ライフサイエンスコーパス: PFS

1 PFS benefit was maintained with lenvatinib versus placeb

2 PFS did not differ with age in either treatment arm.

3 PFS was also improved with eribulin versus dacarbazine (

4 PFS was also longer with IRd vs placebo-Rd in patients w

5 PFS was improved with IRd vs placebo-Rd in both high-ris

6 PFS was significantly different between these groups in

7 PFS was significantly improved with PAG treatment overal

8 Ten of the 11 PFS-associated pathways correlated with microbial divers

9 (n = 23), an objective response rate of 39%, PFS of 6.7 months, and duration of response of 19.6 week

10 There were 758 deaths and 787 PFS events.

11 A total of 93 PFS events occurred.

12 ls of OS (hazard ratio, 1.132; P = .026) and PFS (hazard ratio, 1.454; P = .017).

13 had an OS HR of 0.98 (95% CI, 0.80-1.19) and PFS HR of 0.48 (95% CI, 0.42-0.56).

14 led an OS HR of 0.69 (95% CI, 0.63-0.75) and PFS HR of 0.82 (95% CI, 0.76-0.89).

15 with a positive evaluation at baseline, and PFS was improved in this group (30-month PFS, 78.7% v 56

16 umbers of ALK-rearranged or ALK-CNG CTCs and PFS was observed.

17 ignificantly with nonprogressive disease and PFS.

18 s were conducted between imaging metrics and PFS.

19 without disease progression at 6 months, and PFS duration and overall survival (OS) were secondary en

20 se quantitative relationship between MRD and PFS, and to support general applicability of MRD surroga

21 ssociated with significantly superior OS and PFS compared with dacarbazine.

22 mograms provided useful prediction of OS and PFS for patients with OPSCC treated with primary radiati

23 In the validation set, OS and PFS models were well calibrated, and OS and PFS were sig

24 ethylation were associated with lower OS and PFS rates (p < 0.05).

25 PFS models were well calibrated, and OS and PFS were significantly different across tertiles of nomo

26 To develop and validate nomograms for OS and PFS, we used a derivation cohort of 493 patients with OP

27 e an independent prognostic factor in OS and PFS.

28 cted those reporting results for both OS and PFS.

29 t cycle 1 day 8 correlated with response and PFS.

30 Median overall survival and PFS for all patients were 250 months (95% confidence int

31 between quartiles of (68)Ga-DOTATATE TV and PFS (P = .001) and disease-specific survival (P = .002).

32 The primary end point was centrally assessed PFS.

33 pies to this patient population years before PFS results are mature.

34 nts with the objective of achieving the best PFS.

35 tus was associated with significantly better PFS overall (hazard ratio [HR], 0.41; 95% CI, 0.36-0.48;

36 This was associated with better PFS and OS.

37 istics showed higher discrimination for both PFS and OS in Cox models that included MRD (as opposed t

38 18a, were significantly associated with both PFS and OS in the univariate analysis and were still sta

39 cGVHD was significantly lower with ATLG, but PFS and OS also were lower.

40 nificantly shorter in women with a high CMI (PFS, 2.1 months; OS, 12.3 months) versus a low CMI (PFS,

41 1 months; OS, 12.3 months) versus a low CMI (PFS, 5.8 months; OS, 21.7 months).

42 In contrast, PFS was inferior in ABVD-treated patients receiving 20 G

43 nium skewness tended toward a less favorable PFS (hazard ratio, 3.48; 95% confidence interval [CI], 0

44 ADC-PET correlation leads to less favorable PFS.

45 es of ADC-PET correlation had more favorable PFS (hazard ratio, 0.17; 95% CI, 0.03-0.89 [P = 0.036]),

46 ) for OS and 0.70 (95% CI, 0.66 to 0.74) for PFS, and bias-corrected indices were similar.

47 atients (P < 0.0001, hazard ratio of 6.8 for PFS; P < 0.0001, hazard ratio of 6.6 for OS).

