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1 gated PLN-induced tumor growth and increased progression-free survival.
2 Primary endpoint was 1-year progression-free survival.
3 pheral T cells was prognostic on overall and progression-free survival.
4 The primary end point was progression-free survival.
5 7 is associated with significantly decreased progression-free survival.
6 The primary endpoint was progression-free survival.
7 toxic effects, objective tumor response, and progression-free survival.
8 Primary end point was investigator assessed progression-free survival.
9 pression in melanoma correlated with shorter progression-free survival.
10 We also assessed progression-free survival.
11 stic value of the IMiD-14 gene signature for progression-free survival.
12 cells inversely correlated with overall and progression-free survival.
13 ligorecurrent prostate cancer (PCa) improves progression-free survival.
14 kinases CDK4 and CDK6 substantially improve progression-free survival.
15 The primary end point was 2-year progression-free survival.
16 ast cancer on the basis of an improvement in progression-free survival.
17 The primary outcome was progression-free-survival.
18 t favorable in terms of (1) hazard ratio for progression-free survival (0.13; 95% credible interval,
19 3.7 weeks [18.1-20.0]; hazard ratio [HR] for progression-free survival 1.28, 95% CI 0.99-1.65, p=0.06
20 ; 95% CI, 0.90-2.08; P = .15), as was median progression-free survival (1.9 vs 2.0 months; HR, 1.61;
21 or in the 75th percentile or higher (median progression-free survival 11.6 months and 16.9 months fo
22 XL2 in the 50th percentile or higher (median progression-free survival 11.7 months and 14.3 months fo
23 here was no significant difference in median progression free survival (12 months vs 9.3 months; P =
24 CI 37.5-54.6] vs 46.4% [37.5-54.8]); median progression-free survival (23.3 weeks [95% CI 19.6-30.4]
25 HR] 0.56 [95% CI 0.34-0.91], p=0.019; median progression-free survival 4.4 months [95% CI 2.1-8.6] vs
26 urvival (OS; 4 years, 30%; 5 years, 28%) and progression-free survival (4 and 5 years, both 13%) appe
27 erapy (HR 0.50 [0.30-0.84], p=0.0084; median progression-free survival 6.3 months [95% CI 2.1-10.4] v
28 mor volume were more likely to have a higher progression-free survival (6.4 vs. 3.74 [P = 0.023] and
32 gnificant association between TIL values and progression-free survival (adjusted HR 0.95, 95% CI 0.90
36 e primary endpoint was investigator-assessed progression-free survival, analysed by intention-to-trea
37 apse, reduced metastasis, and increased both progression-free survival and 1-year disease-free surviv
38 dian follow-up was 50 months (IQR 41-54) for progression-free survival and 51 months (IQR 46-57) for
39 r estimate were 72% (95% CI, 56% to 84%) for progression-free survival and 79% (95% CI, 63% to 89%) f
40 year rates were 68% (95% CI, 55% to 79%) for progression-free survival and 83% (95% CI, 71% to 91%) f
41 combined with ipilimumab resulted in longer progression-free survival and a higher objective respons
42 (177)Lu-Dotatate resulted in markedly longer progression-free survival and a significantly higher res
47 d by IWCLL criteria was associated with 100% progression-free survival and overall survival (median 6
48 quantitative parameters were correlated with progression-free survival and overall survival (OS).
49 wed statistically significant differences in progression-free survival and overall survival among res
50 oints for TH3RESA were investigator-assessed progression-free survival and overall survival in the in
51 fter median follow-up of 35.4 months, 2-year progression-free survival and overall survival rates wer
55 alone, with minimal improvement in dysphagia progression-free survival and overall survival with chem
56 tients with advanced NSCLC results in longer progression-free survival and overall survival with pemb
61 lenalidomide and dexamethasone would improve progression-free survival and provide better response ra
62 e primary endpoint was investigator-assessed progression-free survival and we report the primary anal
63 nd then correlated to overall survival (OS), progression-free survival, and disease progression rate
64 d in an independent cohort with WHO grading, progression-free survival, and disease-specific survival
65 ansplantation prolonged event-free survival, progression-free survival, and overall survival among pa
66 estimated medians for duration of response, progression-free survival, and overall survival were not
68 assessed associations with overall survival, progression-free survival, and survival after disease pr
71 months (IQR 9.1-28.1), the hazard ratio for progression-free survival assessed by an independent rev
74 e primary endpoint, reported previously, was progression-free survival assessed by central review; HR
78 the primary analysis, the estimated rate of progression-free survival at month 20 was 65.2% (95% con
79 linded independent review committee assessed progression-free survival, based on all randomly assigne
82 PT-Cy, we found no significant difference in progression-free survival between patients with or witho
84 factors for unfavorable outcome and compare progression-free survival between those treated and not
85 re were no significant differences in 2-year progression-free survival between WBRT and ASCT: 80% (95
86 ced melanoma improves antitumor response and progression-free survival but with a higher frequency of
90 tic effects of biomarkers were evaluated for progression-free survival by stratified univariate log-r
93 b showed a significant improvement in median progression-free survival compared with chemotherapy (5.
