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1 CL2-positive subgroup (log-rank P < .001 for time to progression).
2 evels by alphaDC1 positively correlated with time to progression.
3 d not experience shorter overall survival or time to progression.
4 here was a 2.75-fold reduction in the median time to progression.
5 The primary end point of the study was time to progression.
6 ovariates predictive of overall survival and time to progression.
7 a higher CD8 count did not have an increased time to progression.
8 A), time to response, response duration, and time to progression.
9 he association of baseline relative CBV with time to progression.
10 ne tumor SUV(max) was associated with longer time to progression.
11 meshwork of SMZL infiltrates correlates with time to progression.
12 lic frequency and pooled overall survival or time to progression.
13 outcomes included safety, response rate, and time-to-progression.
14 and 67.0%]) and a follow-up analysis (median time to progression [23.4 months and 13.1 months]) have
15 , stable disease in 16 patients (80%; median time to progression, 34 mo), and progressive disease in
16 ence in response rates (48% v 43.6%), median time to progression (4.1 v 4.6 months), or overall survi
17 follow-up PET showed a significantly shorter time to progression (47 vs. 119 d; P < 0.001) and overal
18 (22% v 7%, respectively; P < .0001), median time to progression (5.3 v 2.8 months, respectively; P <
19 5.1 months (range, 0.2-27.7 months), median time to progression = 5.1 months (range, 0.2-27.7 months
20 documented relapsed follicular lymphoma and time to progression 6 months or longer from last rituxim
22 superior for FOLFOX4 compared with rIFL for time to progression (9.7 v 5.5 months, respectively; P <
23 henotype and that positively correlated with time to progression, 95% were associated with immune fun
26 atients treated with pemetrexed had a longer time to progression and a longer survival than their cou
27 ce therapy after ASCT significantly improved time to progression and could be considered a standard o
30 ity is an independent factor associated with time to progression and has potential as a predictive im
34 onse to biochemotherapy (P = 0.02) and worse time to progression and overall survival (P = 0.009 and
37 has resulted in a significant improvement in time to progression and overall survival for patients wi
42 ed to the outcome (recurrence-free survival, time to progression and overall survival) in several can
44 hs, no significant differences in the median time to progression and progression-free survival were o
45 of metastatic disease such as pain response, time to progression and progression-free survival, while
46 response rate was the primary end point, and time to progression and safety were secondary end points
54 -free survival (PFS), overall survival (OS), time to progression, and duration of response were also
56 l benefit but also improved quality of life, time to progression, and overall survival compared with
58 nt end points of metastasis prevention, SRE, time to progression, and overall survival in the context
64 er high-dose dexamethasone in response rate, time to progression, and survival in patients with myelo
68 uperior clinical efficacy (overall survival, time-to-progression, and prostate-specific antigen decli
70 trials that use progression-free survival or time to progression as their primary end point, because
71 9c* was an independent prognostic factor for time to progression as well as survival after surgical c
75 assifications were independent predictors of time to progression compared to known clinical prognosti
78 d points of progression-free survival (PFS), time to progression, duration of response, safety, and t
81 ls of HER2 homodimers correlated with longer time to progression following trastuzumab therapy in a c
89 here was no significant difference in median time to progression for the patients with low versus hig
90 nts, as well as time to first metastasis and time to progression for trials in the nonmetastatic CRPC
91 ere was no difference in overall survival or time to progression; for prinomastat versus placebo pati
92 agnetic resonance imaging to predict shorter time-to-progression from mild cognitive impairment to Al
93 myeloma patients showed significantly longer time to progression, higher response rate, and improved
94 deprivation (CAD) have superior survival and time to progression if lower castrate levels of testoste
95 roni-corrected P = .016), as well as shorter time to progression in bortezomib-treated patients (P =
98 ion MR imaging can be used to predict median time to progression in patients with gliomas, independen
99 rrations in terms of frequency and impact on time to progression in patients with smoldering multiple
113 Patients with sCR displayed slightly longer time to progression (median, 62 vs 53 months, respective
115 H and TCH in terms of the primary end point, time to progression (medians of 11.1 and 10.4 months, re
119 ase control-progression-free survival (PFS), time to progression, objective response rate, and durati
120 e uniformity was an independent predictor of time to progression (odds ratio, 4.02; 95% confidence in
122 cluded recurrent FL and prior rituximab with time to progression of >/= 6 months from last dose.
123 ere EDSS score progression (masked assessor, time to progression of >/=1 point from a baseline score
125 idence interval [CI], 2%-30%), with a median time to progression of 12 weeks (interquartile range [IQ
128 -negative SBP patients evolved to MM (median time to progression of 26 months vs not reached; hazard
130 relative CBV of less than 1.75 had a median time to progression of 3585 days, whereas patients with
131 tment cycles in 108 patients showed a 5-year time to progression of 41.7% (95% CI 22.2-60.1) in patie
132 ith relative CBV less than 1.75 had a median time to progression of 4620 days +/- 433 (standard devia
133 sing overall response rate of 36% and median time to progression of 8.5 (6.0, 38.7) mo and overall su
136 , 95% CI 0.67-1.00; p=0.0490), as was median time to progression of pain interference with daily acti
138 e objective clinical response, toxicity, and time to progression of treatment with 9-Nitro-Camptothec
141 domisation, stratified by geographic region, time to progression on first-line therapy, and disease m
143 ractive voice response system, stratified by time to progression on penultimate platinum-based regime
147 esponse, with secondary end points including time to progression, overall survival, and correlation o
148 bicin monotherapy resulted in greater median time to progression, overall survival, and progression-f
150 ncluded objective response in non-CNS sites, time to progression, overall survival, and toxicity.