48 s the prognostic value of CR achievement for PFS and OS across the disease spectrum, regardless of th

49 howed statistically significant benefits for PFS but not for OS.

50 The value of iPET3/4 was also confirmed for PFS (P < 0.0001) and OS (P < 0.0001).

51 sis was an independent prognostic factor for PFS and OS, whereas PET-CT normalization before maintena

52 nce was an independent prognostic factor for PFS.

53 strategy and explored prognostic factors for PFS and OS.

54 ials of immunotherapy drugs were greater for PFS than for OS, with important differences for some dru

55 hreshold effect, the minimal value of HR for PFS to predict a non-null effect on OS.

56 erences by a ratio of HRs (rHRs): the HR for PFS to that for OS.

57 roectodermal tumor nor osteosarcoma) (HR for PFS, 0.39; 95% CI, 0.18-0.81; P = .01) appeared to benef

58 cohorts receiving more than 3 cycles (HR for PFS, 0.46; 95% CI, 0.23-0.93; P = .03) and those without

59 ng had PFS events, the hazard ratio (HR) for PFS was 0.73 (90% CI, 0.43 to 1.24) with VR-CHOP ( P = .

60 predictive for progression rate but not for PFS/OS.

61 s/BMPCs ratio retained significance only for PFS.

62 erapy as a potential surrogate end point for PFS in first-line FL therapy.

63 rates that CR30 is a surrogate end point for PFS in first-line FL treatment trials.

64 c PCs retained an independent prediction for PFS/OS, whereas the pPCs/BMPCs ratio retained significan

65 ic involvement were adversely prognostic for PFS (P = .006 and .002, respectively) but not OS.

66 tion of the KRAS-variant with p16 status for PFS in patients treated without cetuximab.

67 ared with all other treatment strategies for PFS.

68 onal complete response (CR) in 5 studies for PFS (n = 574) and 6 studies for OS (n = 616).

69 ignificant differences among the studies for PFS and OS.

70 t general applicability of MRD surrogacy for PFS across diverse patient characteristics, treatment re

71 f MRI and PET-CT regarding progression-free (PFS) and overall survival (OS).

72 Primary end points were progression-free (PFS) and overall survival.

73 % confidence interval CI, 4.7-7.4] and glass PFS 5 mo [95% CI, 0.9-9.2], P = 0.53; resin OS 7.7 mo [9

74 OP) and 18% (VR-CHOP) of patients having had PFS events, the hazard ratio (HR) for PFS was 0.73 (90%

75 All studies had PFS as the primary end point, and none were powered for

76 To determine if PFS provides feasible sample sizes for trials with mutat

77 usion This subanalysis demonstrated improved PFS with lenvatinib treatment versus placebo in both age

78 arginine deprivation with ADI-PEG20 improved PFS in patients with ASS1-deficient mesothelioma.

79 elow the median was associated with improved PFS (n = 29, log-rank p = 0.048) and OS (n = 29, log-ran

80 ing modulator, were associated with improved PFS.

81 rginine deprivation correlated with improved PFS.

82 monstrated a significant clinical benefit in PFS and ORR over standard-of-care sunitinib as first-lin

83 Conclusion No significant differences in PFS were observed between the bevacizumab and IFN arms,

84 The largest improvement in PFS was observed in patients with HA-high tumors who rec

85 nib to pemetrexed plus cisplatin resulted in PFS improvement.

86 irmed that ATLG was associated with inferior PFS (hazard ratio, 1.55; 95% CI, 1.05 to 2.28; P = .026)

87 were independently associated with inferior PFS, whereas DHL and partial response ( v complete respo

88 EBBP mutations were associated with inferior PFS.

89 that host-microbiome interactions influence PFS and fibroblast responsiveness.

90 Caution must be taken when interpreting PFS in the absence of OS data.

91 The primary end point is PFS.

92 mber with ALK-CNG on crizotinib and a longer PFS (likelihood ratio test, P = 0.025).

