify microRNAs associated with distant relapse-free survival (DRFS) that provide independent pr

98 d with significantly improved 5-year distant relapse-free survival (DRFS; HR, 0.76; 95% CI, 0.63 to 0

99 The primary outcome was opioid relapse-free survival during 24 weeks of outpatient trea

100 Two-year overall and relapse-free survival estimates are 63% and 49%, respect

101 pment of novel regimens may lead to improved relapse-free survival even in patients with high-risk cy

102 Analyzing invasive cancers only, 5-year relapse-free survival for MamD breast cancer patients wa

103 Median relapse-free survival for patients in cluster 4 was 16 m

104 3-year relapse-free survival for patients who had complete rese

105 oietic cell transplantation offers long-term relapse-free survival for patients with myelofibrosis.

106 R = 0.54; P = .08) were relevant factors for relapse-free survival; for overall survival, FLT3 mutati

107 ned a novel composite end point of GVHD-free/relapse-free survival (GRFS) in which events include gra

108 the 5-year probability of chronic GVHD-free, relapse-free survival (GRFS) is 71%.

109 was associated with a significant benefit in relapse-free survival (hazard ratio [HR], 0.69; P = .036

110 A similar effect was seen for relapse-free survival (hazard ratio, 0.67; 95% CI, 0.47

111 Capecitabine improved relapse-free survival (hazard ratio, 0.86; 95 percent co

112 HR] 0.94 [95% CI 0.68-1.31], p=0.72) nor did relapse-free survival (HR 0.91 [0.67-1.22], p=0.51).

113 95% CI, 0.11-0.87; P = 0.03), and GvHD-free/relapse-free survival (HR, 0.48; 95% CI, 0.29-0.80; P <

114 Seropositive donors also had no influence on relapse-free survival (HR, 1.04; 95% CI, 0.97 to 1.11; P

115 val (OS; hazard ratio [HR], 2.06; P = .003), relapse-free survival (HR, 2.28; P = .002), and event-fr

116 f TGF-beta signaling correlated with reduced relapse-free survival in all patients; however, the stro

117 a conspicuous prognostic marker for overall/relapse-free survival in AML.

118 endpoints were overall survival in AML15 and relapse-free survival in AML17; outcome data were meta-a

119 mours and low interleukin-11 correlates with relapse-free survival in breast cancer patients.

120 s of HBP1 and WIP1 correlated with decreased relapse-free survival in breast cancer patients.

121 R-205 is highly associated with poor distant relapse-free survival in breast cancer patients.

122 of disease and is negatively associated with relapse-free survival in breast cancer.

123 ession significantly correlated with shorter relapse-free survival in ER(-) patients who were treated

124 in expression, metastasis-free survival, and relapse-free survival in estrogen receptor-positive case

125 High GGI is associated with decreased relapse-free survival in patients receiving either endoc

126 and DBC1 expression correlated with shorter relapse-free survival in patients with advanced CRC.

127 associated with significantly worse distant relapse-free survival in patients with ER-positive cance

128 n deprivation did not improve the 4-year PSA relapse-free survival in patients with positive margins,

129 is paracrine signalling predicts overall and relapse-free survival in stage I non-small cell lung can

130 Overall and relapse-free survival in the present study compared favo

131 interferon did not contribute to survival or relapse-free survival in this group of patients.

132 r prognostic factor for overall survival and relapse-free survival in total patients and also in norm

133 Exploratory analyses of distant relapse-free survival indicated a 22% improvement (HR, 0

134 nal intrathecal chemotherapy is required for relapse-free survival, indicating subclinical CNS manife

135 The 5-year relapse-free survival is 82% (95% CI, 72 to 92).

136 Whether prostate-specific antigen relapse-free survival is an appropriate surrogate for ov

137 pse ranges from 10 to 40%, and, as a result, relapse-free survival is inferior.

138 significantly associated with short time of relapse-free survival (log-rank P = .037) and short time

139 er and bone metastasis ( P </= .02), shorter relapse-free survival (median, 13 v 34 months; P = .01),

140 patients up to 5 years for overall survival, relapse-free survival, modified Rodnan skin score, and p

141 MRD and CRLF2 expression predicted a poorer relapse-free survival; no difference was seen between ca

142 5% CI, 0.76 to 0.95), and an adjusted HR for relapse-free survival of 0.86 (95% CI, 0.77 to 0.95).

