ライフサイエンスコーパス: ASCT

1 ASCT can safely be performed without transfusion support

2 ASCT is feasible in selected patients with EATL and can

3 ASCT is involved in ATP production, whereas ACH is not,

4 ASCT results might well be implemented by improving the

5 ASCT was performed on day 4.

6 ASCT will likely remain an important platform to develop

7 to fatty acids is also abolished in this ACH/ASCT double mutant.

8 After ASCT, 122 patients received rituximab, and 120 patients

9 ay patients, absence of MRD at day 100 after ASCT was highly predictive of a favorable outcome (PFS,

10 Consolidation with bortezomib after ASCT in bortezomib-naive patients improves PFS without i

11 w 3-IS levels within the first 10 days after ASCT were associated with significantly higher transplan

12 isease or better in the first 100 days after ASCT.

13 Several factors affected EFS after ASCT (P < .05), including relapsed disease within 12 mon

14 benefit with lenalidomide maintenance after ASCT in patients with NDMM when compared with placebo or

15 e centrally randomly assigned 3 months after ASCT to receive 20 doses of bortezomib given during 21 w

16 both associated with inferior outcomes after ASCT in patients with rel/ref DLBCL.

17 nd survival in critically ill patients after ASCT.

18 progression among patients with POEMS after ASCT.

19 4-year event-free survival (EFS) rates after ASCT were 52% and 53% for the rituximab and observation

20 ansplantation (ASCT) or having relapse after ASCT have a low likelihood of cure.

21 t eligible for ASCT or who had relapse after ASCT.

22 ot eligible for ASCT or having relapse after ASCT.

23 prior treatments, and 75% had relapsed after ASCT.

24 The impact of maintenance rituximab after ASCT is not known.

25 e group and do not recommend rituximab after ASCT.

26 d and nine patients (25%) achieved sCR after ASCT.

27 Improved long-term outcome is seen after ASCT with achievement of sCR when compared with lesser d

28 cies, lenalidomide maintenance therapy after ASCT significantly improved time to progression and coul

29 orse overall survival (P = .05) 1 year after ASCT.

30 domized clinical trials comparing MR against ASCT should be considered and randomized clinical trials

31 Although ASCT remains a potentially curative approach, these pati

32 singly been used to rescue failures after an ASCT.

33 t of these patients subsequently received an ASCT.

34 tients proceeded to stem-cell collection and ASCT.

35 mmunochemotherapy, high-dose cytarabine, and ASCT, younger MCL patients with deletions of CDKN2A (p16

36 reated with high-dose chemotherapy (HDC) and ASCT without transfusions.

37 of high doses of antimetabolites, R-HDS, and ASCT is feasible and effective in patients age 18 to 70

38 n intensive induction regimen before HDT and ASCT was not associated with improved survival after adj

39 after high-dose radio-chemotherapy (HDT) and ASCT.

40 roups was SIC in 26% and 23% of patients and ASCT in 28% and 18% of patients, respectively.

41 This analysis compares the results of SC and ASCT for TRIL with de novo diffuse large B-cell lymphoma

42 and DLBCL have similar outcomes with SC and ASCT; this therapy should be considered the standard of

43 INTERPRETATION: WBRT and ASCT are both feasible and effective as consolidation th

44 WBRT and ASCT were both effective, and achieved the predetermined

45 r progression-free survival between WBRT and ASCT: 80% (95% CI 70-90) in group D and 69% (59-79) in g

46 SIC, PET2(+)/PET4(-) patients were assigned ASCT, and PET4(+) patients were treated with the investi

47 rtion of patients with measurable disease at ASCT receiving gemcitabine, busulfan, and melphalan who

48 Among patients with measurable disease at ASCT, 16 of 65 patients (24.6%, 95% CI 14.2-35.0) in the

49 Before ASCT, adverse events (AEs) occurred in 98% of patients,

50 PET-positive patients received augICE before ASCT.

51 one, cytarabine, and cisplatin (DHAP) before ASCT.

52 tients with relapsed or refractory HL before ASCT.

53 Functional imaging status before ASCT was the only factor significant for event-free surv

54 -MRD, with a significant interaction between ASCT effect and PB-MRD response ( P = .024 and .027 for

55 concluded that acetate is produced from both ASCT and ACH; however, only ASCT is responsible, togethe

56 ravenously over 30 min on 1 day, followed by ASCT (control group).