93 nse (odds ratio, 5.56; P = .0006) and longer PFS (hazard ratio [HR], 0.38; P = .011) and OS (HR, 0.17

94 n of PD-L1 in responding patients and longer PFS with increased T-lymphocyte infiltrates, irrespectiv

95 r primary treatment had significantly longer PFS compared with women who underwent OBS.

96 Median PFS for patients who underwent OBS was 26.4 months, comp

97 Median PFS was 4.4 months with C20, 5.1 months with C25, and 5.

98 Median PFS was 6.2 versus 2.8 months (hazard ratio, 1.36; 95% C

99 Median PFS was longer in patients with normal PTEN (13.5 v 6.7

100 s (95% Confidence Interval 8.1-14.2); median PFS was 3.5 months (95% Confidence Interval 2.4-4.7).

101 cebo], 20.6 months v 15.2 months) and median PFS gain of 4.0 months (HR, 0.49; 95% CI, 0.30 to 0.82;

102 of 39 months from random assignment, median PFS was not reached for lenalidomide maintenance versus

103 d overall survival vs the comparator; median PFS was not reached in the subgroup of CLL patients with

104 sease free or had persistent disease, median PFS was superior for those who received HMT (81.1 v 30.0

105 ility of "operational cure" was high; median PFS was 12 years, and the 10-year OS rate was 94%.

106 nib treatment significantly increased median PFS (8.2 v 5.6 months) and was associated with a 34% red

107 red with near-CR or partial response (median PFS, 27, 27, and 29 months, respectively; median OS, 59,

108 Results Median PFS and OS were significantly shorter in women with a hi

109 utive days of ibrutinib had a shorter median PFS vs those missing <8 days (10.9 months vs not reached

110 The median PFS by central review was 16.6 months (95% CI, 12.9 to 1

111 Neither the median PFS nor overall survival was reached.

112 By site review, the median PFS times were 15.4 months (95% CI, 12.6 to 17.2 months)

113 ete and 11 partial responses, and the median PFS was 4.8 months.

114 The median PFS was 52.8 months for the lenalidomide group and 23.5

115 The median PFS was 7.7 months v 7.3 months, respectively.

116 The median OS was 13 months and the median PFS was 9 months.

117 al (PFS) requires extended follow-up (median PFS, > 7 years).

118 ative stem cell transplant (SCT) with median PFS not reached.

119 he younger and older age groups, with median PFS of 20.2 versus 3.2 months (hazard ratio [HR], 0.19;

120 (95% CI, 0.462-0.888; P = .007), with median PFS of 20.6 vs 15.6 months.

121 al [CI], 0.321-0.918; P = .021), with median PFS of 21.4 vs 9.7 months; in standard-risk patients, HR

122 and PFS was improved in this group (30-month PFS, 78.7% v 56.8%, respectively).

123 onomic chemotherapy does not improve 6-month PFS, compared with placebo, among pediatric patients wit

124 o associations were observed between 9-month PFS milestone ratio and OS HR (R2 = 0.19; 95% CI, 0.03-0

125 at 12 or 9 months and OS HR but not 9-month PFS or 6-month ORR milestones and OS HR.

126 progression-free survival [PFS] >6 months), PFS, and overall survival (OS), both alone and in the co

127 improved outcomes with neither median OS nor PFS reached.

128 ion This study met its primary end points of PFS and TE event rate.

129 cose at re-assessment was also predictive of PFS (p = 0.037), as confirmed in models including BMI an

130 al therapy or chemotherapy was predictive of PFS for men with mCRPC.

131 and before maintenance was not predictive of PFS or OS.

132 a CMR was the only significant predictor of PFS and CSS (P < 0.0001).

133 Week 4 CMI was a strong predictor of PFS, even in the presence of circulating tumor cells ( P

134 We also evaluated surrogacy of PFS for OS by the coefficient of determination and the s

135 ge cohort of patients with NETs, in terms of PFS and disease-specific mortality.

