ライフサイエンスコーパス: PFS

1 PFS for patients with esophageal cancer was associated w

2 PFS was noninferior (HR, 1.00; 95% CI, 0.65 to 1.53) and

3 PFS was significantly improved in the adjuvant group (15

4 PFS, determined from objective tumor measurements perfor

5 PFS, overall survival (OS), peripheral-blood minimal res

6 6), DOR (median, NR v 5.0 months; P = .014), PFS (median, NR v 3.3 months; P = .020), and OS (1-year

7 ed tumors for ORR (55.2% v 74.1%; P = .037), PFS (8.4 v 11.5 months; P = .026), and OS (2-year rate:

8 e comparison of paclitaxel plus ART (week 48 PFS 50%, 32 to 67; n=59) and etoposide plus ART (20%, 6

9 Week-48 PFS rates were higher in the paclitaxel plus ART arm tha

10 Patients with CMB/LCA (n = 45) had 37% 5y-PFS, 62% 5y-OS, and 39% 5y-CSI-free survival.

11 d more frequently than the SHH-INF group (5y-PFS, 93%; n = 28) or group 4 patients (5y-PFS, 83%; n =

12 dation cohort, without prognostic impact (5y-PFS: iSHH-I, 73%, v iSHH-II, 83%; P = .25; n = 99).

13 Group 3 patients (5y-PFS, 36%; n = 14) relapsed more frequently than the SHH-

14 5y-PFS, 93%; n = 28) or group 4 patients (5y-PFS, 83%; n = 6; P < .001).

15 = 42) had 93% progression-free survival (5y-PFS), 100% overall survival (5y-OS), and 93% CSI-free (5

16 An additional 8 patients had a PFS > 6 months.

17 Uncertainty was explored using alternative PFS estimates and considering all symptomatic grade 2 or

18 Although PFS was not associated with size, site, or age, it was s

19 with improved LRC (HR, 0.321; P = 0.015) and PFS (HR, 0.402; P = 0.043).

20 ntly improved LRC (HR, 0.259; P = 0.036) and PFS (HR, 0.242; P = 0.017) compared with patients with a

21 ith P < .0001 against a null rate of 5%, and PFS was 11.4 months (90% CI, 8.4 to 16.3 months); respon

22 n PSA decline of greater or equal to 50% and PFS.

23 Median DOR and PFS were not reached; 84% and 85% of ibrutinib and zanub

24 al outcome, with significantly longer OS and PFS in responders than in nonresponders according to all

25 arison purposes, the resultant 2-year OS and PFS rates allowing for that dropout rate were 59.6% and

26 by resection had significantly worse OS and PFS than patients receiving first-line chemotherapy foll

27 ain estimated hazard ratios (HRs) for OS and PFS were 0.76 (0.71-0.82) and 0.81 (0.73-0.89) in a rand

28 l (PFS), and objective response rate; OS and PFS were also analyzed according to estrogen-receptor st

29 OS and PFS were calculated using multivariable Cox proportional

30 The OS and PFS were significantly different between responders and

31 s to be significantly associated with OS and PFS.

32 value of (64)Cu-DOTATATE SUV(max) for OS and PFS.

33 etic mutations and GC affected MRD rates and PFS.

34 Response depth, time to major response, and PFS are impacted by MYD88 and CXCR4 mutation status.

35 ation between prior (177)Lu-PSMA therapy and PFS, and a positive association between PSA decline of g

36 1%; 95% CI: 46%, 73%; P = 0.034), as well as PFS (73%; 95% CI: 58%, 83% compared with 50%; 95% CI: 36

37 A negative association between PFS and carriers of any A at NLRP1 rs12150220 and AA for

38 CNS-PFS (intracranial progression or death) and overall surv

39 Median CNS-PFS was 9.9 months in the tucatinib arm versus 4.2 month

40 39% with nivolumab and 17% with dacarbazine; PFS rates were 28% and 3%, respectively.

41 ogical features associated with differential PFS between the treatment arms, including new immunomodu

42 ) nor tumor mutational burden differentiated PFS in either study arm.