57 , tandem melphalan (100 mg/m(2)) followed by ASCT (MEL100-ASCT), 4 cycles of lenalidomide-prednisone

58 Bortezomib-induction followed by ASCT and lenalidomide consolidation-maintenance is a val

59 cyclophosphamide, and busulfan, followed by ASCT and no radiotherapy.

60 received high-dose chemotherapy followed by ASCT.

61 t strategy of cardiac transplant followed by ASCT.

62 rvival and OS were significantly improved by ASCT in those with a < 4-log reduction in PB-MRD.

63 group D) and carmustine-thiotepa conditioned ASCT (carmustine 400 mg/m(2) on day -6, and thiotepa 5 m

64 a positron emission tomography (PET)-driven ASCT or standard immunochemotherapy (SIC) consolidation

65 , and in younger patients eligible for early ASCT.

66 ith multiple myeloma relapsing after a first ASCT.

67 tiple myeloma at first relapse after a first ASCT.

68 elapsed after more than 24 months from first ASCT.

69 participate or had no financial coverage for ASCT in a clinical trial and instead received melphalan

70 Three patients originally not eligible for ASCT became eligible.

71 iaNet (ELN) classification were eligible for ASCT in first remission.

72 osensitive relapse of DLBCL not eligible for ASCT or having relapse after ASCT.

73 ve relapse of DLBCL who are not eligible for ASCT or who had relapse after ASCT.

74 B-MRD may be used as a predictive factor for ASCT indication.

75 se of VTD rather than VCD in preparation for ASCT.

76 a comparatively safe and active regimen for ASCT in patients with refractory or relapsed myeloma.

77 The median time from ASCT to second-line therapy was 24.3 months.

78 The median time to progression (TTP) from ASCT of patients achieving sCR was significantly longer

79 Median follow-up from ASCT was 37.2 months.

80 tes were 93%, 60%, and 32% at 2.5 years from ASCT for all patients with low-, intermediate-, and high

81 osis relapsing within the first 2 years from ASCT should be considered for an allogeneic transplantat

82 HCT-ASCT with thiotepa and carmustine is an effective treatm

83 nt was complete response at day 30 after HCT-ASCT in all registered eligible patients who received at

84 ing induction and one [1%] 4 weeks after HCT-ASCT).

85 patients without complete response after HCT-ASCT.

86 induction treatment; 73 (92%) commenced HCT-ASCT.

87 During HCT-ASCT, the most common grade 3 toxicity was fever (50 [68

88 t course, patients commenced intravenous HCT-ASCT (rituximab 375 mg/m(2) [day 1], carmustine 400 mg/m

89 o investigate the safety and efficacy of HCT-ASCT in patients with newly diagnosed primary CNS lympho

90 th autologous stem cell transplantation (HCT-ASCT) is supposed to overcome the blood-brain barrier an

91 Rituximab maintenance after HDC-ASCT is safe and significantly prolongs PFS but not OS i

92 for 4 weeks) or observation (NP) before HDC-ASCT and to maintenance rituximab (M+; 375 mg/m(2) once

93 nd autologous stem-cell transplantation (HDC-ASCT) in patients with relapsed follicular lymphoma (FL)

94 nd autologous stem cell transplantation (HDC-ASCT).

95 7%, and 26 (81%) patients proceeded with HDC-ASCT.

96 Moreover, HDC/ASCT is the only strategy that is assessed in comparison

97 questions on efficacy and feasibility of HDC/ASCT, as well as the best candidates for this strategy,

98 e critically analyze reported studies on HDC/ASCT in PCNSL and discuss its current role and future pe

99 by autologous stem cell transplantation (HDC/ASCT) or nonmyeloablative chemotherapy, the former suppo

100 The rationale for using HDC/ASCT in PCNSL patients is based on the fact that the del

101 Worldwide experience with HDC/ASCT is limited to few single-arm phase 2 trials, but ov

102 (2) for four 21-day cycles, followed by HDCT-ASCT.

103 Post-HDCT-ASCT, combined CR/nCR rates were 85% (VTD) and 77% (VTDC

104 y-autologous stem-cell transplantation (HDCT-ASCT), were randomly assigned to bortezomib 1.3 mg/m(2),

105 he same before/after the introduction of HDM-ASCT.