136 gnificant benefit with lapatinib in terms of PFS and overall survival ( P > .05 for each).

137 predicted a significant treatment effect on PFS (hazard ratio, 0.69).

138 was developed to predict treatment effect on PFS using treatment effect on PB-MRD.

139 ent effect on PB-MRD and treatment effect on PFS.

140 ther CR30 could predict treatment effects on PFS.

141 stic factor without significant influence on PFS and OS after (90)Y TARE.

142 -varying effects of somatic mutation load on PFS in this cohort (n = 25, p = 0.044).

143 1273) provided data on the impact of MRD on PFS, and 12 studies (n = 1100) on OS.

144 The impact of MRD status on PFS and OS was assessed by pooling data from relevant tr

145 No differences in imaging response or PFS correlates were found for different treatment cohort

146 numerically higher with C25 versus D75; pain PFS was numerically improved with D75 versus C25.

147 /CC genotypes were associated with patients' PFS (HRadj = 1.21, 95% CI = 1.03-1.43, P adj = 0.021 for

148 ard-risk cytogenetics, and improves the poor PFS associated with high-risk cytogenetic abnormalities.

149 ere was no significant difference to predict PFS or OS within this study.

150 Primary PFS favored nintedanib (hazard ratio [HR], 0.56; 95% CI,

151 ent induction regimens anticipated prolonged PFS.

152 a CR or PR to R-CHOP significantly prolonged PFS in elderly patients with DLBCL.

153 tatus was strongly associated with prolonged PFS (median, 63 months; P < .001) and OS (median not rea

154 receiving MVA-5T4, independently prolonging PFS (5.0 vs 2.5 months; hazard ratio [HR], 0.48; 95% CI,

155 lved-field RT to extended-field RT regarding PFS was confirmed (HR, 1.0; 95% CI, 0.8 to 1.2).

156 ncluded overall survival, local and regional PFS, distant metastasis-free survival, quality of life,

157 FCR improved complete remission, PFS and overall survival vs the comparator; median PFS w

158 esin group than the (90)Y glass group (resin PFS 6.1 mo [95% confidence interval CI, 4.7-7.4] and gla

159 point but only 177 with a total motor score PFS.

160 monotypic PCs was associated with a shorter PFS and OS compared with patients with <0.1% monotypic P

161 th a pPCs/BMPCs ratio of </=5% had a shorter PFS compared with patients with pPCs/BMPCs ratio >5% (2-

162 r MR ADC postgadolinium skewness and shorter PFS (hazard ratio, 2.56; 95% CI, 1.11-5.91 [P = 0.028]),

163 CT was associated with significantly shorter PFS for both patients with BRCA-mutant HGSOC (multiple r

164 CT was an indicator of significantly shorter PFS for both patients with BRCA-mutant HGSOC and those w

165 ostgadolinium kurtosis tended toward shorter PFS (hazard ratio, 1.30; 95% CI, 0.98-1.74 [P = 0.073]).

166 e were significantly correlated with shorter PFS (P = .006, P = .0001, P = .002, and P = .0001, respe

167 ere the only factors correlated with shorter PFS (P = .01 and P = .0003, respectively).

168 d higher but not statistically significantly PFS and OS rates in the (90)Y resin group than the (90)Y

169 For required sample size, PFS with a motor diagnosis or total motor score progress

170 n = 157, respectively) had markedly superior PFS, OS, and ORR compared with patients with right-sided

171 ovement in median progression-free survival (PFS) (5.1 vs 1.3 months; P = .008; hazard ratio [HR], 3.

172 e was observed in progression-free survival (PFS) (Kaplan-Meier P value = 0.0166) between patients de

173 strated prolonged progression-free survival (PFS) after treatment with fludarabine-cyclophosphamide-r

174 ary outcomes were progression-free survival (PFS) and disease-specific mortality during a median foll

175 The 2-year OS, progression free survival (PFS) and local control (LC) in oligometastatic and polym

176 dy endpoints were progression-free survival (PFS) and overall survival (OS) assessed by Kaplan-Meier

177 ed with prolonged progression-free survival (PFS) and overall survival (OS) compared with near-CR or

178 ed with a shorter progression-free survival (PFS) and overall survival (OS) compared with patients wi

179 ht NER genes with progression free survival (PFS) and overall survival (OS) in 710 NSCLC patients.

