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1 state cancer and are associated with reduced progression free survival.
2 represent a worse prognostic factor for PCa progression free survival.
3 the accuracy of the 2 methods for predicting progression-free survival.
4 M and identify patients with prolongation of progression-free survival.
5 The primary objective was to determine the progression-free survival.
6 rize patients with glioblastoma according to progression-free survival.
7 he primary outcome was investigator-assessed progression-free survival.
8 c (18)F-DOPA WBMB (>7.5) was associated with progression-free survival.
9 gative predictive values were calculated for progression-free survival.
10 oestradiol uptake was associated with longer progression-free survival.
11 d during relapse and correlated with shorter progression-free survival.
12 An additional endpoint was progression-free survival.
13 ints were overall survival and imaging-based progression-free survival.
14 nformation about overall survival instead of progression-free survival.
15 e correlation between staining intensity and progression-free survival.
16 extensive nodularity (MBEN; n = 42) had 93% progression-free survival (5y-PFS), 100% overall surviva
17 study reported no significant improvement in progression-free survival (a primary endpoint) with week
19 e primary endpoint was investigator-assessed progression-free survival according to Response Evaluati
22 ifferent from the intention-to-treat primary progression-free survival analysis of ICON8, which defin
24 iations between gene expression features and progression free survival and response to treatment were
26 Patients responding to R-CHOP had median progression-free survival and OS times of 5.4 and 9.8 ye
27 nse Evaluation Criteria in Solid Tumours 1.1 progression-free survival and overall survival (group A
31 h a median follow-up of 533 days, the 1-year progression-free survival and overall survival for all e
32 stuzumab and capecitabine resulted in better progression-free survival and overall survival outcomes
33 azitaxel significantly improved radiographic progression-free survival and overall survival versus ab
34 a median follow-up of 11 months, the 1-year progression-free survival and overall survival were 23%
37 show a clinically meaningful improvement in progression-free survival and was associated with more a
38 s third-line or fourth-line therapy improved progression-free survival and was better tolerated compa
39 latinum led to superior overall survival and progression-free survival, and a higher proportion of pa
41 e primary endpoint was investigator-assessed progression-free survival, and analyses included all pat
42 ated with response to neoadjuvant treatment, progression-free survival, and overall survival as end p
43 ulation frequencies with treatment response, progression-free survival, and overall survival was also
46 an follow-up of 18.9 months (IQR 10.4-23.8), progression-free survival as assessed by the study inves
47 ee survival analysis of ICON8, which defined progression-free survival as the time from randomisation
51 s in the olaparib arm achieved longer median progression-free survival, assessed by blinded independe
58 ensitivity analysis of investigator-assessed progression-free survival at the overall survival databa
59 s with glioblastoma is controversial because progression-free survival benefit did not translate into
60 f PARP inhibitors, which have demonstrated a progression-free survival benefit in the BRCAm cohort.
62 respecified two-sided alpha of 0.2 in median progression-free survival between group A (8.3 months, 9
63 (n=1552), the difference in estimated median progression-free survival between the CDKI plus fulvestr
66 and abemaciclib, have significantly improved progression-free survival by a number of months when com
70 e first-line setting significantly prolonged progression-free survival compared with a fixed-duration
71 ignificant improvement in post-randomization progression-free survival compared with intermittent dos
74 dition of capivasertib prolonged a composite progression-free survival (cPFS) end point that included
77 a primary endpoint of investigator-assessed progression-free survival, defined as time from date of
78 %; p < 0.001), a significantly longer median progression-free survival duration (1.7 months [95% conf
80 rogression-free survival (Jan 30, 2019), 112 progression-free survival events had occurred, 49 (71%)
87 The primary endpoints (overall survival and progression-free survival) have been published previousl
88 n/100 g +/- 21 for ypT0-1; P = .01), shorter progression-free survival (hazard ratio = 0.97; 95% conf
89 d was independently associated with inferior progression-free survival (hazard ratio, 1.5; P = .02) a
91 y reflecting its effectiveness for extending progression-free survival; however, these parameters wer
92 ignificantly reduced GBM growth and improved progression free survival in two clinically relevant ort
93 icantly enhanced tumor growth inhibition and progression-free survival in an aggressive model of undi
96 No difference was observed between median progression-free survival in group B (5.7 months, 95% CI
99 pathways may postpone resistance and extend progression-free survival in many cancer indications.