106 an/autologous stem cell transplantation [HDM-ASCT]) and 2000 (introduction of immunomodulatory drugs

107 t underwent a syngeneic allograft and 25 HDM/ASCT (16 of whom subsequently received a reduced-intensi

108 < 1% of circulating plasma cells before HDM/ASCT.

109 he remaining patients underwent a second HDM/ASCT followed by 1 year of bortezomib, lenalidomide, dex

110 nd autologous stem cell transplantation (HDM/ASCT) followed by either allogeneic transplantation or b

111 ter salvage chemotherapy (ST) and before HDT-ASCT by modern criteria.

112 No other pre-HDT-ASCT risk factors significantly impacted PFS or OS.

113 atients with rel/ref DLBCL proceeding to HDT-ASCT, with ST response assessment by FDG-PET according t

114 rameter flow cytometry at day +100 after HDT/ASCT (hazard ratio 8.0; P = .005) were the only independ

115 in CR at risk of early progression after HDT/ASCT in whom novel treatments should be investigated.

116 of 241 patients in CR at day +100 after HDT/ASCT who were enrolled in the Spanish GEM2000 (n = 140)

117 could optimise the chance of cure after HDT/ASCT.

118 Therefore, dose-dense induction and HDT/ASCT are a rational up-front strategy in transplantation

119 should be a negative FDG-PET scan before HDT/ASCT.

120 Dose-dense induction followed by HDT/ASCT was well tolerated and led to long-term PFS in 44%

121 ib/thalidomide/dexamethasone followed by HDT/ASCT; n = 276).

122 riamycin, and dexamethasone) followed by HDT/ASCT; n = 319] and GEM2005<65y (randomized induction wit

123 ry 12 h, day 1) before consideration for HDT/ASCT.

124 ho lose their CR status within 1 year of HDT/ASCT (unsustained CR) have poor prognosis.

125 transplanted with negative FDG-PET, pre-HDT/ASCT after 1 or 2 SLT programs, had an EFS of > 80%, ver

126 ent as per protocol proceeded to receive HDT/ASCT.

127 ome by incorporating novel agents in the HDT/ASCT setting.

128 3-40) were PET-negative and proceeded to HDT/ASCT.

129 e score of 1 or 2) proceeded directly to HDT/ASCT; those with persistent abnormalities on PET receive

130 ence of disease progression proceeded to HDT/ASCT; those with progressive disease were study failures

131 apy and autologous stem-cell transplant (HDT/ASCT) for patients with relapsed or refractory Hodgkin's

132 py/autologous stem cell transplantation (HDT/ASCT) and novel agents has significantly improved surviv

133 py/autologous stem cell transplantation (HDT/ASCT) is a surrogate for prolonged survival in multiple

134 A total of 115 underwent HDT/ASCT, with 90 in complete remission at 3 months post-tra

135 patients proceeded to consolidation with HDT/ASCT.

136 nts needing an alternative to SIC, including ASCT.

137 lete response (CR) rate was 33% after MEL100-ASCT, 48% after LP and 53% after L maintenance.

138 halan (100 mg/m(2)) followed by ASCT (MEL100-ASCT), 4 cycles of lenalidomide-prednisone consolidation

139 id sequence identity between family members, ASCTs function quite differently from the EAATs and GltP

140 sfamide, etoposide, epirubicin/methotrexate)-ASCT [corrected] was piloted from 1998 for patients elig

141 Non-ASCT first-line regimen changed with 65% of patients in

142 r improvement differing for the ASCT and non-ASCT groups.

143 In the non-ASCT group, greatest gains were after 2005 (4-year OS, 3

144 ely driven by improved VGPR rates in the non-ASCT population.

145 The widespread availability of ASCT and use of novel agents in the upfront setting of m

146 stem cell transplantation (ASCT), instead of ASCT in ineligible patients or as salvage.

147 in patients who relapsed within 3 months of ASCT.

148 First, RNAi-mediated repression of ASCT in the ACH null background abolishes acetate produc

149 Nevertheless, the results of ASCT are not universally uniform in all groups of patien

150 inical trials and aims to define the role of ASCT in the era of novel agents.

151 This Spotlight examines the role of ASCT in the era of novel drugs and argues that ASCT shou

152 nance approaches have challenged the role of ASCT.