180 s correlated with progression-free survival (PFS) and overall survival (OS) in patients with glioblas

181 ollow-up, the 2-y progression-free survival (PFS) and overall survival (OS) were 51% and 67%, respect

182 Both progression-free survival (PFS) and overall survival (OS) were lower with ATLG (2-y

183 3%; P < .01), but progression-free survival (PFS) and overall survival (OS) were similar in both grou

184 ycles, as well as progression-free survival (PFS) and overall survival (OS), was assessed using logis

185 tcomes, including progression-free survival (PFS) and overall survival (OS).

186 cal benefit rate, progression-free survival (PFS) and overall survival (OS).

187 were compared for progression-free survival (PFS) and overall survival, and a multivariable Cox regre

188 ary end point was progression-free survival (PFS) assessed by modified Response Evaluation Criteria i

189 ate (P = .04) and progression-free survival (PFS) at 5 and 10 years (P < .0001).

190 ced longer median progression-free survival (PFS) compared with those with lower DI regardless of del

191 The median progression-free survival (PFS) for all patients was 9.6 weeks (95% CI 8.0 to 15.7

192 mab improved both progression-free survival (PFS) for the first year (HR, 0.31; 95% CI, 0.10-0.94; P

193 nib could predict progression-free survival (PFS) in a cohort of ALK-rearranged patients.

194 ate end point for progression-free survival (PFS) in chronic lymphocytic leukemia (CLL) based on 3 ra

195 survival (OS) and progression-free survival (PFS) in CS patient samples with a follow-up spanning 234

196 To compare progression-free survival (PFS) in patients with LA-SCCHN treated with standard-fra

197 survival (OS) and progression-free survival (PFS) in trials of US Food and Drug Administration-approv

198 date, the median progression-free survival (PFS) is 17.9 months.

199 Progression-free survival (PFS) is the composite of a motor diagnosis or a progress

200 of 12.5%, median progression-free survival (PFS) of 14 months, and 2-year PFS of 20.4%.

201 RT), with 15-year progression-free survival (PFS) of 73% versus 52% (hazard ratio [HR], 0.5; 95% CI,

202 rial assessed the progression-free survival (PFS) of bevacizumab or interferon alfa-2b (IFN-alpha-2b)

203 cal endpoints and progression-free survival (PFS) or cause-specific survival (CSS).

204 ed MRD status and progression-free survival (PFS) or overall survival (OS) in 20 or more patients fol

205 erall local tumor progression-free survival (PFS) per nodule (including initial treatment failures) w

206 -line FL therapy, progression-free survival (PFS) requires extended follow-up (median PFS, > 7 years)

207 icantly prolonged progression-free survival (PFS) versus placebo in patients with radioiodine-refract

208 strated prolonged progression-free survival (PFS) versus placebo or observation in several randomized

209 p of 15.6 months, progression-free survival (PFS) was 17.4 months and overall survival was not reache

210 years, the 2-year progression-free survival (PFS) was 60% (95% CI, 55% to 65%) and the 2-year overall

211 Progression-free survival (PFS) was calculated as a composite end point of progress

212 Progression-free survival (PFS) was the primary end point.

213 version 1.1), and progression-free survival (PFS) were determined.

214 tive outcome, and progression-free survival (PFS) were evaluated by using logistic regression and Cox

215 nt improvement in progression-free survival (PFS) with ixazomib-lenalidomide-dexamethasone (IRd) comp

216 c chemotherapy on progression-free survival (PFS) with that of placebo in pediatric patients with pri

217 6 months, 9-month progression-free survival (PFS), 9-month overall survival (OS), and 12-month OS.

