ライフサイエンスコーパス: OS

1 OS at 3 years for the whole cohort was 85.2%.

2 OS rates were compared with the age-, sex-, and country-

3 OS, progression-free survival (PFS), and safety were ana

4 HR 1.08, 95% confidence interval 1.01-1.16; OS: HR 1.08, 95% confidence interval 1.03-1.14), regardl

5 al acuity had improved to 20/25 OD and 20/20 OS.

6 rs (10-year bRFS, 39%; DMFS, 73%; PCSS, 86%; OS, 80%) and luminal A prostate cancers (10-year bRFS, 4

7 rs (10-year bRFS, 41%; DMFS, 73%; PCSS, 89%; OS, 82%).

8 Although OS at 12 months had the strongest association with OS HR

9 rgeted therapy trials vs chemotherapy had an OS HR of 0.98 (95% CI, 0.80-1.19) and PFS HR of 0.48 (95

10 progression, which did not translate into an OS difference.

11 Conclusion We report an OS benefit in patients who received AC versus observatio

12 notherapy trials vs chemotherapy revealed an OS HR of 0.69 (95% CI, 0.63-0.75) and PFS HR of 0.82 (95

13 o, 1.79; 95% CI, 1.23 to 2.60; P = .002) and OS (hazard ratio, 1.75; 95% CI, 1.21 to 2.54; P = .003).

14 6%, P = .02), TFS (76% vs 94%, P < .01), and OS (79% vs 94%, P = .03).

15 o, 1.55; 95% CI, 1.05 to 2.28; P = .026) and OS (hazard ratio, 1.74; 95% CI, 1.12 to 2.71; P = .01).

16 evel were associated with PFS (P = 0.04) and OS (P = 0.04).

17 vel who had excellent 5-year EFS (98.1%) and OS (100%).

18 S of 87% each (HR, 1.0; 95%, 0.6 to 1.5) and OS of 94% each (HR, 0.9; 95% CI, 0.5 to 1.6), respective

19 were significantly associated with BCSS and OS (P < 0.0001).

20 ated with neoadjuvant chemotherapy, BCSS and OS were associated with approximated subtype and chemoth

21 The DFS and OS at 10 years postactivation were calculated for 1069 p

22 The surprisingly long DFS and OS in these patients represent a challenge to adjuvant c

23 egative prognostic factors regarding DFS and OS, and the occurrence of both is associated with signif

24 Co-primary end points were DFS and OS, based on imaging studies assessed by independent rad

25 our growth, increases cisplatin efficacy and OS.

26 HTS and FC showed similar 5-year EFS and OS for MRD-positive and -negative patients using an MRD

27 earlier use of HD-araC led to better EFS and OS in AAML0431 than in past COG studies.

28 cell, Philadelphia chromosome), and EFS and OS.

29 CSS) (p < 0.00001), between elevated LMR and OS (p < 0.00001)/CSS (p < 0.00001), and elevated PLR and

30 ognostic value of CR achievement for PFS and OS across the disease spectrum, regardless of the type o

31 e significantly associated with both PFS and OS in the univariate analysis and were still statistical

32 Results Median PFS and OS were significantly shorter in women with a high CMI (

33 001)/CSS (p < 0.00001), and elevated PLR and OS (p < 0.00001)/CSS (p = 0.005).

34 roendocrine tumor incidence, prevalence, and OS rates.

35 ranscriptome after the application of PS and OS.

36 Three-year RFS and OS did not differ significantly for patients in the R-CH

37 Three-year RFS and OS rates did not differ significantly for autoSCT (n = 6

38 expression of both genes had poorer RFS and OS than the others (P < 0.001).

39 opean LeukemiaNet, disease-free survival and OS were significantly improved by ASCT in those with a <

40 predictive of progression-free survival and OS.

41 GIST-specific survival and OS.

42 local progression, event-free survival, and OS.

43 or functional monitoring of system xC(-) and OS imaging.

44 imals displayed a rod-dominant phenotype and OSs similar to those seen in the Prph2+/-.

45 early in 2012 for squamous patients because OS for nonplatinum therapy was inferior to platinum ther

46 nts, elevated LMR was associated with better OS (hazard ratio 0.569, 95% confidence interval: 0.478-0

47 pic heterogeneity was associated with better OS in patients treated with androgen receptor signaling

48 igh heterogeneity was associated with better OS in patients treated with taxane chemotherapy.

49 nd selected those reporting results for both OS and PFS.