100 3 activity associating with poor overall and progression-free survival in melanoma patients undergoin
101 metastasis showed a significant reduction in progression-free survival in patients allocated to cetux
102 tion of capivasertib to fulvestrant improved progression-free survival in patients with aromatase inh
103 fe and tolerable and significantly increased progression-free survival in patients with BRAF(V600) mu
104 is interim analysis, with partial alpha from progression-free survival in patients with CPS of 10 or
105 ed in significant and durable improvement in progression-free survival in patients with germline BRCA
106 ib and the MEK inhibitor trametinib improves progression-free survival in patients with metastatic an
107 of a theranostic agent in markedly improving progression-free survival in patients with metastatic ga
108 ine platinum-based chemotherapy and prolongs progression-free survival in patients with metastatic ur
109 emotherapy as first-line treatment prolonged progression-free survival in patients with metastatic ur
110 cell dose, is associated with longer OS and progression-free survival in patients with relapsed CLL.
111 docetaxel was previously reported to improve progression-free survival in platinum-refractory, advanc
112 ibitor-treated patients (n=2252), the median progression-free survival in the CDKI plus aromatase inh
114 all survival analysis (May 31, 2019), median progression-free survival in the intention-to-treat popu
115 e primary endpoint was investigator-assessed progression-free survival in the intention-to-treat popu
116 Primary endpoints were overall survival and progression-free survival in the intention-to-treat popu
117 ed the combination treatment for group A and progression-free survival in the intention-to-treat popu
118 for olaparib was also seen for imaging-based progression-free survival in the overall population (coh
119 .6-1.9) in the triplet therapy group, median progression-free survival is 1.2 years (95% CI 1.7-not r
121 metabolic response, toxicity (CTCAE), local progression-free survival (LPFS) and patient perception
122 patients (de novo) had an ORR of 44%, median progression-free survival (mPFS) of 6 months, and 16% CR
123 esponse and maintained this response, with a progression-free survival of 29 months at last assessmen
124 exhibited an enrichment in response rate and progression-free survival of 44% and 6.2 months vs 19% a
125 cantly better long-term survival with 5-year progression-free survival of 49% vs 30%, 34%, and 23%, r
126 gnificant differences were found between the progression-free survival of iPET- and iPET+ patient gro
128 plantation and a plethora of new agents, the progression-free survival of patients with PTCLs needs t
131 without obinutuzumab significantly improved progression-free survival over obinutuzumab-chlorambucil
132 Participants were monitored for safety, progression-free survival, overall survival (OS), and im
133 response, disease control rate at 32 weeks, progression-free survival, overall survival, and pharmac
134 ry end points included duration of response, progression-free survival, overall survival, and safety.
135 duration of response, disease control rate, progression-free survival, overall survival, and safety.
137 nt difference in overall survival (P = .75), progression-free survival (P = .79), or response duratio
140 e primary endpoint was investigator-assessed progression-free survival per Response Evaluation Criter
141 primary endpoints were investigator-assessed progression-free survival per Response Evaluation Criter
142 ORR), immune-related adverse events (irAEs), progression free survival (PFS) and overall survival (OS
143 cantly and positively associated with longer progression free survival (PFS) in patients treated with
145 verse TME associated with 17 fewer months of progression-free survival (PFS) (95% confidence interval
146 as continuous variable, was associated with progression-free survival (PFS) (hazard ratio [HR] = 0.9
147 C) (hazard ratio [HR], 0.279; P = 0.011) and progression-free survival (PFS) (HR, 0.276; P = 0.006).
148 rolactin (PRL) levels (p = 0.02) and shorter progression-free survival (PFS) (p = 0.02) compared to p
149 R segment counts were associate with longer progression-free survival (PFS) [hazard ratio (HR) 0.32,
150 les predictive for overall survival (OS) and progression-free survival (PFS) after (225)Ac-PSMA-617 t
152 red, by Cox proportional hazards regression, progression-free survival (PFS) after relapse (second PF
153 ement strategies, overall survival (OS), and progression-free survival (PFS) among patients with PMNS
155 S and BMS < 4 were associated with prolonged progression-free survival (PFS) and overall survival (OS
157 e TMTV(REF) in terms of prognostic value for progression-free survival (PFS) and overall survival (OS
158 algorithm were applied to predict patients' progression-free survival (PFS) and overall survival (OS
160 terruptions and delays, quality of life, and progression-free survival (PFS) and overall survival (OS
161 After median follow-up of 56 months, 5-year progression-free survival (PFS) and overall survival (OS
165 We developed an imaging signature to predict progression-free survival (PFS) by fitting an L1-regular
166 x plus rituximab (VenR) resulted in improved progression-free survival (PFS) compared with bendamusti
168 ere the only abnormalities with an effect on progression-free survival (PFS) for both treatment group
170 ating-characteristic analyses using a median progression-free survival (PFS) of >= 9 mo and overall s
173 Thrombosis was not associated with inferior progression-free survival (PFS) or overall survival (OS)
174 this subset, the 1-year overall survival and progression-free survival (PFS) probabilities were 86% a
175 e interval [CI], 78.9-99.9) and an estimated progression-free survival (PFS) rate at 24 months of 91.