43 ontrast, no significant difference in either PFS or OS was observed with the addition of PCV in the I

44 rapy and received reduced RT had encouraging PFS similar to patients in ACNS0122 who received full-do

45 f 79.2% (95% CI, 57.9-92.9) and an estimated PFS rate at 24 months of 87.2% (95% CI, 57.2-96.7) with

46 g/mL by week 8 was associated with favorable PFS and OS, while having prior episodes of PD and the ti

47 ts with ERCC1 levels < 1.7 receiving FOLFOX, PFS and response rate were statistically superior to IT,

48 , for OS and 15.5 vs. 2.2 mo, P < 0.001, for PFS, respectively).

49 hazard ratio was 0.50 (range, 0.32-0.77) for PFS.

50 V and Dmax(patient) were adverse factors for PFS (P = 0.027 and P = 0.0003, respectively) and for OS

51 SF3B1 as independent prognostic factors for PFS with GClb, whereas for VenG, only del(17p) was signi

52 ases were independent prognostic factors for PFS.

53 (patient) (>58 cm) yielded 3 risk groups for PFS (P = 0.0003) and OS (P = 0.0011): high with 2 advers

54 th (64)Cu-DOTATATE PET/CT was prognostic for PFS but not OS.

55 tatistically significant HR was reported for PFS in the glioma patients (HR = 1.23, 95% CI: 0.41, 3.7

56 e to those observed in the overall trial for PFS (hazard ratio [HR], 0.43; 95% CI, 0.28 to 0.64; P <

57 displayed a significant prognostic value for PFS and OS in DLBCL patients.

58 he optimal TMTV cutoff for progression-free (PFS) and overall survival (OS) was determined and confir

59 Differences in progression-free (PFS) and overall survival (OS) were evaluated using log-

60 have significantly longer progression-free (PFS) and overall survival (OS), and are better matched t

61 cinoma and how the progression events impact PFS.

62 elate with TMTV/survival, BCL2 >70% impacted PFS and could be stratified by TMTV.

63 High vs low TMTV significantly impacted PFS and OS, independent of maintenance treatment.

64 A-EPOCH-R was more toxic and did not improve PFS or OS compared with R-CHOP.

65 on-eligible patients with MM did not improve PFS or OS.

66 py was an independent predictor for improved PFS and OS and can be proposed as the standardized crite

67 IDELA improved PFS and OS compared with rituximab alone in patients wit

68 n was associated with significantly improved PFS but not OS after PSW analysis.

69 ysis, AHCT remained associated with improved PFS (HR, 0.70; 95% CI, 0.59 to 0.84; P < .05) but not im

70 of IMiD maintenance associates with improved PFS and OS.

71 lysis, this decline correlated with improved PFS and overall survival, especially when combined with

72 lets + bevacizumab and provides advantage in PFS, ORR, and R0 resection rate at the price of a modera

73 The difference in PFS was considered significant with a hazard ratio of 0.

74 l analyses showed significant differences in PFS between response categories classified by each of th

75 The absolute differences in PFS were -30% (95% CI -52 to -8) for the comparison of p

76 There was no improvement in PFS in patients receiving afatinib plus cetuximab compar

77 ted clinical benefit-specifically, increased PFS-in patients with symptomatic and progressive MTC.

78 TMTV was a strong prognosticator of inferior PFS and OS.

79 ctors independently associated with inferior PFS and OS were as follows: TP53 aberration, prior treat

80 symptoms, with no difference in intracranial PFS and OS, and should be considered a standard of care

81 not differ significantly in OS, intracranial PFS, or toxicity.

82 or response rate and longer, albeit limited, PFS, with toxicity of the combination regimen comparable

83 enefit, reduced hyperprogression, and longer PFS among patients treated with ICIs.

84 signed to FOLFOXIRI + bevacizumab had longer PFS (median, 12.2 v 9.9 months; HR, 0.74; 95% CI, 0.67 t

85 nd TBR(max) predicted a significantly longer PFS and OS (both P <= 0.03; univariate survival analyses

86 her BAF segment counts were linked to longer PFS (HR 0.49, p = 0.022) and OS (HR 0.49, p = 0.052).