218 ll survival (OS), progression-free survival (PFS), actuarial distant metastasis, and locoregional rec

219 ted with inferior progression-free survival (PFS), and DHL was associated with poorer overall surviva

220 ll survival (OS), progression-free survival (PFS), and distant metastasis-free survival (DMFS) (Hazar

221 disease RR (mRR), progression-free survival (PFS), and molecular biomarker analysis.

222 survival (OS) and progression-free survival (PFS), and odds ratios (OR) for objective response rate (

223 ti-5T4 responses, progression-free survival (PFS), and overall survival (OS).

224 istogram metrics, progression-free survival (PFS), and overall survival.

225 OS, progression-free survival (PFS), and safety were analyzed.

226 as they relate to progression-free survival (PFS), fibroblast function, and leukocyte phenotypes.

227 tween the CMI and progression-free survival (PFS), overall survival (OS), and disease status at first

228 We described progression-free survival (PFS), overall survival (OS), and histologic transformati

229 Progression-free survival (PFS), overall survival (OS), and objective response rate

230 ity of remission, progression-free survival (PFS), overall survival (OS), and safety outcomes of pati

231 y end points were progression-free survival (PFS), response rate, and toxicity.

232 rimary end point, progression-free survival (PFS), was evaluated in 183 patients with centrally confi

233 survival (OS) and progression free survival (PFS), with AUC of 0.976 and 0.932, respectively.

234 survival (OS) and progression-free survival (PFS).

235 ary end point was progression-free survival (PFS).

236 d to response and progression-free survival (PFS).

237 ession to predict progression-free survival (PFS).

238 response rate and progression-free survival (PFS).

239 ary end point was progression-free survival (PFS).

240 included safety; progression-free survival (PFS); tumor, prostate-specific antigen, and pain respons

241 y end points were progression-free survival (PFS; overall) and thromboembolic (TE) event rate.

242 R) at week 6, the progression free-survival (PFS), overall survival (OS), and safety profile of cetux

243 s for progression-free and overall survival (PFS and OS, respectively) in early-stage I and II non-sm

244 h DCB (defined as progression-free survival [PFS] >6 months), PFS, and overall survival (OS), both al

245 ondary end points included overall survival, PFS by HA level, and objective response rate.

246 The PFS curves of the Track mutation carriers showed good ex

247 The PFS hazard ratio was 0.56 (95% CI, 0.33-0.96), with a me

248 ia and age x pack-years interaction; and the PFS model also included marital status, weight loss, and

249 es a significant OS benefit and confirms the PFS benefit with lenalidomide maintenance after ASCT in

250 With a median follow-up of 46 months, the PFS of panitumumab plus accelerated-fractionation RT was

251 of MRD(-) rates between arms, the log of the PFS hazard ratio decreased by -0.188 (95% confidence int

252 Correlation of the CR30 odds ratio with the PFS hazard ratio was evaluated by both linear regression

253 This PFS benefit was consistent across subgroups with individ

254 tional burden showed stronger correlation to PFS than did the change in number of lesions.

255 hs), the 6- and 12-month overall local tumor PFS rates for the 75 treated nodules were 87% (95% confi

256 factors associated with overall local tumor PFS.

257 only factor linked with overall local tumor PFS.

258 d midtreatment was the strongest univariable PFS predictor (hazard ratio, 1.97; 95% CI, 1.44 to 2.71;

259 1; P = .017), which was confirmed in updated PFS analyses (HR, 0.54; 95% CI, 0.33 to 0.87; P = .010).

260 The primary end point was PFS as defined by the proportion of patients without dis

261 Primary end point was PFS.

262 The primary end point was PFS; secondary end points included overall survival (OS)

263 CNG was the strongest factor associated with PFS (HR, 4.485; 95% confidence interval, 1.543-13.030, P

264 and the serum AFP level were associated with PFS (P = 0.04) and OS (P = 0.04).