50 -70 km downwind of the OS) are controlled by OS emissions; > 50% of the monthly mean HNCO arose from

51 rds regression analyses were used to compare OS of patients in the two treatment groups.

52 Conclusion OS was higher with MAC, but this was not statistically s

53 nalyses by risk group demonstrated decreased OS and EFS in the standard-risk group only (HR, 1.9; 95%

54 Together, this points to dissociative OS-SET (SET to a sigma* orbital concerted with C-Cl brea

55 TET2 removes aberrant DNAm during OS through interacting with DNA methyltransferases (DNMT

56 Final OS among patients not receiving previous pelvic radiothe

57 ce index was 0.76 (95% CI, 0.72 to 0.80) for OS and 0.70 (95% CI, 0.66 to 0.74) for PFS, and bias-cor

58 Data were pooled using HRs for OS of LCC vs RCC according to fixed or random-effects mo

59 ethods To develop and validate nomograms for OS and PFS, we used a derivation cohort of 493 patients

60 was observed for DFS ( P = .04) but not for OS ( P = .07).

61 lly significant benefits for PFS but not for OS.

62 Outcomes for OS presenting with unresectable metastases or recurrent

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

64 had independent prognostic significance for OS, while combined RDW and NLR scores stratified patient

65 Conclusion MFS is a strong surrogate for OS for localized prostate cancer that is associated with

66 otherapy drugs were greater for PFS than for OS, with important differences for some drugs, which is

67 KRAS-variant, p16 status, and treatment for OS (HR, for KRAS-variant, cetuximab and p16 positive, 0.

68 Odds ratios were calculated for OSs, and periodontal parameters were assessed using anal

69 idated these results in an independent human OS tumor cohort and in 15 different tumor data sets obta

70 Conclusion Ipilimumab did not improve OS in patients with metastatic castration-resistant pros

71 to concurrent chemoradiation did not improve OS.

72 independent on-treatment marker for improved OS (P = .004, HR 6.8 [1.8-25.3]).

73 OLFIRI plus cetuximab significantly improved OS relative to the respective comparators (FOLFIRI and F

74 atments (HMA and LEN) significantly improved OS.

75 ative management is associated with improved OS and GSS in AYA patients, including those with metasta

76 F/MEK and PD-1 were associated with improved OS benefit compared with all other treatments except CTL

77 , C-->PORT remained associated with improved OS compared with CRT in cohort one (hazard ratio, 1.35;

78 ial metastases were associated with improved OS.

79 There was no significant difference in OS between BRAF/MEK and PD-1 (HR, 1.02; 95% credible int

80 , and there was no statistical difference in OS between the sequencing groups for cohort two (hazard

81 No differences in OS or second neoplasias were observed in in both trials.

82 No statistical difference was found in OS after 52 weeks (P = 0.122), whereas a statistically s

83 continued to show significant improvement in OS compared with the chemotherapy-alone groups: 16.8 mon

84 There was no evidence of improvement in OS for any other patient subgroups defined by HBV and HC

85 Drug-related improvements in OS were, however, widely distributed across therapeutic

86 Even larger increases in OS between these periods were noted in distant-stage gas

87 Similar patterns were seen in OS.In TNBC (n = 174), 5-year BCSS was higher in patients

88 ins of DNAm and 5hmC occur simultaneously in OS, and knocking down TET2 dynamically alters this balan

89 Increased OS was observed in patients who received D + T with base

90 nt surgery was not associated with increased OS when compared with CRT (adjusted hazard ratio [HR], 1

91 of radiotherapy, is associated with inferior OS in patients with EGFR-mutant NSCLC who develop brain

92 The following were associated with inferior OS on multivariable analysis: age (hazard ratio [HR], 3.

93 uced dosing was not associated with inferior OS relative to standard dosing.