143 The model projected 15-year relapse-free survival of 52% and 43% with and without PM

144 /B, and PTPRM; ERG DNA deletions; and 4-year relapse-free survival of 94.7% +/- 5.1%, compared with 6

145 Correlation of relapse-free survival of breast cancer patients (n=2878)

146 ficantly reduced distant-metastasis-free and relapse-free survival of breast cancer patients who unde

147 After adjustment for covariates, the relapse-free survival of patients achieving CR was longe

148 p53 and ER target genes that can predict the relapse-free survival of patients with ER+ breast cancer

149 dian follow-up of 33 months, the hematologic relapse-free survival of the entire evaluable study coho

150 Responders enjoyed relapse-free survivals of 92% and 76%, respectively, at

151 , perioperative transfusion had no effect on relapse-free survival on multivariate analysis.

152 d ecto-CRT were all associated with improved relapse-free survival, only CRT exposure significantly c

153 erence was not significantly associated with relapse-free survival or grade 3 or 4 toxicity.

154 ted soft-tissue sarcoma showed no benefit in relapse-free survival or overall survival.

155 ighly associated with time to event, such as relapse-free survival or overall survival.

156 gnificant differences in the response rates, relapse-free survival, or disease-free survival between

157 kemic blasts correlates with poor overall or relapse-free survival, our data suggest that a combinati

158 eic hematopoietic stem-cell transplantation, relapse-free survival, overall survival, and adverse eve

159 Five-year incidence of relapse, relapse-free survival, overall survival, and nonrelapse

160 differences in rates of distant recurrence, relapse-free survival, overall survival, or late toxicit

161 In addition, relapse-free survival, overall survival, safety as deter

162 n into two distinct subgroups with different relapse-free survival (P < 0.03).

163 wing significant univariate association with relapse-free survival (P < 0.05) in the present study wa

164 emission and was highly associated with poor relapse-free survival (P = .008).

165 with increased vasostatin levels had longer relapse-free survival (P = .04) and specifically benefit

166 mphocytes was an independent risk factor for relapse-free survival (p = 0.002) and overall survival (

167 nd decreased overall survival (P = 0.00004), relapse-free survival (P = 0.0119), and metastasis-free

168 -2(+) phenotype was associated with improved relapse-free survival (P = 0.04) and disease-specific su

169 fic survival, disease-free survival, distant relapse-free survival, pathological complete response, a

170 IL-6 tumors had shorter overall survival and relapse-free survival periods when compared with patient

171 Five-year relapse-free survival ranged from 62% to 73% for FCC/DLB

172 The hema-tologic relapse-free survival rate of a subgroup of 9 patients w

173 The expression of VEGF and the relapse-free survival rate of breast cancer patients are

174 The actuarial 3-year relapse-free survival rate was 30% (95% confidence inter

175 Among those who achieved a CR, the 5-year relapse-free survival rate was 43% in the DA+GO group an

176 hat dietary fat reduction would increase the relapse-free survival rate.

177 Two-year relapse-free survival rates (28% vs 39%, P = .843) and m

178 s, the 2-year estimated overall survival and relapse-free survival rates are 92% and 78%, respectivel

179 a median follow-up of 4 years (IQR 3.0-4.9), relapse-free survival rates for radiotherapy and carbopl

180 Five-year relapse-free survival rates were 94%, 78%, and 45%, resp

181 nt EBV serologic status on overall survival, relapse-free survival, relapse incidence, nonrelapse mor

182 No differences in CR, relapse-free survival, relapse, or OS were seen between

183 ied before the median time to alloHSCT, only relapse-free survival remained significantly superior in

184 = 0.03 and P = 0.04) of overall survival and relapse-free survival, respectively.

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

186 whether class I antigen expression impacted relapse-free survival (RFS) after adjuvant therapy with

187 ine Tumor Society (ENETS) are prognostic for relapse-free survival (RFS) after surgical resection.

188 or absence of various prognostic factors on relapse-free survival (RFS) and disease-specific surviva

189 ted to be significant prognostic factors for relapse-free survival (RFS) and OS.

190 These data were collated in relation to relapse-free survival (RFS) and overall survival (OS) at

191 We compared relapse-free survival (RFS) and overall survival (OS) de

192 tor (GM-CSF) and peptide vaccination (PV) on relapse-free survival (RFS) and overall survival (OS) in

193 chemotherapy (PCT) is associated with higher relapse-free survival (RFS) and overall survival (OS) ra

194 Results Relapse-free survival (RFS) and overall survival (OS) ra

195 Those receiving VbMF achieved higher relapse-free survival (RFS) and overall survival (OS) th

196 Median relapse-free survival (RFS) and overall survival (OS) ti

197 (range, 21 to 161 months), estimated 5-year relapse-free survival (RFS) and overall survival (OS) we

198 rospectively defined primary end points were relapse-free survival (RFS) and overall survival (OS).