265 d age remained significantly associated with PFS after adjusting for stage and tumor weight.

266 was significantly positively associated with PFS; tumors with higher values of ADC-PET correlation ha

267 or clinical covariates, DRD association with PFS remained significant.

268 kurtosis) had a significant association with PFS, although a higher PET postgadolinium skewness tende

269 Volume-based PET metrics correlate with PFS and OS and could be used for risk assessment in stag

270 untington disease trials can be planned with PFS, and there is evidence of generalizability of this a

271 ative correlation is associated with a worse PFS, which may indicate higher-grade elements within the

272 -variant treated without cetuximab had worse PFS than patients without the KRAS-variant (HR, 2.59; 95

273 baseline to week 4 was associated with worse PFS ( P < .001) and progressive disease at first restagi

274 ek 4 was independently associated with worse PFS (hazard ratio, 1.79; 95% CI, 1.23 to 2.60; P = .002)

275 receptor pathways, was associated with worse PFS.

276 The 2-y PFS and OS for iPET3/4-positive (n = 28) and iPET3/4-neg

277 TMTV </= 230 cm(3) and iPET3/4-negative [2-y PFS/OS, 79%/85%]; TMTV > 230 cm(3) and iPET3/4-negative

278 plus 30 Gy IF-RT was confirmed with 10-year PFS of 87% each (HR, 1.0; 95%, 0.6 to 1.5) and OS of 94%

279 6.7 years, and the estimated 5- and 10-year PFS rates for patients treated with R-CHOP were 88.5% (9

280 eiving 20 Gy instead of 30 Gy IF-RT (10-year PFS, 76% v 84%; HR, 1.5; 95% CI, 1.0 to 2.1).

281 0 Gy IF-RT was noninferior to 30 Gy (10-year PFS, 84% v 84%; HR, 1.0; 95% CI, 0.7 to 1.5).

282 th patients with <0.1% monotypic PCs (2-year PFS 31% vs 87%; P < .0001; 2-year OS 87% vs 98%, P = .02

283 th patients with <2.5% monotypic PCs (2-year PFS 41% vs 56%, P = .007; 2-year OS 55% vs 70%; P = .01)

284 h patients with pPCs/BMPCs ratio >5% (2-year PFS 43% vs 55%; P = .02), but without OS difference (2-y

285 free survival (PFS) of 14 months, and 2-year PFS of 20.4%.

286 as third-line or later therapy with a 2-year PFS of 49% (95% CI, 36% to 61%).

287 ed HDCT as second-line therapy with a 2-year PFS of 63% (95% CI, 57% to 68%), and 61 patients receive

288 The 4-year PFS in patients with DEL compared with those with non-DE

289 ear OS was 56% versus 67% ( P = .10); 4-year PFS in patients with DHL compared with those with non-DH

290 rrent DEL and DHL had a poor outcome (4-year PFS, 0%).

291 % was associated with better outcome (4-year PFS, 84% vs 35%; 4-year OS, 91% vs 57%; P < .0001), what

292 In ePET-positive patients, 5-year PFS improved from 77.4% for standard ABVD + INRT to 90.6

293 ients with ABC-like DLBCL without DE (5-year PFS rate, 39% [95% CI,19% to 59%] v 68% [95% CI, 52% to

294 that of patients in the GCB subgroup (5-year PFS rate, 68% [95% CI, 52% to 85%] v 85% [95% CI, 74% to

295 In ePET-negative patients, 5-year PFS rates in the F group were 99.0% versus 87.1% (HR, 15

296 COPPesc + INRT significantly improved 5-year PFS.

297 Five-year PFS was 22% (95% CI, 12%-32%); 5-year actuarial distant

298 Three-year PFS and overall survival for all patients were 71.4% and

299 Three-year PFS for 27 patients with Ki-67 LI >/= 15% was 48.5% comp

300 Two-year PFS rates were 77.6% with R-CHOP and 82.0% with VR-CHOP;