ライフサイエンスコーパス: relapse-free

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

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

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

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

5 on is associated with an increased period of relapse-free and overall survival (P=0.006 and 0.016, re

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 ar to have excess toxicity, and have similar relapse-free and overall survival compared to noncarrier

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

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

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

12 vant chemotherapy has led to improvements in relapse-free and overall survival in patients with breas

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

14 t chemotherapy regimens have improvements in relapse-free and overall survival similar to younger pat

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

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

17 g-rank analyses identified factors affecting relapse-free and overall survival, and regression models

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

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

20 ers was tested by treatment interactions for relapse-free and overall survival.

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

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

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

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

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

26 om onset of complete remission, 45% remained relapse-free as opposed to 20% on the control arm (P = .

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

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

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

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

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

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

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

34 Three patients remained relapse free during tocilizumab treatment.

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

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

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

38 ciated with significant improvements in both relapse-free (HR 0.92, 95% CI 0.72-1.18 for tumours with

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

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

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

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

43 ly associated with response to chemotherapy, relapse-free, or overall survival (OS).

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

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

46 static tissues was inversely correlated with relapse-free (P<0.0001) and overall (P<0.0001) survival.

47 Relapse-free patients display lower intra-tumour methyla

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

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

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

51 Conversely, p68 shows no association with relapse-free period, or overall survival, but it is asso

52 .33; P<0.001 for both comparisons), a higher relapse-free rate (79.7% and 78.9%, respectively, vs. 60

53 The primary outcome measure was the 2-year relapse-free rate (RFR) in patients with a negative PET

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

55 -containing chemotherapy experience improved relapse-free (RFS) and overall survival (OS) compared wi

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

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

58 >/= 0.51 was associated with an unfavorable relapse-free (RFS, P = .0008) and overall survival (OS,

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

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

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

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

63 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 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).

81 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 <

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 38-gene expression classifier predictive of relapse-free survival (RFS) could distinguish 2 groups w

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

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

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

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

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

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

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

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

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

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

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

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

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

116 1989 to 1993 v 68% in 1999 to 2002), and the relapse-free survival (RFS) subsequently improved from 8

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 5% confidence interval [CI], 1.04-1.81), and relapse-free survival (RFS; P = .005; HR, 1.52; 95% CI,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 59% in CHD, respectively, and the estimated relapse-free survival at 2 years was 81% and 40% for the

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

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

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

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

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

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

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

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

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

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

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

175 3-year relapse-free survival for patients who had complete rese

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

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

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

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

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

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

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

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

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

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

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

193 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).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 8 of 77 patients, 23.4%) had longer times of relapse-free survival than patients with small or no del

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

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

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

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

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

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

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

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

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

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

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

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

224 <100 x 10(9)/L) was achieved in another 25%; relapse-free survival was 66.7% at 12 months (median res

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

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

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

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

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

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

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

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

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

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

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

236 Relapse-free survival was significantly superior in pati

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

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

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

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

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

242 9; 95% CI, 0.46-1.01; P = 0.06 for GvHD-free/relapse-free survival).

243 , 81.5% vs 89.2% (log-rank test, P = .429;); relapse-free survival, 96.6% vs 92.4% (P = .2); visual a

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

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

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

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

248 9%; relapse, nonrelapse mortality, GVHD-free relapse-free survival, and overall survival at 1 year we

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 = 0.03 and P = 0.04) of overall survival and relapse-free survival, respectively.

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

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

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

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

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

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

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

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

274 expression is significantly correlated with relapse-free survival.

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

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

277 The primary end point was relapse-free survival.

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

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

280 The primary end point was relapse-free survival.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 ose, and the number of patients who remained relapse-free while the glucocorticosteroid dosage was ta

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