87 ations) independently correlates with longer PFS (hazard ratio [HR], 0.63; 95% confidence interval [C

88 and vincristine) was associated with longer PFS (HR, 0.32; P = .003; HR, 0.13; P < .001) and OS (HR,

89 se on venetoclax were associated with longer PFS after BTKi salvage (P = .044 and P = .029, respectiv

90 hemoglobin level were associated with longer PFS and OS (all Ps < 0.05).

91 0.42, P = 0.043) was associated with longer PFS.

92 Median PFS and OS were 3.4 and 15.1 mo, respectively.

93 Median PFS and OS were 62 and 139 months, respectively.

94 Median PFS by BICR was 9.1 months (95% CI, 7.3 to 11.3) for bin

95 Median PFS was 13.3 months (90% CI, 12 months to not available/

96 Median PFS was 5.1 months (95% CI, 3.5 to 6.9 months) for all p

97 Median PFS was 7 months (95% CI 5-8) for patients with grade >=

98 Median PFS was 8.3 months (95% CI, 5.7 to 10.9 months).

99 18) to combination treatment, with a median PFS of 1.8 months versus 3.7 months versus 3.3 months, r

100 The IDELA/R-to-IDELA group had a median PFS of 20.3 months (95% CI, 17.3 to 26.3 months) after a

101 The 24-month PFS rate was 48.3%, and median PFS time was 16.8 months (95% CI, 4.6 months to not esti

102 After data cutoff, median PFS was 10.5 years in the rituximab maintenance arm comp

103 95% CI, 7.6 months to not estimable), median PFS was 7.4 months (95% CI, 5.3 to 8.7 months), and medi

104 The estimated median PFS and OS were 15.2 mo (95% CI, 13.1-17.4) and 18 mo (9

105 Estimated median PFS was significantly longer with Gef+C than Gef (16 mon

106 assignment follow-up of 13.5 months, median PFS was longer with continuous versus 1-year fixed-durat

107 follow-up of 22.4 months, respective median PFS, DOR, and OS were 6.7 months, not reached, and 25.3

108 , FOLFOX had a statistically superior median PFS compared with IT (5.7 v 2.9 months; hazard ratio, 0.

109 The median PFS and OS were 22 and 53 mo, respectively.

110 In patients with MYD88(WT), the median PFS was 0.4 years (P < .01 for three-way comparisons).

111 atients reached 6-month PFS6, and the median PFS was 1.7 months (95% CI, 1.4 to 1.8 months).

112 ss than or equal to 55% (n = 53), the median PFS was 11 mo and the median OS was 22 mo.

113 The median PFS was 5.5 months (95% CI, 3.4 to 9.5 months), and the

114 The 6-mo PFS rates were 94%, 48%, and 0% for World Health Organiz

115 The 24-month PFS rate was 48.3%, and median PFS time was 16.8 months

116 clax resistance mutation (estimated 24-month PFS, 69%).

117 ave not been reached; the estimated 45-month PFS was 62% (95% confidence interval, 51% to 71%).

118 rvival (PFS) was 3.4 months, and the 6-month PFS rate was 15% (90% CI, 8% to 31%).

119 e was 22% (90% CI, 4.1% to 55%), and 6-month PFS rate was 56% (90% CI, 31% to 100%).

120 ded progression-free survival (PFS), 6-month PFS, and overall survival.

121 With a median follow-up of 36 months, PFS and overall survival remain superior to bendamustine

122 R, 0.31; 95% CI, 0.11-0.85; P = .02) but not PFS (HR, 0.47; 95% CI, 0.19-1.13; P = .09).

123 of 36 months, the Kaplan-Meier estimates of PFS were 86% (95% confidence interval [CI], 76.6-91.9) f

124 However, the accuracy of prediction of PFS at 24 mo after (64)Cu-DOTATATE PET/CT SRI was modera

125 DOTATATE SUV(max) was 43.3 for prediction of PFS, with a hazard ratio of 0.56 (95% confidence interva

126 Both TMTV results were predictive of PFS (hazard ratio, 2.3 and 2.6 for TMTV(PARS) and TMTV(R

127 tio of >=0.1 was an independent predictor of PFS (HR 2.5, P = 0.01) and OS (HR 2.2, P = 0.03).