153 e assessed the effect of CHIP at the time of ASCT on subsequent outcomes, including TMN, cause-specif

154 ion (ASCT) for lymphoma, CHIP at the time of ASCT would be associated with an increased risk of myelo

155 120 patients (29.9%) had CHIP at the time of ASCT, which was associated with an increased rate of TMN

156 e prognostic impact of DEL and DHL status on ASCT outcomes in patients with rel/ref DLBCL.

157 oduced from both ASCT and ACH; however, only ASCT is responsible, together with the F(0)/F(1)-ATP syn

158 with AL regardless of previous treatment or ASCT candidacy.

159 8 patients were randomly assigned to WBRT or ASCT (59 patients per group) and constitute the study po

160 Post-ASCT, 4-year EFS was 45% for TRIL and 46% for DL.

161 On multivariable analysis, post-ASCT response of sCR was an independent prognostic facto

162 rmed whole-exome sequencing on pre- and post-ASCT samples from 12 patients who developed TMN after au

163 M with progressive or relapsing disease post-ASCT but was associated with a higher incidence of grade

164 lapse contained superior properties for post-ASCT outcome prediction.

165 set of high-risk patients with inferior post-ASCT outcomes in two independent external validation coh

166 m cell transplantation, as well as into post-ASCT consolidation therapy, and in the maintenance setti

167 ne expression-based prognostic model of post-ASCT outcomes (RHL30), and two independent cohorts were

168 ating novel STs, conditioning regimens, post-ASCT maintenance, or allogeneic stem cell transplantatio

169 he concurrent controls received similar post-ASCT maintenance.

170 In an intention-to-treat analysis, the post-ASCT CR rate was higher with VTD than with TD (46% vs 24

171 se identifies patients with unfavorable post-ASCT outcomes.

172 ssion differences and associations with post-ASCT outcomes.

173 ents who received a transplant, bMTV and pre-ASCT PET were independently prognostic; 3-year EFS for p

174 independently prognostic; 3-year EFS for pre-ASCT PET-positive patients with low bMTV was 86%.

175 anted for patients who fail to normalize pre-ASCT functional imaging.

176 but there was an increase in the use of pre-ASCT bortezomib induction and of unattenuated melphalan

177 e, bMTV improved the predictive power of pre-ASCT PET.

178 008), in addition to proliferation rate, pre-ASCT cytogenetics, and performance status.

179 TMN specimen were also detectable in the pre-ASCT specimen.

180 disease at least 18 months after a previous ASCT from 51 centres across the UK.

181 multiple myeloma relapsing after a previous ASCT were re-induced with intravenous bortezomib (1.3 mg

182 atients with prior refractory disease, prior ASCT, and prior alloSCT; however, no responses were seen

183 e analysis included 44 patients who received ASCT for EATL between 2000 and 2010.

184 were recorded, both in patients who received ASCT.

185 ified an RCT in patients with NDMM receiving ASCT followed by lenalidomide maintenance versus placebo

186 djustment for the MIPI in patients receiving ASCT.

187 Salvage ASCT increases overall survival during consolidation of

188 treatments, and 32 were receiving a salvage ASCT.

189 ug, or both, or who were receiving a salvage ASCT.

190 ceive either high-dose melphalan and salvage ASCT (n=89) or oral weekly cyclophosphamide (n=85).

191 igh-dose melphalan (200 mg/m(2)) and salvage ASCT or weekly oral cyclophosphamide (400 mg/m(2) per we

192 4 adverse events with PAD induction, salvage ASCT, and cyclophosphamide were: neutropenia (125 [43%]

193 The delay of salvage ASCT to third-line treatment or later might not confer t

194 ancies were reported in 12 patients (salvage ASCT [n=7] vs oral weekly cyclophosphamide [n=5]).

195 high-dose melphalan 200 mg/m(2) plus salvage ASCT or oral cyclophosphamide (400mg/m(2) per week for 1

196 efficacy of high-dose melphalan plus salvage ASCT when compared with cyclophosphamide in patients wit

197 to compare high-dose melphalan plus salvage ASCT with cyclophosphamide in patients with relapsed mul

198 ion shows continued advantage in the salvage ASCT group compared with the weekly cyclophosphamide gro

199 ease progression was superior in the salvage ASCT group compared with the weekly cyclophosphamide gro

200 overall survival was superior in the salvage ASCT group compared with weekly cyclophosphamide group (

201 , and 63 [76%] of 83 patients in the salvage ASCT group vs 11 [13%] of 84 patients in the cyclophosph

202 sion was significantly longer in the salvage ASCT than in the cyclophosphamide group (19 months [95%

203 sufficient PBSCs were randomised to salvage ASCT (n=89) or cyclophosphamide (n=85).