199 Coprimary end points were relapse-free survival (RFS) and overall survival (OS).

200 r week for 48 weeks (arm B) and observed for relapse-free survival (RFS) and overall survival.

201 of the probabilities of overall survival and relapse-free survival (RFS) and the cumulative incidence

202 Secondary end points included relapse-free survival (RFS) and TRM.

203 Relapse-free survival (RFS) at 5 years was 17% versus 7%

204 variables were analyzed for association with relapse-free survival (RFS) by Cox proportional hazards

205 38-gene expression classifier predictive of relapse-free survival (RFS) could distinguish 2 groups w

206 Overall survival (OS) and relapse-free survival (RFS) data demonstrate continued s

207 determine the association of each gene with relapse-free survival (RFS) for 433 patients who receive

208 rvival analysis showed significantly shorter relapse-free survival (RFS) for those with high expressi

209 analysis evaluated overall survival (OS) and relapse-free survival (RFS) in a phase 2 study of the bi

210 significantly correlated with an unfavorable relapse-free survival (RFS) in breast cancer patients (H

211 and provided the most powerful predictor of relapse-free survival (RFS) in multivariable analysis (h

212 aclitaxel (WP) followed by FEC would improve relapse-free survival (RFS) in operable breast cancer.

213 Relapse-free survival (RFS) is a powerful measure of tre

214 The median relapse-free survival (RFS) of 31 patients with localize

215 We also determined overall 5-year relapse-free survival (RFS) of all stage III patients se

216 ognostic impact on overall survival (OS) and relapse-free survival (RFS) only in the NPM1+ subgroup (

217 Estimated 5-year relapse-free survival (RFS) rate is 50% in arm 1 and 48%

218 who achieved complete remission, the 3-year relapse-free survival (RFS) rate was 47.4% and overall s

219 Early studies reported 10-year relapse-free survival (RFS) rates higher than 90% withou

220 ohorts in event-free survival (EFS), OS, and relapse-free survival (RFS) seen in univariate analysis

221 1989 to 1993 v 68% in 1999 to 2002), and the relapse-free survival (RFS) subsequently improved from 8

222 plantation based on cytogenetics, age, and a relapse-free survival (RFS) time that was more than or e

223 the effect of PBBs at the time of CR-MDA on relapse-free survival (RFS) time.

224 e of relapse and death: the hazard ratio for relapse-free survival (RFS) was 0.79 (95% CI, 0.64 to 0.

225 Relapse-free survival (RFS) was 52% in the alloSCT group

226 Relapse-free survival (RFS) was not significantly associ

227 The Kaplan-Meier estimates of 3-year relapse-free survival (RFS) were 56% for related and 59%

228 s after the diagnosis, overall survival, and relapse-free survival (RFS) were assessed.

229 dences of relapse, nonrelapse mortality, and relapse-free survival (RFS) were estimated at 19.5%, 15.

230 ly relevant genes and their association with relapse-free survival (RFS) were evaluated using microar

231 Overall survival (OS), relapse-free survival (RFS), and complete remission rate

232 included, the 5-year overall survival (OS), relapse-free survival (RFS), and distant RFS (DRFS) esti

233 d the cumulative incidence of relapse (CIR), relapse-free survival (RFS), and overall survival (OS) f

234 The 5-year event-free survival, relapse-free survival (RFS), and overall survival (OS) r

235 Data on treatment toxicity, relapse-free survival (RFS), and overall survival (OS) w

236 determine the association between BB intake, relapse-free survival (RFS), and overall survival (OS).

237 ed donor transplantation), overall survival, relapse-free survival (RFS), nonrelapse mortality, and a

238 tem-cell transplantation (HSCT) realization, relapse-free survival (RFS), overall survival (OS), and

239 The primary end point was overall survival; relapse-free survival (RFS), relapse-free interval, and

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

241 less than 1.30 for the primary end point of relapse-free survival (RFS).

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

243 The primary efficacy end point was relapse-free survival (RFS).

244 used to calculate overall survival (OS) and relapse-free survival (RFS).

245 ot only for achieving remission but also for relapse-free survival (RFS).

246 osis (P =.014) were associated with improved relapse-free survival (RFS).