177 SD and HD arms, respectively, 5-year OS and progression-free survival (PFS) rates were 32.1% and 23%
184 , which demonstrated significantly prolonged progression-free survival (PFS) with first-line avelumab
186 se rate (ORR); secondary end points included progression-free survival (PFS), 6-month PFS, and overal
188 rmed data extraction; overall survival (OS), progression-free survival (PFS), and overall response ra
189 tcomes were toxicity, response to treatment, progression-free survival (PFS), and overall survival (O
190 points included duration of response (DOR), progression-free survival (PFS), and overall survival (O
191 ives included objective response rate (ORR), progression-free survival (PFS), duration of response (D
192 d points included major response rate (MRR), progression-free survival (PFS), duration of response (D
195 for the other study, which provided data on progression-free survival (PFS), no statistically signif
196 ival (OS), and secondary end points included progression-free survival (PFS), objective response rate
198 included overall survival (OS), intracranial progression-free survival (PFS), toxicity, and patient-r
204 linical or radiographic characteristics with progression-free survival (PFS; by RECIST) were evaluate
205 e, aiming to achieve similar outcome (2-year progression-free survival [PFS] >= 90%) with reduced tre
207 to 19.4% (n = 6/31; second line) and median progression-free survival ranging from 5.5 months (fourt
209 5.9 years (range, 0.5-10 years), the 6-year progression-free survival rate of patients who underwent
211 and bevacizumab achieved better overall and progression-free survival rates than sorafenib in unrese
212 he RVd group progressed; respective 24-month progression-free survival rates were 95.8% and 89.8%.
213 t the overall survival database lock, median progression-free survival remained significantly improve
217 ctively categorized 28 patients according to progression-free survival (short-term or long-term) with
218 ing P-AscH(-) have demonstrated increases in progression free survival, suggesting a reduction in met
219 plus obinutuzumab had a significantly longer progression-free survival than did patients given chlora
220 ib led to significantly longer imaging-based progression-free survival than the physician's choice of
224 achieve a PSA50 was associated with shorter progression-free survival, time on treatment, and overal
225 ved rates of stringent complete response and progression-free survival versus bortezomib, thalidomide
227 ant and clinically meaningful improvement in progression-free survival versus placebo-chemotherapy am
229 rant, and trastuzumab significantly improved progression-free survival versus standard-of-care chemot
236 nths (5.6-NE) in the EZH2(WT) cohort; median progression-free survival was 13.8 months (10.7-22.0) an
241 estrant-treated patients (n=396), the median progression-free survival was 18.6 months (95% CI 14.8-2
247 second planned interim analysis, the median progression-free survival was 34.6 months (95% CI 28.8-3
249 duration of response was 5.5 months, median progression-free survival was 4.2 months, and median ove
252 r the atezolizumab monotherapy group, median progression-free survival was 5.6 months (95% CI 3.6-7.4
257 ponse was 79% (95% CI, 54 to 94), and 1-year progression-free survival was 64% (95% CI, 37 to 82).
261 o 0.71; P<0.001), and the median duration of progression-free survival was 7.8 months and 5.6 months,
264 from the time of CAR T-cell infusion, median progression-free survival was 8.3 months (95% CI, 6.0 to
265 d trials, the difference in estimated median progression-free survival was 8.8 months in favour of CD
266 fidence interval [CI], 55 to 81), and 1-year progression-free survival was 82% (95% CI, 69 to 90).
268 mong patients with CPS of 10 or more, median progression-free survival was 9.7 months with pembrolizu
269 ponse was 73% (95% CI, 62 to 82), and 1-year progression-free survival was 92% (95% CI, 82 to 97).
274 ow-up of 28.3 months (IQR 25.6-33.1), median progression-free survival was longer with acalabrutinib-
277 follow-up of approximately 17 months, median progression-free survival was not reached in the KdD gro
278 months (IQR 46-59), no difference in median progression-free survival was observed (RVd 33.64 months
285 -free survival of the phase 3 ALCYONE trial, progression-free survival was significantly longer with
292 int was independent review facility-assessed progression-free survival, which has been reported previ
296 linical trials clearly demonstrated improved progression-free survival with targeted therapy over che
297 ent in independent review committee-assessed progression-free survival with venetoclax versus placebo
299 continued to show significant improvement in progression-free survival, with no new safety concerns.
300 irumab plus docetaxel significantly improves progression-free survival, without a significant improve