94 rapy is associated with improved overall and progression-free survival compared with conventional rad
96 hase 3 RADIANT-4 trial, everolimus increased progression-free survival compared with placebo in patie
97 e ipilimumab improves objective response and progression-free survival compared with standard-dose ip
98 e alone only achieves modest improvements in progression-free survival compared with that for chemoth
99 condary end points were time to progression, progression-free survival, conversion to partial hepatec
101 , and key secondary endpoints were dysphagia progression-free survival (defined as a worsening of at
104 0.58, 95% CI 0.36-0.86; p=0.0071), although progression-free survival did not differ between treatme
105 e lymphoma; however, improvements in EFS and progression-free survival did not translate into longer
106 he primary outcome was investigator-assessed progression-free survival evaluated with use of an order
107 nalysis (Aug 1, 2016), 31 patients had had a progression-free survival event (15 with AZD8931 and 16
108 esign methodology triggered by occurrence of progression-free survival events in the placebo group.
109 nd conducted after approximately 120 and 200 progression-free survival events, respectively, occurred
110 tating treatment did not result in prolonged progression-free-survival, fewer toxic effects, or impro
111 nation), in addition to overall survival and progression-free survival from time of randomisation.
114 umour size (>5 cm) was associated with worse progression-free survival (hazard ratio 2.25, 95% CI 1.3
115 disease, 1.0; 95% CI, 0.6 to 1.6; P = .93), progression-free survival (HR, 1.1; 95% CI, 0.6 to 1.8;
120 objective was to demonstrate improvement in progression-free survival in patients with COX-2 index >
122 sis groups, rucaparib significantly improved progression-free survival in patients with platinum-sens
126 val in the intention-to-treat population and progression-free survival in the PTEN-low (by immunohist
128 isons included 2-year overall survival (OS), progression-free survival, local failure, distant metast
129 in plasma were associated with the shortest progression-free survival (median 2.6 months, 95% CI 1.3
135 ths (12.7 to not estimable), with a 12 month progression-free survival of 68% (50-81), whereas in the
137 eeks on, 1 week off, based on improvement in progression free survival over placebo (4.8 vs. 0.9 mont
138 regimen in a phase 3 study to show superior progression-free survival over chemotherapy in patients
139 ens with the hope of demonstrating long-term progression-free survival over cyclophosphamide, doxorub
140 RETATION: Dacomitinib significantly improved progression-free survival over gefitinib in first-line t
142 teria in Solid Tumors [RECIST] version 1.1), progression-free survival, overall survival (OS), and PD
143 rmine whether previous radiotherapy affected progression-free survival, overall survival, and pulmona
145 ples and investigated their association with progression-free survival, overall survival, clinicopath
146 ortion of patients with an overall response, progression-free survival, overall survival, haematologi
150 ciations of 25 rSNPs in eight NER genes with progression free survival (PFS) and overall survival (OS
151 ve performance for overall survival (OS) and progression free survival (PFS), with AUC of 0.976 and 0
152 he disease control rate (DCR) at week 6, the progression free-survival (PFS), overall survival (OS),
153 n OR had a significant improvement in median progression-free survival (PFS) (5.1 vs 1.3 months; P =
154 3 recent studies have demonstrated prolonged progression-free survival (PFS) after treatment with flu
156 o) and whether their volumes correlated with progression-free survival (PFS) and overall survival (OS
157 (EFS; 4-year EFS, 31% vs 43%; P < .01), but progression-free survival (PFS) and overall survival (OS
158 monotypic PCs was associated with a shorter progression-free survival (PFS) and overall survival (OS
159 With a median of 43 mo of follow-up, the 2-y progression-free survival (PFS) and overall survival (OS
161 etabolic response after 4 cycles, as well as progression-free survival (PFS) and overall survival (OS
162 negativity was not associated with prolonged progression-free survival (PFS) and overall survival (OS
164 better complete response rate (P = .04) and progression-free survival (PFS) at 5 and 10 years (P < .
166 th the KRAS-variant, cetuximab improved both progression-free survival (PFS) for the first year (HR,
167 -CNG)] monitored on crizotinib could predict progression-free survival (PFS) in a cohort of ALK-rearr
168 moimmunotherapy as a surrogate end point for progression-free survival (PFS) in chronic lymphocytic l
169 F1 methylation and overall survival (OS) and progression-free survival (PFS) in CS patient samples wi
171 fect sizes between overall survival (OS) and progression-free survival (PFS) in trials of US Food and
174 th a complete response rate of 12.5%, median progression-free survival (PFS) of 14 months, and 2-year
176 between metabolic or clinical endpoints and progression-free survival (PFS) or cause-specific surviv
177 Eligible studies reported MRD status and progression-free survival (PFS) or overall survival (OS)
179 d study end point for first-line FL therapy, progression-free survival (PFS) requires extended follow
180 ransplantation (ASCT) demonstrated prolonged progression-free survival (PFS) versus placebo or observ
185 mutation status, cytoreductive outcome, and progression-free survival (PFS) were evaluated by using
186 dy demonstrated a significant improvement in progression-free survival (PFS) with ixazomib-lenalidomi
187 are the effect of metronomic chemotherapy on progression-free survival (PFS) with that of placebo in
188 response rate (ORR) within 6 months, 9-month progression-free survival (PFS), 9-month overall surviva
189 lan-Meier analysis of overall survival (OS), progression-free survival (PFS), actuarial distant metas
190 DEL and DHL were associated with inferior progression-free survival (PFS), and DHL was associated
191 h significantly worse overall survival (OS), progression-free survival (PFS), and distant metastasis-
192 d ratios (HRs) for overall survival (OS) and progression-free survival (PFS), and odds ratios (OR) fo
193 lysis of the kinetics of anti-5T4 responses, progression-free survival (PFS), and overall survival (O
194 ffusion coefficient (ADC) histogram metrics, progression-free survival (PFS), and overall survival.
