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 (2)) was an independent predictor of shorter relapse free survival.

3 ted with CCR2 expression and correlated with relapse free survival.

4 st cancer patients correlated with decreased relapse-free survival.

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

6 d in PCa tissues and associated with shorter relapse-free survival.

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

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

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

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

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

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

13 expression is significantly correlated with relapse-free survival.

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

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

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

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

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

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

20 CCL7 and CCL8 were associated with decreased relapse-free survival.

21 N/HMGA2/EZH2 signaling predictive of reduced relapse-free survival.

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

23 The primary end point was relapse-free survival.

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

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

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

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

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

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

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

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

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

33 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

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

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

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

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

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

39 , 81.5% vs 89.2% (log-rank test, P = .429;); relapse-free survival, 96.6% vs 92.4% (P = .2); visual a

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

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

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

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

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

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

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

47 Secondary endpoints focused on safety, relapse-free survival and biomarker analysis.

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 Secondary endpoints were relapse-free survival and overall survival.

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

60 Here, we report 5-year results for relapse-free survival and survival without distant metas

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

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

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

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

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

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

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

68 n independent predictor of poor EFS, distant relapse-free survival, and OS.

69 9%; relapse, nonrelapse mortality, GVHD-free relapse-free survival, and overall survival at 1 year we

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

71 Four-year event-free survival, relapse-free survival, and overall survival rates were 6

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

73 , yet the parameters for achieving sustained relapse-free survival are not fully delineated.

74 nce of aggressive breast cancers and reduces relapse-free survival, as well as enhances BCSC self-ren

75 59% in CHD, respectively, and the estimated relapse-free survival at 2 years was 81% and 40% for the

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

77 fenib plus trametinib significantly improved relapse-free survival at 3 years.

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

79 The primary end point was relapse-free survival at month 28.

80 ciles seem to derive a substantial long-term relapse-free survival benefit from targeted therapy (HR

81 To confirm the stability of the relapse-free survival benefit, longer-term data were nee

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

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

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

85 The primary end point was biochemical relapse-free survival (bRFS).

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

87 es in refractory/relapsed TTP and increasing relapse-free survival; caplacizumab targets the von Will

88 ns and CYP2D6 genotypes were associated with relapse-free survival (censored at the time of tamoxifen

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

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

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

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

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

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

95 The primary outcome was relapse-free survival, defined as the time from randomis

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

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

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

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

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

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

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

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

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

105 Major relapse-free survival estimates at month 28 were 100% (C

106 Relapse-free survival estimates at month 28 were 96% (95

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

108 ersus-host disease (GVHD), and GVHD-free and relapse-free survival following transplantation from var

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

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

111 3-year relapse-free survival for patients who had complete rese

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

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

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

115 howed higher leukemia-free survival and GVHD/relapse-free survival (GRFS).

116 The primary endpoint (GvHD-free, relapse-free survival [GRFS]) was defined as the time fr

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

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

119 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).

120 t chemotherapy indicated significantly worse relapse-free survival (HR = 0.29 (95% CI 0.08-0.98), p =

121 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 <

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

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

124 95% CI, 3.37 to 12.10; P < .001), decreased relapse-free survival (HR, 2.94; 95% CI, 1.84 to 4.69; P

125 elate with poor metastasis-free survival and relapse-free survival in affected patients.

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

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

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

129 than the median was prognostic for prolonged relapse-free survival in both treatment groups.

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

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

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

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

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

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

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

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

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

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

140 onal burden was independently prognostic for relapse-free survival in the placebo group (high TMB, to

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

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

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

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

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

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

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

148 When HCT does produce prolonged relapse-free survival, it commonly reflects graft-versus

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

150 ociated with poor disease-specific survival, relapse-free survival, lung-specific relapse, and liver-

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

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

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

154 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).

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

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

157 tabases, we uncover a remarkable decrease in relapse-free survival of breast cancer patients expressi

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

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

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

161 Median relapse-free survival of responders was 18.54 months (95

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 of 88 patients with similar risk AML had 54% relapse-free survival (P = 0.002).

177 was an independent predictor of overall and relapse-free survival (P = 0.007 and P < 0.001, respecti

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

179 CTCs showed significant shorter overall and relapse-free survival (P = 0.038 and P = 0.004, respecti

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

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

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

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

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

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

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

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

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

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

190 The primary endpoint was relapse-free survival, reported elsewhere.

191 = 0.03 and P = 0.04) of overall survival and relapse-free survival, respectively.

192 rove prognosis for overall survival (OS) and relapse free survival (RFS) outcomes.

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

194 val (DRFI) (94.1% vs. 85.0%, P < 0.0001) and relapse-free survival (RFS) (90.0% vs. 80.5%, P = 0.0003

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

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

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

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

199 s have reported significant benefits in both relapse-free survival (RFS) and overall survival (OS) fo

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

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

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

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

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

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

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

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

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

209 38-gene expression classifier predictive of relapse-free survival (RFS) could distinguish 2 groups w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 1989 to 1993 v 68% in 1999 to 2002), and the relapse-free survival (RFS) subsequently improved from 8

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

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

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

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

229 Relapse-free survival (RFS) was the primary endpoint of

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

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

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

233 liplatin chemotherapy (GEMOX) would increase relapse-free survival (RFS) while maintaining health-rel

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

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

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

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

238 were cumulative incidence of relapse (CIR), relapse-free survival (RFS), and overall survival (OS).

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

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

241 Here, we report relapse-free survival (RFS), overall survival (OS), and

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

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

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

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

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

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

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

249 The primary objective was to evaluate median relapse-free survival (RFS).

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

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

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

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

254 fic OS (HR 2.29 [1.5-3.48], p = 0.0004), and relapse-free survival (RFS; HR 1.92 [1.34-2.76], p = 0.0

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

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

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

258 5% confidence interval [CI], 1.04-1.81), and relapse-free survival (RFS; P = .005; HR, 1.52; 95% CI,

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

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

261 8 of 77 patients, 23.4%) had longer times of relapse-free survival than patients with small or no del

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

263 trametinib resulted in significantly longer relapse-free survival than placebo in patients with rese

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

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

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

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

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

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

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

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

272 Relapse-free survival was 100% at a median of 44 months

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

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

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 who achieved a complete response, the median relapse-free survival was 6.0 months (95% CI, 4.1 to 6.5

279 <100 x 10(9)/L) was achieved in another 25%; relapse-free survival was 66.7% at 12 months (median res

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

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

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

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

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

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

286 nths after the initial response, the rate of relapse-free survival was estimated to be 65% (79% among

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

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

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

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

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

292 Relapse-free survival was significantly superior in pati

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

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

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

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

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

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