204 ised patients had died at follow-up: salvage ASCT (n=31 [35%]) versus oral weekly cyclophosphamide (n

205 ame degree of advantage as seen with salvage ASCT at first relapse.

206 ty conditioning allograft and seven a second ASCT followed by maintenance).

207 onger than 2 years may benefit from a second ASCT.

208 tion from glucose, as opposed to both single ASCT and ACH mutants.

209 vestigational strategies other than standard ASCT.

210 CT in the era of novel drugs and argues that ASCT should continue to be considered for eligible patie

211 production, whereas ACH is not, because the ASCT null mutant is approximately 1000 times more sensit

212 ient mortality were ICU admission during the ASCT conditioning phase or the use of reduced-intensity

213 ion points for improvement differing for the ASCT and non-ASCT groups.

214 bunit, which is lethal when performed in the ASCT null background but not in the wild-type cells or t

215 In the ASCT population, the greatest gains were after 2010 (4-y

216 ormation regarding prognostic factors in the ASCT setting that can allow to discriminate specific gro

217 lete or partial remission at the time of the ASCT.

218 The ASCTs (alanine, serine, and cysteine transporters) belon

219 contrast, neutral amino acid exchange by the ASCTs does not require protons or the counter-transport

220 dulatory imide drugs, time from diagnosis to ASCT, and cytogenetic risk.

221 highly effective induction regimen prior to ASCT.

222 hieved complete response and 64 proceeded to ASCT.

223 s with HL who relapsed or were refractory to ASCT, panobinostat monotherapy demonstrated antitumor ac

224 gan R/P, 31%; and (5) suboptimal response to ASCT and second-line therapy as consolidation, 4%.

225 er VcR-CVAD induction performed similarly to ASCT and may improve response duration.

226 urces are acetate:succinate CoA-transferase (ASCT) and an unknown enzymatic activity.

227 in which acetate:succinate CoA-transferase (ASCT) replaces the enzymatic step typically performed by

228 dition, pre-autologous stem cell transplant (ASCT) (18)FDG-PET response to SLT predicts outcome.

229 reated with autologous stem cell transplant (ASCT) at Mayo Clinic.

230 (HDC) with autologous stem-cell transplant (ASCT) may provide an alternative to address chemoresista

231 lization of autologous stem cell transplant (ASCT) was similar across all periods, about one-third of

232 py (SC) and autologous stem cell transplant (ASCT).

233 dergoing an autologous stem-cell transplant (ASCT).

234 uximab, and autologous stem-cell transplant (ASCT).

235 rating autologous stem cell transplantation (ASCT) and novel agents into treatment regimens.

236 ns for autologous stem-cell transplantation (ASCT) and overall prognosis.

237 T) and autologous stem-cell transplantation (ASCT) are frequently used in an attempt to improve outco

238 y with autologous stem-cell transplantation (ASCT) as first-line treatment in patients with diffuse l

239 ays of allogeneic stem-cell transplantation (ASCT) at our institution.

240 tor of allogeneic stem cell transplantation (ASCT) benefit.

241 alvage autologous stem-cell transplantation (ASCT) compared with oral cyclophosphamide in patients wi

242 ion of autologous stem cell transplantation (ASCT) consolidation instead of MR.

243 after autologous stem-cell transplantation (ASCT) demonstrated prolonged progression-free survival (

244 rgoing autologous stem-cell transplantation (ASCT) for lymphoma, CHIP at the time of ASCT would be as

245 rgoing autologous stem cell transplantation (ASCT) for multiple myeloma (MM) undergo disease assessme

246 Autologous stem cell transplantation (ASCT) has long been considered frontline therapy for new

247 ole of autologous stem-cell transplantation (ASCT) has not been fully defined.

248 Autologous stem-cell transplantation (ASCT) has shown to provide curative benefit in patients

249 after allogeneic stem cell transplantation (ASCT) in 131 patients.