128 WHO subgroup was a significant predictor of PFS after adjustment for clinical variables and treatmen

129 = 0.01], and was an independent predictor of PFS and OS on multivariable analysis.

130 gnature remained an independent predictor of PFS in multivariable analysis adjusting for stage, human

131 ed VTE during follow-up had shorter times of PFS (HR, 1.74; 95% CI, 1.19-2.54; P = .004) and OS (HR,

132 iated with significant decreases in times of PFS and OS.

133 heless, distribution of treatment effects on PFS did not vary with expression.

134 ng to PERCIST(MTV) predicted prolonged OS or PFS (P < 0.01), whereas all other imaging criteria and p

135 ORR (P = .63, .29, and .27, respectively) or PFS (P = .28, .27, and .32).

136 of overall and progression-free survival (OS/PFS) in chemorefractory metastatic colorectal cancer (mC

137 = 0.001) with significantly worse outcomes (PFS, 95% CI 6-36, 49-73 versus 74-90 months) who were no

138 ionary parameters strongly predict patients' PFS and OS.

139 S (HR = 1.27, 95% CI: 1.01, 1.59) and poorer PFS (HR = 1.46, 95% CI: 1.17, 1.82).

140 failure time model was developed to predict PFS, which was represented as a nomogram and an online c

141 The accuracy was moderate for predicting PFS (57%) at 24 mo after (64)Cu-DOTATATE PET/CT.

142 atment metabolic tumor volume for predicting PFS, with a C-index of 0.72 versus 0.67 (training) and 0

143 that TBR(max) changes predicted a prolonged PFS (P = 0.012) and changes of MTV a prolonged OS (P = 0

144 therapy to gefitinib significantly prolonged PFS and OS but increased toxicity in patients with NSCLC

145 epening of responses and likely to prolonged PFS and OS.

146 nts with RR cHL, and resulted in a promising PFS in a high-risk patient cohort, supporting the testin

147 The median PSA-PFS and overall survival were 3.2 mo (95% confidence int

148 QA-PFS was calculated as progression-free survival function

149 The significant differences in QA-PFS and Q-TWiST confirm the benefit of rucaparib versus

150 Mean QA-PFS was significantly longer with rucaparib versus place

151 Higher IMH was associated with reduced PFS for every standard deviation decrease in the area un

152 Higher MTV was associated with reduced PFS for every standard deviation increase (hazard ratio

153 ases, and showed promising results regarding PFS and OS.

154 zard ratio [HR], 0.6 and 0.47, respectively; PFS: HR, 0.36 and 0.24, respectively).

155 n the efficacy of CTx versus ASCT for second PFS (HR, 0.7; 95% CI, 0.3 to 1.6; P = .39).

156 on-free survival (PFS) after relapse (second PFS) treated with either ASCT or CTx and performed sensi

157 ged > 60 years at relapse had shorter second PFS (hazard ratio [HR], 3.0; P = .0029) and were mostly

158 ho were aged <= 60 years, the 2-year, second PFS rate was 94.0% with CTx (95% CI, 85.7% to 100%) vers

159 positive for PD-L1) at baseline had shorter PFS.

160 nts with low SMI had a significantly shorter PFS (HR = 1.66 [95% CI: 1.05-2.61]; p = 0.0291) at univa

161 ogenic mutations had a significantly shorter PFS (p = 0.005).

162 PI3K/MTOR pathway had significantly shorter PFS than those without these mutations after tyrosine ki

163 unmutated IGHV were associated with shorter PFS.

164 .042); higher GC was associated with shorter PFS.