247 The primary end point was PSA relapse-free survival (RFS).

248 tistically significant improvement in 4-year relapse-free survival (RFS; 96% v 94%; RR = 0.44; P = .0

249 ted for covariates, HDC was found to prolong relapse-free survival (RFS; hazard ratio [HR], 0.87; 95%

250 with high-risk stage I NSCLC who had shorter relapse-free survival (RFS; hazard ratio [HR], 2.35; 95%

251 F1high) associated with significantly better relapse-free survival (RFS; P < .001), overall survival

252 deprivation therapy (FFADT; P = .0011), and relapse-free survival (RFS; P < .001).

253 tion for overall survival (OS; P = .005) and relapse-free survival (RFS; P = .002) than did MRD statu

254 5% confidence interval [CI], 1.04-1.81), and relapse-free survival (RFS; P = .005; HR, 1.52; 95% CI,

255 urvival (OS; PINAOS) and the other regarding relapse-free survival (RFS; PINARFS), were derived from

256 strated an association between TS intensity (relapse-free survival [RFS]: risk ratio [RR] = 1.46, P =

257 may decrease acute GVHD without compromising relapse-free survival, separating the graft-versus-tumor

258 quential, 86%; concurrent, 81%; P = .64), or relapse-free survival (sequential, 76%; concurrent, 85%;

259 Disease-specific survival and relapse-free survival statistics were calculated by usin

260 8 of 77 patients, 23.4%) had longer times of relapse-free survival than patients with small or no del

261 tion were found to be associated with longer relapse-free survival than patients without ID1 increase

262 s on day 19 was more closely associated with relapse-free survival than was lack of detectable residu

263 with an increased copy number and a shorter relapse-free survival time (P = 0.027, log-rank test).

264 association between high EDI3 expression and relapse-free survival time in both endometrial (P < 0.00

265 Of nine surviving responders, median relapse-free survival time was 72 months (95% confidence

266 way activation was associated with increased relapse-free survival time.

267 es based on E2F activity with differences in relapse-free survival times.

268 ts with GVHD versus those with GVHD-free and relapse-free survival using quantitative reverse-transcr

269 sters, patients in cluster 4 had an inferior relapse-free survival vs patients in cluster 1 (log-rank

270 The median relapse free-survival was about 19 months in patients wh

271 magglutinin disease (CHD; average, 60%); the relapse-free survival was 100% for WAIHA at +6 and +12 m

272 The 5-year relapse-free survival was 100% versus 65% for patients w

273 a median follow-up of 23 months, the median relapse-free survival was 19 months among patients with

274 The median relapse-free survival was 30 months, and the median dise

275 , respectively (P < .001); the corresponding relapse-free survival was 30% and 65% (P < .001).

276 Relapse-free survival was 5 months (range, 0-19).

277 p of 2.8 years, the estimated 3-year rate of relapse-free survival was 58% in the combination-therapy

278 <100 x 10(9)/L) was achieved in another 25%; relapse-free survival was 66.7% at 12 months (median res

279 At 3 years, the rate of relapse-free survival was 68% in the capecitabine group

280 ars (after eight relapse-related deaths) and relapse-free survival was 70% at 5 years.

281 confidence interval 48-96 months) and 5-year relapse-free survival was 75% (95% confidence interval 3

282 Four-year relapse-free survival was 80% and progression-free survi

283 The 3-year relapse-free survival was 90.9% (83.5%-99%) over the bio

284 patients who achieved hematologic CR, 3-year relapse-free survival was 91% with DAS and 88% with IM 4

285 The rate of relapse-free survival was higher in the mycophenolate mo

286 end point of chronic GVHD-free survival and relapse-free survival was higher with ATG.

287 Relapse-free survival was longer in group 1 (P = .049).

288 Compared with observation, better relapse-free survival was recorded in patients allocated

289 In contrast, the difference for relapse-free survival was significant (HR, 1.27; P = .03

290 site end point of extensive chronic GVHD and relapse-free survival was significantly better for HAPLO

291 Relapse-free survival was significantly superior in pati

292 ults who achieved complete remission, 5-year relapse-free survival was significantly worse for SNP-po

293 Relapse-free survival was similar (adjusted HR 1.02 [0.9

294 The rate of 2-year relapse-free survival was similar in the ATG group and t

295 However, relapse-free-survival was significantly superior in VPA

296 Progression-free survival and clinical relapse-free survival were 90.9% (90% CI, 73.7%-97.1%) a

297 djuvant androgen deprivation did improve PSA relapse-free survival when one or more of these variable

298 The primary end point was relapse-free survival, which was assessed using a Cox pr

299 ssociated with luminal A category and longer relapse-free survival, while that of p53 was associated

300 ed a 30% improvement in the relative risk of relapse-free survival with B/x donors compared with A/A