250 erwent autologous stem-cell transplantation (ASCT) in our institution were eligible for the present s

251 py and autologous stem cell transplantation (ASCT) in patients with newly diagnosed multiple myeloma.

252 before autologous stem-cell transplantation (ASCT) in patients with relapsed or refractory Hodgkin ly

253 T) and autologous stem-cell transplantation (ASCT) in PTCL, the Nordic Lymphoma Group (NLG) conducted

254 before autologous stem-cell transplantation (ASCT) is as effective as and less toxic than standard tr

255 Autologous stem cell transplantation (ASCT) is superior to conventional chemotherapy and is co

256 ) plus autologous stem cell transplantation (ASCT) is the standard of care for chemosensitive relapse

257 py and autologous stem-cell transplantation (ASCT) is unclear.

258 first autologous stem cell transplantation (ASCT) longer than 2 years may benefit from a second ASCT

259 le for autologous stem cell transplantation (ASCT) or having relapse after ASCT have a low likelihood

260 n with autologous stem cell transplantation (ASCT) remain controversial issues when treating patients

261 EVIEW: Autologous stem cell transplantation (ASCT) represents the treatment of choice for primary ref

262 after autologous stem-cell transplantation (ASCT) was investigated for patients with newly diagnosed

263 Autologous stem cell transplantation (ASCT) was retrospectively evaluated as a consolidation o

264 ded to autologous stem cell transplantation (ASCT) whereas PET-positive patients received augICE befo

265 py and autologous stem cell transplantation (ASCT) with no consolidation in bortezomib-naive patients

266 py and autologous stem cell transplantation (ASCT), and in younger patients eligible for early ASCT.

267 ted by autologous stem-cell transplantation (ASCT), as an alternative to whole-brain radiotherapy (WB

268 n, and autologous stem cell transplantation (ASCT), followed by lenalidomide consolidation-maintenanc

269 dosis (AL) before stem cell transplantation (ASCT), instead of ASCT in ineligible patients or as salv

270 le for autologous stem-cell transplantation (ASCT), or for whom this treatment failed, received benda

271 py and autologous stem cell transplantation (ASCT), with or without high-dose cytarabine, in the rand

272 ted by autologous stem-cell transplantation (ASCT).

273 eed to autologous stem cell transplantation (ASCT).

274 ndergo autologous stem-cell transplantation (ASCT).

275 ory to autologous stem-cell transplantation (ASCT).

276 d post-autologous stem cell transplantation (ASCT).

277 after autologous stem-cell transplantation (ASCT).

278 py and autologous stem-cell transplantation (ASCT).

279 py and autologous stem cell transplantation (ASCT).

280 after autologous stem-cell transplantation (ASCT).

281 after autologous stem-cell transplantation (ASCT; n = 397) in intensive-pathway patients and at the

282 The alanine, serine, cysteine transporters (ASCTs) belong to the solute carrier family 1A (SLC1A), w

283 outcome in patients with myeloma undergoing ASCT.

284 Conclusion In patients undergoing ASCT for lymphoma, CHIP at the time of transplantation i

285 ultiple myeloma who had previously undergone ASCT.

286 , and 43 of 49 responding patients underwent ASCT.

287 edian, 10 x 10(6)/kg); 20 patients underwent ASCT.

288 < .001) and in the 85 patients who underwent ASCT as initial consolidation (HR, 7.2; P < .001).

289 herapy-sensitive rel/ref DLBCL who underwent ASCT at two institutions and in whom archival tumor mate

290 ell products from 401 patients who underwent ASCT for non-Hodgkin lymphoma between 2003 and 2010.

291 This remains true for patients who underwent ASCT up front.

292 ed in 445 consecutive patients who underwent ASCT within 12 months of diagnosis of MM.

293 We evaluated 430 MM patients who underwent ASCT within 12 months of their diagnosis and had not ach

294 between patients treated with MR (n = 44) vs ASCT (n = 22).

295 front-line intensive R-HDS chemotherapy with ASCT did not improve the outcome of high-risk patients w

296 A combination of novel drugs with ASCT in a sequential treatment approach can attain long-

297 gh-dose sequential chemotherapy (R-HDS) with ASCT.

298 stration of involved-field radiotherapy with ASCT was marginally significant for EFS (P = .055).

299 l outcomes of 59 POEMS patients treated with ASCT at our institution.

300 ity was more common in patients treated with ASCT than in those who received WBRT.