165 .98; P < 0.001) were associated with shorter PFS; necrosis on pathology (HR, 0.42, P = 0.043) was ass

166 and CD8(+) CAR T cells experienced superior PFS (P = .02 and .04, respectively).

167 therapy (EOCT) was associated with superior PFS compared with low MRD positivity (HR, 0.50) and high

168 7 fewer months of progression-free survival (PFS) (95% confidence interval [CI] 5-29, 49-69 versus 70

169 s associated with progression-free survival (PFS) (hazard ratio [HR] = 0.99; 95% confidence interval

170 ciated with worse progression-free survival (PFS) (HR = 1.51, 95% CI:1.03-2.22, p-value = 0.037) and

171 9; P = 0.011) and progression-free survival (PFS) (HR, 0.276; P = 0.006).

172 34, p = 0.02) and progression free survival (PFS) (HR:1.45, p < 0.001) due to an increase in MM progr

173 0.02) and shorter progression-free survival (PFS) (p = 0.02) compared to patients without the mutatio

174 ciate with longer progression-free survival (PFS) [hazard ratio (HR) 0.32, p < 0.001], and overall su

175 survival (OS) and progression-free survival (PFS) after (225)Ac-PSMA-617 treatment.

176 ts based on their progression-free survival (PFS) after FOLFIRINOX.

177 zards regression, progression-free survival (PFS) after relapse (second PFS) treated with either ASCT

178 urvival (OS), and progression-free survival (PFS) among patients with PMNSGCTs undergoing resection a

179 surgery improved progression-free survival (PFS) and delayed new disease in patients with oligometas

180 Median progression-free survival (PFS) and median overall survival after BTKi initiation w

181 lity of life, and progression-free survival (PFS) and overall survival (OS) at 1, 2, and 3 y.

182 ed with prolonged progression-free survival (PFS) and overall survival (OS) at PM (OS: hazard ratio [

183 es were to assess progression-free survival (PFS) and overall survival (OS) in all patients treated w

184 ove prediction of progression-free survival (PFS) and overall survival (OS) in diffuse large B-cell l

185 56 months, 5-year progression-free survival (PFS) and overall survival (OS) rates were 72% and 84% fo

186 ry endpoints were progression-free survival (PFS) and overall survival (OS) times.

187 Progression-free survival (PFS) and overall survival (OS) were compared between res

188 rmed to calculate progression-free survival (PFS) and overall survival (OS), defined from the start o

189 e events (irAEs), progression free survival (PFS) and overall survival (OS).

190 gnostic value for progression-free survival (PFS) and overall survival (OS).

191 predict patients' progression-free survival (PFS) and overall survival (OS).

192 ll survival (OS), progression-free survival (PFS) and response rate.

193 imary outcome was progression-free survival (PFS) at week 48, using a 15% non-inferiority margin to c

194 ary end point was progression-free survival (PFS) by blinded independent central review (BICR); addit

195 nature to predict progression-free survival (PFS) by fitting an L1-regularized Cox regression model.

196 ulted in improved progression-free survival (PFS) compared with bendamustine plus rituximab (BR) in p

197 Early progression-free survival (PFS) events were associated with low tumor mutational bu

198 with an effect on progression-free survival (PFS) for both treatment groups: GClb (hazard ratio [HR],

199 n of response and progression-free survival (PFS) have not been reached; the estimated 45-month PFS w

200 iated with longer progression free survival (PFS) in patients treated with EGFR-TKIs, while EGFR-DLS

201 one would improve progression-free survival (PFS) in patients with treatment-naive EGFR-mutant non-sm

202 ary end point was progression-free survival (PFS) in the intention-to-treat population.

203 The 2-year progression-free survival (PFS) is 30% (95% confidence interval, 20% to 70%). Subje

204 es using a median progression-free survival (PFS) of >= 9 mo and overall survival (OS) of >= 15 mo as

205 The OS and progression-free survival (PFS) of patients with complete and partial response were

206 Additionally, the progression-free survival (PFS) of stage IV patients was comparatively shorter in f

207 was to determine progression-free survival (PFS) of these patients.

