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 results might well be implemented by improving the

4 ASCT was performed on day 4.

5 ASCT will likely remain an important platform to develop

6 In this retrospective analysis of 161 ASCT patients, we used serial analyses of urinary 3-indo

7 ond-line therapy, 85 received CTx (49%); 70, ASCT (41%); 11, radiotherapy only (6%); and 4, palliativ

8 deepened with further treatment (44.1% after ASCT and 50.2% after consolidation).

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 pembrolizumab in patients with RR cHL after ASCT, hypothesizing that it would improve the progressio

12 , PD-1 blockade given as consolidation after ASCT could improve ASCT outcomes.

13 ogically favorable environment created after ASCT may also represent an opportunity for approaches ut

14 me parameters within the first 10 days after ASCT to identify potential commensal microbiota-sparing

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

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

17 e functions were preserved or improved after ASCT.

18 transfer of vaccine-primed lymphocytes after ASCT is feasible and safe.

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

20 ssion-free survival (PFS) at 18 months after ASCT (primary end point) from 60% to 80%.

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

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

23 ations appear attractive, particularly after ASCT.

24 nd survival in critically ill patients after ASCT.

25 4-year event-free survival (EFS) rates after ASCT were 52% and 53% for the rituximab and observation

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

27 However, relapse after ASCT remains a frequent cause of treatment failure, with

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

29 ot eligible for ASCT or having relapse after ASCT.

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

31 e group and do not recommend rituximab after ASCT.

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

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

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

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

36 mal residual disease (MRD) within 1 yr after ASCT at the previously validated threshold of >=1 malign

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

38 Although ASCT remains a potentially curative approach, these pati

39 singly been used to rescue failures after an ASCT.

40 tients proceeded to stem-cell collection and ASCT.

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

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

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

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

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

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

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

48 WBRT and ASCT are effective consolidation treatments for patients

49 and 87% (95% CI, 77% to 98%) in the WBRT and ASCT arms, respectively.

50 Both WBRT and ASCT met the predetermined threshold (among the first 38

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

52 rded in one and five patients after WBRT and ASCT, respectively.

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

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

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

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

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

58 PET-positive patients received augICE before ASCT.

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

60 tients with relapsed or refractory HL before ASCT.

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

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

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

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

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

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

67 cell product from 629 MM patients treated by ASCT at the Dana-Farber Cancer Institute (2003-2011) det

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

69 ed 1:1 to D-RVd or RVd induction (4 cycles), ASCT, D-RVd or RVd consolidation (2 cycles), and lenalid

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

71 , and in younger patients eligible for early ASCT.

72 ter relapse (second PFS) treated with either ASCT or CTx and performed sensitivity analyses with over

73 tiple myeloma at first relapse after a first ASCT.

74 ith multiple myeloma relapsing after a first ASCT.

75 elapsed after more than 24 months from first ASCT.

76 of ixazomib as maintenance therapy following ASCT.

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

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

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

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

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

82 Randomisation was stratified by intent for ASCT at disease progression for the first randomisation

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

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

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

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

87 Median follow-up from ASCT was 37.2 months.

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

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

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

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

92 patients without complete response after HCT-ASCT.

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

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

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

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

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

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

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

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

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

102 7%, and 26 (81%) patients proceeded with HDC-ASCT.

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

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

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

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

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

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

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

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

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

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

113 < 1% of circulating plasma cells before HDM/ASCT.

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

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

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

117 19-28z CAR T cells following HDT-ASCT were associated with a high incidence of reversible

118 Following HDT-ASCT, effector CD4(+) and CD8(+) immunophenotypes may im

119 tor (CAR) T cells administered following HDT-ASCT.

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

121 Patients underwent standard HDT-ASCT followed by 19-28z CAR T cells on days +2 and +3.

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

123 nd autologous stem cell transplantation (HDT-ASCT) is the standard of care for relapsed or primary re

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

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

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

127 3-40) were PET-negative and proceeded to HDT/ASCT.

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

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

130 le for, or did not intend to have, immediate ASCT.

131 en as consolidation after ASCT could improve ASCT outcomes.

132 lant (ASCT) conditioning regimen may improve ASCT outcomes for MM patients.

133 nts needing an alternative to SIC, including ASCT.

134 ith NDMM received 4 cycles of KRd induction, ASCT, 4 cycles of KRd consolidation, and 10 cycles of KR

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

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

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

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

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

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

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

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

143 ter adjustment for age and a disadvantage of ASCT after the more historic HD10 trial, we did not obse

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

145 in patients who relapsed within 3 months of ASCT.