94 .40-9.62; P = 0.01), and integrity of the IS-OS layer (OR, 2.09; 95% CI, 1.30-3.37; P = 0.003) were a

95 782) from 2000 to 2009 were analyzed for ITT-OS using a Cox model; and tumor recurrence using 2 compe

96 LDLT improves ITT-OS, and it is not a risk factor for tumor recurrence.

97 ally significant difference was found in ITT-OS between LDLT and BDLT groups (73.2% vs 66.7%; P = 0.0

98 The mean (SD) baseline KCCQ-OS score was 42.3 (23.7), indicating substantial health

99 ransthoracic access (mean difference in KCCQ-OS, 3.5 points; 95% CI, -1.4 to 8.4; P < .01 for interac

100 myopathy Questionnaire overall summary (KCCQ-OS) score (range, 0-100 points; higher scores indicate l

101 difference in the KCCQ overall summary [KCCQ-OS] score, 14.1 points; 95% CI, 11.7 to 16.4; P < .01) a

102 h disease specific (16-22 points on the KCCQ-OS scale) and generic health status (3.9-5.1 points on t

103 1 year, with a mean improvement in the KCCQ-OS score of 27.6 (95% CI, 27.3-27.9) points at 30 days a

104 sted by propensity score demonstrated longer OS with HAI: 0.67 (95% CI, 0.59 to 0.76; P < .001).

105 followed by EGFR-TKI resulted in the longest OS and allowed patients to avoid the potential neurocogn

106 WIF1 methylation were associated with lower OS and PFS rates (p < 0.05).

107 Similar 5-year post-LT OS rates (73.2% and 73.0% for Group LDLT and Group BDLT,

108 e implemented using C# and run on Linux, Mac OS X & Windows operating systems.

109 ce code and precompiled binaries (Linux, Mac OS/X, Windows) are available at github.com/aresio/cupSOD

110 Median OS was 16 months for nivolumab versus 14 months for ICC

111 Median OS was found to be inferior in the DPL arm compared with

112 Median OS was superior in surgical (n = 392; 18.0 months) vs no

113 onths to not reached) compared with a median OS among those who had neither high MSI nor MMRD of 20.5

114 CI, 0.1-22.5 months) compared with a median OS among those who were neither high MSI nor MMRD of 19.

115 ed cases had a dismal outcome, with a median OS of 1.8 years, and 50% relapsed at 1.0 years, compared

116 relapsed at 1.0 years, compared to a median OS of 12.7 years for TP53-unmutated cases (P < .0001).

117 ease or progressive disease) showed a median OS of 4.4 mo (1-y and 2-y OS was 33% and 0%, respectivel

118 derived the greatest benefit, with a median OS of 64 months.

119 who had either high MSI or MMRD had a median OS of 9.6 months (95% CI, 0.1-22.5 months) compared with

120 within the first 24 months and had a median OS of only 4.9 months (5-year OS, 11%).

121 alone who had high MSI or MMRD had a median OS that was not reached (95% CI, 11.5 months to not reac

122 up of 34.9 months in arm A and arm B, median OS times were 8.9 and 9.8 months, and 1-year survival ra

123 corresponded with very long-term OS (median OS was not reached after 57 months of median follow-up).

124 27, 27, and 29 months, respectively; median OS, 59, 64, and 65 months, respectively).

125 usted Kaplan-Meier curves showed that median OS was significantly longer for AC versus observation (4

126 The median OS (pravastatin v placebo) was 14.6 months in both group

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

128 eeks (95% CI, 6.1 to 17.4 weeks); the median OS was 13.7 months (95% CI, 8.5 months to not estimable)

129 ystemic chemotherapy (n = 1,442), the median OS was 67 months with HAI and 47 months without HAI ( P

130 apy was inferior to platinum therapy (median OS, 7.6 months [paclitaxel and gemcitabine] v 10.7 month

131 igh-risk categories, corresponding to median OS of 27.7 years (95% CI, 22 to 34 years), 7.1 years (95

132 ed with TP53, EGFR, and MMP members mediated OS development, including angiogenesis, migration and in

133 .5 months to not estimable), with a 12-month OS rate of 54.3% (95% CI, 37.9% to 68.1%).

134 r in women with a high CMI (PFS, 2.1 months; OS, 12.3 months) versus a low CMI (PFS, 5.8 months; OS,

135 3 months) versus a low CMI (PFS, 5.8 months; OS, 21.7 months).

136 hereas the dSC is enriched with the negative OS/DS cells and with cells with large RFs, low evoked FR

137 There was no OS benefit in the experimental arm (median, 21.8 v 24.5

138 in the apical medium following ingestion of OS by human fetal RPE and ARPE19 cells cultured on Trans

139 Lack of OS benefit with upfront surgery persisted in a subset an

140 ated nomograms provided useful prediction of OS and PFS for patients with OPSCC treated with primary

141 The LMR is an independent predictor of OS in patients with CRC undergoing curative resection an

142 asured kinetic properties in the presence of OS with its impact on the Kd for linoleic acid substrate

143 In this study, transcriptional profiles of OS tumors and cell lines derived from humans (n = 49), m

144 a promising biomarker for prognostication of OS and hematologic toxicity in late-stage mCRPC patients

145 We discuss the role of OS-induced changes in protein flexibility in the context

146 that CERKL may regulate the phagocytosis of OSs by the retinal pigment epithelium (RPE).