196 crobial interaction in IPF as they relate to progression-free survival (PFS), fibroblast function, an
198 nt, we examined the durability of remission, progression-free survival (PFS), overall survival (OS),
199 sed to test associations between the CMI and progression-free survival (PFS), overall survival (OS),
201 survival (OS), and secondary end points were progression-free survival (PFS), response rate, and toxi
210 ignificantly by stromal TIL value for either progression-free survival (pinteraction=0.23) or overall
211 cal activity (partial response and prolonged progression-free survival) provides an impetus for furth
212 t a median follow-up of 370 days, the 1-year progression-free survival rate was 58.2% (95% CI, 33.1%-
213 lts The 8-year time to treatment failure and progression-free survival rates were 44% (95% CI, 39% to
215 weighted values of median overall survival, progression-free survival, response rate, and toxic effe
216 reatment with pembrolizumab conferred longer progression-free survival than did platinum-based therap
217 le-agent brentuximab vedotin and show longer progression-free survival than do patients treated with
218 ion was associated with significantly longer progression-free survival than RVD therapy alone, but ov
219 distinct immune composition correlated with progression-free survival, thereby presenting an in-dept
220 RETATION: The sustained responses and median progression-free survival time, combined with a manageab
221 in the intention-to-treat population (median progression free survival times of 12.6 months and 15.4
224 y associated with disease-related mortality, progression-free survival, transplant-related mortality,
226 ed: two used disease-free survival, one used progression-free survival, two used local failure, and o
227 ng the K-allele showed significantly shorter progression-free survival upon palliative treatment with
228 d a significantly worse overall survival and progression-free survival upon receiving cisplatin after
230 TP53 [n = 4], and AKT [n = 1]) with shorter progression-free survival ( v those without cfDNA mutati
231 ant and clinically meaningful improvement in progression-free survival versus chemotherapy in patient
232 termine whether TACE with sorafenib improves progression-free survival versus TACE with placebo.
233 th a median follow up of 25.7 months, median progression-free survival was 10.1 months (T,: 16.6 mont
234 whereas in the T790M-negative group, median progression-free survival was 10.5 months (9.4-14.2), wi
237 months) in 6 trials with data available, and progression-free survival was 12.4 months (95% CI, 10.0-
241 (95% CI, 16.7 to not estimable), and median progression-free survival was 14.2 months (95% CI, 8.3 t
250 an follow-up of 14 months (IQR 7-18), median progression-free survival was 20.8 months (95% CI 16.6-2
252 atio, 0.95; 95.54% CI, 0.73 to 1.24); median progression-free survival was 3.1 months versus 3.7 mont
260 After a minimum follow-up of 6 years, median progression-free survival was 43 months and median durat
263 92 patients with IMiD-14 low scores; 3 year progression-free survival was 52% (95% CI 42-64) for the
266 he 48 patients with PTEN-low tumours, median progression-free survival was 6.2 months (95% CI 3.6-9.1
267 K pathway-activated patients (n=372), median progression-free survival was 6.8 months (95% CI 4.9-7.1
268 ients with known PI3K status (n=851), median progression-free survival was 6.8 months (95% CI 5.0-7.0
270 At a minimum follow-up of 18 months, median progression-free survival was 8.4 months for patients wh
272 median follow-up of 13.1 months, the median progression-free survival was 8.8 (95% CI, 4.6-15.4) mon
278 e ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients wi
281 s not reported for these 2 studies, although progression-free survival was reported to be between 55%
287 signment, open-label, phase 3 TH3RESA study, progression-free survival was significantly longer with
291 The estimated 1-year overall survival and progression-free survival were 40% and 37%, respectively
293 The median time to progression and median progression-free survival were significantly longer in t
294 all survival, disease-specific survival, and progression-free survival were the primary end points.
295 rvival, disease-specific survival (DSS), and progression-free survival were the primary endpoints.
296 ual disease-based algorithm to predict short progression-free survival, which might be incorporated i
297 o a statistically significant improvement in progression-free survival, which, however, did not trans
298 of the previous RADIANT-4 findings of longer progression-free survival with everolimus, our findings
300 phagus Gefitinib trial demonstrated improved progression-free survival with the epidermal growth fact
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