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

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

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

149 120 patients (29.9%) had CHIP at the time of ASCT, which was associated with an increased rate of TMN

150 geographical variations exist in the use of ASCT, especially between the United States and Europe in

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

152 8 patients were randomly assigned to WBRT or ASCT (59 patients per group) and constitute the study po

153 SL were randomly assigned to receive WBRT or ASCT as consolidation treatment after induction chemothe

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

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

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

157 eloma as well as maintenance approaches post-ASCT.

158 izumab was successfully administered as post-ASCT consolidation in patients with RR cHL, and resulted

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

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

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

162 plete response (sCR) rate by the end of post-ASCT consolidation, favored D-RVd vs RVd (42.4% vs 32.0%

163 to 8 cycles, starting within 21 days of post-ASCT discharge.

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

165 he concurrent controls received similar post-ASCT maintenance.

166 se identifies patients with unfavorable post-ASCT outcomes.

167 ssion differences and associations with post-ASCT outcomes.

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

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

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

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

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

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

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

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

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

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

178 were recorded, both in patients who received ASCT.

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

180 Salvage ASCT increases overall survival during consolidation of

181 treatments, and 32 were receiving a salvage ASCT.

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

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

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

185 4 adverse events with PAD induction, salvage ASCT, and cyclophosphamide were: neutropenia (125 [43%]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 phalan (200 mg/m(2)) conditioning and single ASCT within 12 months of diagnosis.

202 vestigational strategies other than standard ASCT.

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

204 Recent studies suggest that ASCT reestablishes immune equilibrium and thus represent

205 It is amply clear from these trials that ASCT will continue to play an important role in manageme

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

207 The efficacy end points tended to favor the ASCT arm.

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

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

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

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

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

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

214 he introduction of more effective therapies, ASCT continues to play an important role in overall mana

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

216 hieved complete response and 64 proceeded to ASCT.

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

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

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

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

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

222 emotherapy, autologous stem cell transplant (ASCT) and long-term immunomodulatory drug (IMiD) mainten

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

224 followed by autologous stem cell transplant (ASCT) conditioned with IV busulfan + melphalan vs melpha

225 -CD38 to an autologous stem cell transplant (ASCT) conditioning regimen may improve ASCT outcomes for

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

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

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

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

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

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

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

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

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

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

236 lowing autologous stem cell transplantation (ASCT) can delay disease progression and prolong survival

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

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

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

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

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

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

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

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

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

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

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

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

249 ion of autologous stem cell transplantation (ASCT) into a carfilzomib-lenalidomide-dexamethasone (KRd

250 Autologous stem cell transplantation (ASCT) is a standard of care in eligible patients and res

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

252 wed by autologous stem cell transplantation (ASCT) is standard frontline therapy for transplant-eligi

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

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

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

256 py and autologous stem cell transplantation (ASCT) or conventional chemotherapy (CTx).

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

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

259 Autologous stem cell transplantation (ASCT) remains the standard of care for patients with rel

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

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

262 blood autologous stem cell transplantation (ASCT) was the mainstay of therapy for patients who were

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

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

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

266 during allogeneic stem cell transplantation (ASCT), and loss of diversity correlates with acute GI gr

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 andard autologous stem cell transplantation (ASCT).

273 after autologous stem-cell transplantation (ASCT).

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

275 ediate autologous stem-cell transplantation (ASCT).

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

277 eed to autologous stem cell transplantation (ASCT).

278 ndergo autologous stem-cell transplantation (ASCT).

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

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

281 outcome in patients with myeloma undergoing ASCT.

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

283 ultiple myeloma who had previously undergone ASCT.

284 , and 43 of 49 responding patients underwent ASCT.

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

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

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

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

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

290 e also demonstrated the feasibility of using ASCT at the time of first relapse rather than as a compo

291 ant difference in the efficacy of CTx versus ASCT for second PFS (HR, 0.7; 95% CI, 0.3 to 1.6; P = .3

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

293 Tx (95% CI, 85.7% to 100%) versus 83.3% with ASCT (95% CI, 71.8% to 94.8%).

294 nfirmed the survival benefit associated with ASCT in myeloma.

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 Patients with NDMM treated with KRd with ASCT achieved high rates of sCR and MRD-negative disease

299 with CTx (n = 33 of 49; 67%) and rarely with ASCT (n = 8; 16%).

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