147 in polysaccharide (PS) and oligosaccharide (OS) base wine composition and concentration were found a

148 f HR for PFS to predict a non-null effect on OS.

149 or diploidy but had no significant effect on OS.

150 ent evidence that the effect of sorafenib on OS is dependent on patients' hepatitis status.

151 S (hazard ratio, 0.97; 95% CI, 0.79-1.18) or OS advantage (hazard ratio, 0.99; 95% CI, 0.74-1.32).

152 found no significant improvement in BCSS or OS for women undergoing CPM (BCSS: HR 1.08, 95% confiden

153 CS, surgical type does not influence DDFI or OS after adjusting for known prognostic factors in young

154 rall survival of patients with osteosarcoma (OS) has improved little in the past three decades, and b

155 and young adult patients with osteosarcoma (OS).

156 >67) was the strongest predictor of overall (OS) and disease free survival (DFS) (p = 0.00001; p = 0.

157 were prognostic: among nonsquamous patients, OS HRs for positive versus negative were ERCC1, 1.11 ( P

158 Periodontal inflammation and self-perceived OSs were poorer among CSs than among vaping individuals

159 s retained an independent prediction for PFS/OS, whereas the pPCs/BMPCs ratio retained significance o

160 dictive for progression rate but not for PFS/OS.

161 e lymphoma cells) had a shorter TTF and poor OS independent of both MIPI score and Ki-67 index.

162 Postprogression OS was not significantly different between the chemother

163 onse assessed with adapted criteria predicts OS and RS in these patients, who can thus be assessed fo

164 negative effect of adenovirus reactivation (OS, P = .67; NRM, P = .64).

165 re selected later in the process and require OS and other pluripotency TFs.

166 rgery is the standard of care for resectable OS in those younger than 40 years.

167 oactivated one rhodopsin per Galphat the rod OS swelling response reached a saturated elongation of 1

168 ind the H2O membrane permeability of the rod OS to be (2.6 +/- 0.4) x 10(-5) cms(-1), comparable to t

169 The photoreceptor outer segment (OS) is a unique modification of the primary cilium, spec

170 f phagocytized photoreceptor outer segments (OS).

171 egeneration of photoreceptor outer segments (OSs) and increased apoptosis of retinal cells, including

172 t long-term defects in their outer segments (OSs), which were less severe when more photoreceptors we

173 have early progression of disease and short OS.

174 with a higher relapse incidence and shorter OS.

175 alysis, AC was associated with a significant OS benefit (hazard ratio, 0.77 [95% CI, 0.68 to 0.88]; P

176 his meta-analysis demonstrates a significant OS benefit and confirms the PFS benefit with lenalidomid

177 nfounders, there was no longer a significant OS difference (adjusted hazard ratio [HRadj], 0.92; 95%

178 and microRNA expression during oral siphon (OS) regeneration in Ciona robusta, and the derived netwo

179 Specific, OS-induced conformational changes are detected both at t

180 ormed using starch octenyl succinate (starch-OS) were used to stabilize nisin and thymol in cantaloup

181 Cl breakage) in alkanes compared to stepwise OS-SET (SET to a pi* orbital followed by C-Cl cleavage)

182 Results In the LPS subgroup, OS was significantly improved: 15.6 versus 8.4 months (h

183 Subsequent OS was measured after achieving EFS24 or from the time o

184 n was associated with significantly superior OS and PFS compared with dacarbazine.

185 ement was associated with improved survival (OS: 69.5% vs 53.7%, P = .04; GSS: 71.5% vs 56.7%, P = .0

186 p between elevated NLR and overall survival (OS) (p < 0.00001)/ cancer specific survival (CSS) (p < 0

187 tios (HRs) and 95% CIs for overall survival (OS) and CRC-specific survival.

188 Overall survival (OS) and disease-free survival (DFS) were evaluated among

189 a prognostic biomarker of overall survival (OS) and hematologic toxicity and as a tool for response

190 biomarker predicting worse overall survival (OS) and metastasis-free survival (MFS).