151 ral randomised trials have reported improved time-to-progression, overall survival, or both in metast
154 d IL-12p70 levels positively correlated with time to progression (P = 0.019, log-rank), as did T-cyto
155 only, hippocampal atrophy predicted shorter time-to-progression (P < 0.001) while Abeta load did not
158 objectives included safety and tolerability, time to progression, progression-free survival, and over
160 improved the rate of complete remission, and time to progression, progression-free survival, and over
162 ter B-cell-like DLBCL (log-rank P < .001 for time to progression, progression-free survival, disease-
163 umors), median survival increased by 36% and time to progression/progression-free survival increased
165 riginal protocol but instead was added after time-to-progression results were analyzed, and that not
167 CBV (>1.75) have a significantly more rapid time to progression than do patients who have gliomas wi
168 s on CT at 2 months had significantly longer time to progression than those who did not respond (P =
169 time of KS diagnosis did not have a shorter time to progression than those who were antiretroviral n
170 rtezomib had higher response rates, a longer time to progression (the primary end point), and a longe
172 tments for patients with MDS, increasing the time to progression to acute myelogenous leukemia and im
177 e-free survival as the primary end point and time to progression, toxicity, disease-specific survival
178 tus was an independent prognostic factor for time to progression (TTP) (hazard ratio [HR], 2.7; P = .
181 ponse to HDT-ASCT leads to an improvement in time to progression (TTP) and overall survival (OS).
182 aseline to first follow-up was compared with time to progression (TTP) by using a Cox proportional ha
184 were significantly (P < .01) associated with time to progression (TTP) during ADT, remaining so in mu
191 ly 40% for patients with neither; the median time to progression (TTP) was 10.47 versus 3.46 years (P
195 nfirmed response, overall response rate, and time to progression (TTP) was evaluated based on all 10
201 aboratory toxicity levels, imaging response, time to progression (TTP), 90-day mortality, and surviva
203 objective of determining the response rate, time to progression (TTP), and overall survival (OS) amo
204 OX expression with time to metastasis (TTM), time to progression (TTP), and overall survival (OS).
205 o higher overall response rate (ORR), longer time to progression (TTP), and progression-free survival
206 -free survival (PFS), overall survival (OS), time to progression (TTP), and safety were assessed.
207 dary end points were time to response (TTR), time to progression (TTP), duration of response (DOR), a
208 estingly, there was a striking difference in time to progression (TTP), duration of response, and ove
211 ) was the primary end point; others included time to progression (TTP), overall survival (OS), and to
212 esponse rate (RR); secondary end points were time to progression (TTP), overall survival, and toxicit
213 as overall survival; secondary outcomes were time to progression (TTP), progression-free survival (PF
214 survival (OS) and secondary end points were time to progression (TTP), response rate (RR), progressi
215 Secondary and tertiary end points included time to progression (TTP), response rate, and overall su
217 d points include radiographic response rate, time to progression (TTP), toxicity, and symptom improve
218 y end points included overall survival (OS), time to progression (TTP), VEGF levels, and molecular st
219 and CHL patients (75% vs 73%; P = .610), the time to progression (TTP), which also includes the devel
226 5% CI, 1.15 to 1.73; P = .03) and the median time to progression (TTP, 5.7 months v 3.6 months; HR, 1
227 control rate (DCR, 56.5% v 33.3%; P = .04), time to progression (TTP, 9.05 v 2.7 months; P = .02), a
228 ponse rates (RR; 28% v 15.5%; P = .0009) and time to progression (TTP; 6.2 v 4.4 months; P = .0009) w
229 all and complete response rates (P < .0001), time to progression (TTP; P < .0001), response duration
231 this patient population and to determine the time-to-progression (TTP) and time-to-subsequent-chemoth
232 In this report, we update survival (OS) and time-to-progression (TTP) data for the Intergroup trial
233 fter a median follow-up of 66 months, median time-to-progression (TTP) was 55 months and median progr
234 e correlated with the radiographic response, time-to-progression (TTP), and overall survival (OS).
235 e response rate, duration of response (DOR), time-to-progression (TTP), overall survival (OS), and sa
236 tion of AFP response to radiologic response, time-to-progression (TTP), progression-free survival (PF
240 hazard ratio for the independently assessed time to progression was 0.49 (95% confidence interval, 0
243 At the median follow-up of 2.5 years, median time to progression was 1.1 year for lenalidomide alone
266 of 40 patients; 95% CI, 16% to 44%), median time to progression was 5 months (95% CI, 3 to 8 months)
267 a median follow-up of 19 months, the median time to progression was 5 months, median survival was 11
273 events for progression-free survival, median time to progression was 6.4 months in the sorafenib-doxo
278 th a median follow-up of 12.2 months, median time to progression was 8.3 months (95% CI, 5.5 to 9.9 m
280 was 13.1 months and not reached, and median time to progression was 8.3 months and not reached, resp
285 rameters and standard criteria with measured time to progression was assessed by using Kaplan-Meier a
287 median of 16.4 months follow-up, the median time to progression was not reached for patients in the
288 ling in RAS-induced tumorigenesis, decreased time to progression was observed for some KRAS-mutant tu
289 HCC, no radiographic responses were seen and time to progression was short, which suggests minimal si
290 n follow-up of 31 months (IQR 19-42), median time to progression was significantly longer in the salv
291 a median follow-up of 40 months, the median time to progression was significantly longer in the trea
298 such patterns differentiated short from long time-to-progression with 90% (27/30) sensitivity and 80%
299 pal atrophy and Abeta load predicted shorter time-to-progression with comparable power (hazard ratio
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