208 ted with inferior progression-free survival (PFS) or overall survival (OS), apart from inferior OS fo

209 monstrated longer progression-free survival (PFS) over bortezomib and dexamethasone (Vd) in patients

210 rall survival and progression-free survival (PFS) probabilities were 86% and 59%, respectively.

211 and an estimated progression-free survival (PFS) rate at 24 months of 91.5% (95% CI, 70.0-97.8) with

212 The median 5-year progression-free survival (PFS) rate for all patients was not reached, and was 70%

213 ly, 5-year OS and progression-free survival (PFS) rates were 32.1% and 23% and 18.3% and 13% (P = .05

214 mary endpoint was progression-free survival (PFS) stratified by mutation profiles in ctDNA.

215 The median progression-free survival (PFS) was 2 and 3.9 months in the nivolumab and nivolumab

216 The median progression-free survival (PFS) was 3.4 months, and the 6-month PFS rate was 15% (9

217 y, whereas median progression-free survival (PFS) was 3.7 months and 8.0 months, respectively (P = .0

218 The progression-free survival (PFS) was 32% +/- 6%, and the overall survival (OS) was 7

219 Median progression-free survival (PFS) was 5.6 months (95% CI, 1.9 to 7.4 months); the PFS

220 Progression-free survival (PFS) was a secondary endpoint.

221 Median DOR and progression-free survival (PFS) were 11.0 and 4.5 months in all patients and were n

222 se rate (ORR) and progression-free survival (PFS) were calculated.

223 icantly prolonged progression-free survival (PFS) with first-line avelumab + axitinib versus sunitini

224 Durability of progression-free survival (PFS) with ibrutinib can vary by patient subgroup.

225 nt improvement in progression-free survival (PFS) with tucatinib.

226 d points included progression-free survival (PFS), 6-month PFS, and overall survival.

227 yses included OS, progression-free survival (PFS), and objective response rate; OS and PFS were also

228 ll survival (OS), progression-free survival (PFS), and overall response rate were compared between an

229 nse to treatment, progression-free survival (PFS), and overall survival (OS).

230 f response (DOR), progression-free survival (PFS), and overall survival (OS).

231 ator of response, progression-free survival (PFS), and overall survival.

232 ponse rate (ORR), progression-free survival (PFS), duration of response (DoR), and overall survival (

233 ponse rate (MRR), progression-free survival (PFS), duration of response (DOR), disease burden, and sa

234 ll survival (OS), progression-free survival (PFS), duration of response (DOR), safety, ORR according

235 ent end points of progression-free survival (PFS), event-free survival, duration of response, and ove

236 End points were progression-free survival (PFS), freedom from transformation, and overall survival

237 y was assumed for progression-free survival (PFS), if the upper limit of the 95% CI for the hazard ra

238 provided data on progression-free survival (PFS), no statistically significant HR was reported for P

239 d points included progression-free survival (PFS), objective response rate (ORR), and safety.

240 y end points were progression-free survival (PFS), objective response rate (ORR), R0 resection rate,

241 Progression-free survival (PFS), OS, and adverse events were also assessed.

242 y end points were progression-free survival (PFS), overall response rate (ORR), overall survival (OS)

243 OS), intracranial progression-free survival (PFS), toxicity, and patient-reported symptom burden.

244 d points included progression-free survival (PFS), toxicity, and quality of life (QOL).

245 l end points were progression-free survival (PFS), toxicity, biomarkers of response as determined by

246 overall (OS) and progression-free survival (PFS).

247 ional control and progression free survival (PFS).

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

249 survival (OS), or progression-free survival (PFS).

250 benefit rate and progression-free survival (PFS).

251 seline on patient progression-free survival (PFS).

252 point was 3-year progression-free survival (PFS).

253 CIST) version 1.1 progression-free survival (PFS).

254 meta-analysis was progression-free survival (PFS).

255 ary end point was progression-free survival (PFS); secondary end points included overall survival (OS

256 racteristics with progression-free survival (PFS; by RECIST) were evaluated by Cox regression and Kap

257 aphic or clinical progression free-survival (PFS) by using the Johns Hopkins University modified-Adna

258 r outcome (2-year progression-free survival [PFS] >= 90%) with reduced treatment-related neurotoxicit

259 d not progressed (progression-free survival [PFS] population).