191 predictive performance for overall survival (OS) and progression free survival (PFS), with AUC of 0.9

192 ls of WIF1 methylation and overall survival (OS) and progression-free survival (PFS) in CS patient sa

193 tment effect sizes between overall survival (OS) and progression-free survival (PFS) in trials of US

194 ient-specific estimates of overall survival (OS) and progression-free survival (PFS).

195 the primary end point and overall survival (OS) as the secondary end point.

196 model was used to compare overall survival (OS) between RT dose groups, accounting for age, sex, rac

197 on-free survival (PFS) and overall survival (OS) compared with near-CR or partial response (median PF

198 n-free survival (TFS), and overall survival (OS) compared with those without ACAs with the following

199 Surrogates for overall survival (OS) could expedite the evaluation of new adjuvant therap

200 e, we report the coprimary overall survival (OS) end point of CheckMate 037, which has previously sho

201 significant improvement in overall survival (OS) for the eribulin arm, with a manageable toxicity pro

202 s to analyze the impact on overall survival (OS) from the addition of postoperative radiation with or

203 Overall survival (OS) has improved, with inflection points for improvement

204 ion-free survival (PFS) or overall survival (OS) in 20 or more patients following treatment.

205 dent prognostic factor for overall survival (OS) in a post hoc analysis of the Mainsail trial.

206 ssess EFS24 and subsequent overall survival (OS) in large, multinational PTCL cohorts.

207 reatment failure (TTF) and overall survival (OS) in mantle cell lymphoma (MCL) is based on the clinic

208 (HAI) was associated with overall survival (OS) in patients who had a complete resection of colorect

209 on-free survival (PFS) and overall survival (OS) in patients with glioblastoma (GBM).

210 index and associated with overall survival (OS) in the 145 specimens collected prior to initiation o

211 t prostate cancer (mCRPC), overall survival (OS) is significantly improved with cabazitaxel versus mi

212 The primary end point was overall survival (OS) of patients who were prescribed standard starting do

213 The 8-year overall survival (OS) rate was 83% (95% CI, 79% to 87%), with no significa

214 se-free survival (RFS) and overall survival (OS) rates at 3 years were 80% and 87%, respectively, for

215 ion prevalence, and 5-year overall survival (OS) rates.

216 The median overall survival (OS) was 30 months (95% confidence interval, 6-54) from s

217 , 5-year EFS was 89.9% and overall survival (OS) was 93.0%.

218 Overall survival (OS) was examined using a propensity score-matched analys

219 ecific survival (BCSS) and overall survival (OS) were analyzed.

220 issions and have excellent overall survival (OS) with current treatment.

221 event-free survival (EFS), overall survival (OS), and cumulative incidence of local progression (CILP

222 ssion-free survival (PFS), overall survival (OS), and disease status at first restaging.

223 patient-reported toxicity, overall survival (OS), and distant disease-free survival.

224 ssion-free survival (PFS), overall survival (OS), and objective response rate (ORR) were assessed acc

225 ssion-free survival (PFS), overall survival (OS), and safety outcomes of patients treated on this tri

226 Primary end point was overall survival (OS), and secondary end points were progression-free surv

227 Clinical outcomes included overall survival (OS), event-free-survival, nonrelapse mortality (NRM), an

228 ondary end points included overall survival (OS), objective response rate, and safety.

229 Kaplan-Meier analysis of overall survival (OS), progression-free survival (PFS), actuarial distant

230 Overall survival (OS), quality of life (QoL), and safety.

231 on-free survival (PFS) and overall survival (OS), was assessed using logistic regression and Cox mode

232 ined prognostic impact for overall survival (OS), whereas TP53 mutations (HR, 6.9; P < .0001) and MIP

233 was associated with poorer overall survival (OS).

234 se that were predictive of overall survival (OS).

235 Overall survival (OS).

236 gression-free survival and overall survival (OS).

237 jective response rate, and overall survival (OS).

238 A209-004, including 3-year overall survival (OS).

239 Primary end point was overall survival (OS).

240 ng cancer (ES-SCLC) to the overall survival (OS).

241 pathological outcomes and overall survival (OS).

242 ssion correlates with poor overall survival (OS).

243 with significantly better overall survival (OS).

244 r-free surivival (TFS) and overall survival (OS).

245 , event-free survival, and overall survival (OS).

246 d locoregional control and overall survival (OS).

247 with different lengths of overall survival (OS): a median of 1.1, 2.6, and 8.6 years, respectively (

248 3; P < .001) and a shorter overall survival (OS; hazard ratio [HR], 10.99; P < .001).

