ライフサイエンスコーパス: relapse-free

1 2015 in Ontario, Canada, who were alive and relapse free 30 days after treatment completion (index d

2 ange, 15 to 62 months), 20 patients remained relapse free (5-year progression-free survival [PFS] +/-

3 Eighteen patients (60%) became relapse free after rituximab treatment.

4 On treatment, 43% patients were relapse free, although this increased to 64% when relaps

5 tients followed for >/=1 year, 21 (50%) were relapse-free and alive without systemic immunosuppressio

6 Relapse-free and overall survival and the incidence of s

7 of achieving complete remission and inferior relapse-free and overall survival as compared with FAB M

8 py was superior to capecitabine in improving relapse-free and overall survival for older women with e

9 eased risk of distant metastasis and reduced relapse-free and overall survival in breast cancer patie

10 was significantly associated with decreased relapse-free and overall survival in ER(+) breast cancer

11 Three-year relapse-free and overall survival ranged from 48% to 52%

12 A durable impact on both relapse-free and overall survival was seen only with the

13 ly-stage breast cancer would have equivalent relapse-free and overall survival with capecitabine comp

14 el of heterogeneity correlates with times of relapse-free and overall survival.

15 ongly associated with higher CIR and shorter relapse-free and overall survival.

16 rom those with high relapse rate and adverse relapse-free and overall survival.

17 Median relapse-free and overall survivals were 7 and 11 months,

18 Median relapse-free and overall survivals were 8 and 11 months,

19 Here, we compared disease-free, relapse-free, and overall survival between the patient g

20 to NSGCT, yielding 10-year disease-specific, relapse-free, and overall survival rates of 100%, 98%, a

21 mplete remission rates, inferior event-free, relapse-free, and overall survival.

22 atients in the interferon beta 1a group were relapse-free at 2 years compared with 278 (65%) patients

23 atients in the interferon beta 1a group were relapse-free at 2 years compared with 78% of patients in

24 nd the probability that a patient would have relapse-free B-cell aplasia was 73% (95% CI, 57 to 94).

25 s compared with 43% in patients who remained relapse free but full donor chimeras at 9 months post-tr

26 of 56 patients in the tocilizumab group were relapse-free compared with 29 (56%) of 52 patients in th

27 in relapsed/refractory patients than matched relapse-free controls (median baseline vitamin D, 21.4 n

28 tandard regimen and reduce treatment time to relapse-free cure by 75%.

29 ment is well founded, as demonstrated by 90% relapse-free cure rates in FMT treatment for recurrent C

30 ing and standard regimens, respectively, and relapse-free cure was obtained after 3 and 6 mo of treat

31 ation antibiotic therapy required to achieve relapse-free cure.

32 Three patients remained relapse free during tocilizumab treatment.

33 The primary efficacy endpoint was relapse-free efficacy at 6 months from initial dose (ie,

34 Relapse-free efficacy at 6 months was 57.7% (95% CI 43-7

35 tion were significant prognostic factors for relapse-free (hazard ratio [HR] 1.59, 95% CI 1.32-1.92,

36 that predicts tendency to relapse or remain relapse-free in antineutrophil cytoplasmic antibody (ANC

37 Six of the 10 long-term survivors remained relapse-free, including 4 who received allogeneic stem c

38 idence interval (CI) = 0.2-0.87) and distant relapse-free interval (HR = 0.31, CI = 0.13-0.76) compar

39 erall survival; relapse-free survival (RFS), relapse-free interval, and toxicity were secondary end p

40 il antigen, to be positively correlated with relapse-free, metastasis-free, or overall survival in br

41 sed pCR rates, but whether this will improve relapse-free or overall survival is unknown.

42 ients with CTCs showed significantly shorter relapse-free (P < 0.001) and overall survival (P < 0.001

43 CTC detection indicated significantly worse relapse-free (P < 0.001) and overall survival (P = 0.007

44 Relapse-free patients display lower intra-tumour methyla

45 patient (annual relapse rate), proportion of relapse-free patients, and proportion of patients with 3

46 Annualized relapse rate and proportion of relapse-free patients, as well as the proportion of pati

47 had a significantly greater probability of a relapse-free period (P<0.001), independent of ANCA serot

48 BD, providing control of symptoms and longer relapse-free periods.

49 eta1/alphaV integrin dual targeting achieved relapse-free radiosensitization and prevented metastatic

50 finities of at least 10 nM were required for relapse-free regression.

51 f HPV association, was a strong predictor of relapse-free (RFS) and overall survival (OS) (p < 0.001,

52 Relapse-free (RFS) and overall survival (OS) of AML+13 p

53 yses, DNMT3A(mut) did not impact event-free, relapse-free (RFS), or overall survival (OS) in either t

54 >/= 0.51 was associated with an unfavorable relapse-free (RFS, P = .0008) and overall survival (OS,

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

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

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

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

59 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 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).

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

79 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 <

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

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

82 95% CI, 3.37 to 12.10; P < .001), decreased relapse-free survival (HR, 2.94; 95% CI, 1.84 to 4.69; P

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 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

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

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

139 5% confidence interval [CI], 1.04-1.81), and relapse-free survival (RFS; P = .005; HR, 1.52; 95% CI,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Secondary endpoints were relapse-free survival and overall survival.

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

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

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

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

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

161 59% in CHD, respectively, and the estimated relapse-free survival at 2 years was 81% and 40% for the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 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).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 8 of 77 patients, 23.4%) had longer times of relapse-free survival than patients with small or no del

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

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

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

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

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

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

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

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

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

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

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

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

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

222 <100 x 10(9)/L) was achieved in another 25%; relapse-free survival was 66.7% at 12 months (median res

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

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

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

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

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

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

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

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

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

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

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

234 Relapse-free survival was significantly superior in pati

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

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

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

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

239 9; 95% CI, 0.46-1.01; P = 0.06 for GvHD-free/relapse-free survival).

240 , 81.5% vs 89.2% (log-rank test, P = .429;); relapse-free survival, 96.6% vs 92.4% (P = .2); visual a

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

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

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

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

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

246 9%; relapse, nonrelapse mortality, GVHD-free relapse-free survival, and overall survival at 1 year we

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 expression is significantly correlated with relapse-free survival.

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

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

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

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

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

286 The primary end point was relapse-free survival.

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

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

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

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

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

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

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

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

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

296 ast cancer correlate and are associated with relapse-free tumors.

297 hs of eculizumab treatment, 12 patients were relapse free; two had had possible attacks.

298 Patients who continued, alive and relapse free, were censored at their last known follow-u

299 Seven patients (44%) remained relapse free with a mean follow-up of 47 (range, 18-81)

300 follow-up of 48 months, 17 patients remained relapse free, with a 2-year event-free survival rate of