260 w conversion to detectable MRD and sustained PFS after completion of 2 years of venetoclax-rituximab

261 suffer from secondary pollen food syndrome (PFS).

262 T has significant association with long-term PFS and MFS in localized PCa.

263 hemotherapy provides a significant long-term PFS, but not OS, benefit over observation.

264 he 3' end of the RNA target site (called the PFS).

265 ersus 1-year fixed-duration treatment in the PFS (not reached v 32.5 months; HR, 0.61 [95% CI, 0.37 t

266 5.6 months (95% CI, 1.9 to 7.4 months); the PFS rate at 6 months was 39.5%.

267 ility to risk-stratify patients according to PFS.

268 uous versus 1-year fixed-duration treatment (PFS population: 24.7 months v 9.4 months; hazard ratio [

269 pretreatment parameters was performed using PFS and overall survival (OS) end-points.

270 by using the Wilcoxon rank sum test and with PFS by using the log-rank test.

271 x(patient) was significantly associated with PFS (P = 0.0014) whereas both factors remained significa

272 and ECOG PS as independently associated with PFS and OS.

273 SMA treatment was negatively associated with PFS in both univariate and multivariate analyses.

274 T pathway mutations were not associated with PFS, overall survival, or objective response after CPI.

275 from last PD to vaccine were associated with PFS.

276 and postoperative STMs were associated with PFS.

277 ch was associated with a significantly worse PFS (p = 0.00079).

278 umber of sites >2 were associated with worse PFS (P < .05).

279 o any A carriers, were associated with worse PFS in KRAS wild-type (wt) patients (HR = 1.94, 95% CI:1

280 tology (P = .005) were associated with worse PFS.

281 to high-risk versus low-risk groups with 2-y PFS rates of 59.1% versus 89.4% (hazard ratio, 4.4; 95%

282 = 0.0011): high with 2 adverse factors (4-y PFS and OS of 50% and 53%, respectively, n = 18), low wi

283 The 1-year PFS probabilities in all evaluable patients were 38% and

284 patients in the >=90% group (n = 20), 1-year PFS was 55%, compared with 94% in the <90% group (n = 17

285 agnosis with significantly different 10-year PFS (100%, 91%, 0% for scores of 0, 1, >=2, respectively

286 ntly improved in the adjuvant group (15-year PFS, 29% v 36%, hazard ratio [HR], 1.25 [95% CI, 1.07 to

287 ection failed to achieve the targeted 2-year PFS of 90%.

288 nd SHH-II, which were associated with 2-year PFS rates of 30.0% (95% CI, 1.6% to 58.4%) and 66.7% (95

289 For those who achieved CR/CRi, the 3-year PFS estimate was 83%.

290 The 3-year PFS rates for all 804 patients combined were 47%, 74%, a

291 l of 473 patients underwent PC-RPLND; 5-year PFS for patients with pure teratoma in PC-RPLND specimen

292 The 5-year PFS rate was not reached in arm 1 (3.2%; 95% CI, 0% to 1

293 The 5-year PFS rates were 91.1% after RT, 90.5% after CMT, 77.8% af

294 With median follow-up of 2.3 years, 5-year PFS was 61.9% (95% CI, 57.1% to 66.2%) for those with te

295 a median follow-up of 96 months, the 5-year PFS was 67% (95% CI, 54% to 82%) and the 5-year OS was 8

296 At a 25% 5-year PFS, improvements in life expectancy were smaller (3.4 y

297 n optimistic scenario, assuming a 35% 5-year PFS, tisagenlecleucel increased life expectancy by 4.6 y

298 Five-year PFS and OS in the entire cohort were 87.1% and 98.3%, re

299 Four-year PFS and OS rates were higher with VenR than BR, at 57.3%

300 Two-year PFS and overall survival rates were 52% (95% CI, 32.4% t