249 information was available (overall survival [OS] was reported in the article as hazard ratio (HR) acc

250 ific survival [PCSS], 78%; overall survival [OS], 69%), followed by basal prostate cancers (10-year b

251 se recurrence, 3- or 5-year overall survival(OS) and disease free survival(DFS) between the two appro

252 Omenn syndrome (OS) is a rare severe combined immunodeficiency associate

253 ed immunodeficiency (LS) and Omenn syndrome (OS).

254 le baseline corresponded with very long-term OS (median OS was not reached after 57 months of median

255 eic acid substrate binding, we conclude that OS binding brings about an increase in rate constants fo

256 The OS curves crossed, so life expectancy was used: 15.7 mon

257 The OS emissions of nontraditional toxic species such as HNC

258 The OS rate for all NETs improved from the 2000-2004 period

259 ogous organelles, the primary cilium and the OS share common building blocks and molecular machinery

260 50% of the monthly mean HNCO arose from the OS.

261 Although these unique features of the OS have been well documented, their implications in prot

262 The secondary HNCO downwind of the OS was enhanced by up to a factor of 20 relative to its

263 ray ( approximately 10-70 km downwind of the OS) are controlled by OS emissions; > 50% of the monthly

264 of crossover after disease progression, the OS benefit was observed in older patients, suggesting th

265 stratifies pRCC type 1 tumors with regard to OS and CSS.

266 r-sphere reductive single electron transfer (OS-SET) has been proposed for such different processes a

267 n in wild-type bone marrow (BM)-transplanted OS mice in peripheral blood and hematopoietic organs, su

268 The primary end point was OS 18 months post-random assignment based on an intent-t

269 The primary end point was OS.

270 Primary outcomes were OS (analysed in the intention-to-treat population) and a

271 In this study, we examined whether OS phagocytosis was linked to ketogenesis.

272 The wine OS amounts varied between 97 and 139mg/L.

273 0 Gy (V40) was significantly associated with OS on adjusted analysis ( P < .05).

274 used to identify covariates associated with OS.

275 12 months had the strongest association with OS HR, it may not be the optimal time for future trials,

276 -HB released were temporally correlated with OS phagocytic burst after light onset.

277 atient level, Kendall's tau correlation with OS was 0.85 and 0.91 for DFS and MFS, respectively.

278 a show that LV-mediated GT for patients with OS significantly ameliorates the immunodeficiency, even

279 symptoms in patients with LS and those with OS.

280 -1.45; P = .04) were associated with a worse OS.

281 e) showed a median OS of 4.4 mo (1-y and 2-y OS was 33% and 0%, respectively) (P < 0.001).

282 One-year and 2-y OS were 79% and 47%, respectively.

283 The 2-year OS in oligometastatic patients with the chemotherapy + r

284 The 2-year OS was 67.3% and 69.6% in the N3I1 and N1I3 arms, respec

285 The 2-year OS, progression free survival (PFS) and local control (L

286 tients with double mutation had worse 3-year OS of 18%, compared with 35% without double mutation (P

287 L was 28% versus 57% ( P = .013), and 4-year OS was 25% versus 61% ( P = .002).

288 s 48% versus 59% ( P = .049), and the 4-year OS was 56% versus 67% ( P = .10); 4-year PFS in patients

289 evealed no significant differences in 5-year OS (36.7% vs. 44.6%, p = 0.4289) or 5-year LTP (73.3% vs

290 Kaplan-Meier analysis demonstrated a 5-year OS of 81% in LP compared with 78% in RP and 76% in OP (P

291 risk categories were delineated, with 5-year OS of 91% in low-risk, 66% in intermediate-risk (HR, 3.2

292 ere delineated for the MIPSS70 model; 5-year OS was 95% in low-risk, 70% in intermediate-risk, and 29

293 d had a median OS of only 4.9 months (5-year OS, 11%).

294 Conclusion With an 83% 8-year OS rate, long-term follow-up of the FOLL05 trial confirm

295 Five-year OS for patients receiving HMA, LEN, and MISC was 36.5%,

296 Five-year OS in SCRT and ConvRT arms was 86% and 91%, respectively

297 Five-year OS was 86.8% and 78.8% for patients treated at GR and at

298 Ten-year OS rates were 75% in the hypofractionation group and 64%

299 Two-year OS, progression-free survival, local failure, and distan

300 ng was -1.1 mum/year (OD) and -1.2 mum/year (OS).