ライフサイエンスコーパス: MRD

1 MRD assessment can provide real-time information about t

2 MRD at the end of induction therapy of 10(-2) cells or m

3 MRD at the end of induction therapy was high (>=10(-2) c

4 MRD evaluation by next-generation sequencing (NGS) has a

5 MRD is an important predictor of survival in ALL, and re

6 MRD measurements, available for 146 of the 204 patients,

7 MRD negativity should be considered as one of the most r

8 MRD tests included blood and bone marrow (BM) flow cytom

9 MRD was assessed in 1,100 bone marrow samples from 397 p

10 MRD was evaluated by polymerase chain reaction analysis

11 MRD was measured by using standardized real-time quantit

12 MRD was measured in peripheral blood (PB) from treatment

13 MRD, identified as a new prognostic factor for ML-DS pat

14 MRD-negative status was strongly associated with prolong

15 py, CR rates were 100% versus 88% (P = .11), MRD-free CR rates 97% versus 24% (P < .0001, primary end

16 Day 22 MRD was positive in 57 of 121 randomly assigned evaluabl

17 Among 34 MRD-negative patients with MM and a phenotypic pattern o

18 ma, the response rate was 70%, including 50% MRD-negative complete responses, at 400 mug/d, the MTD f

19 io of event-free survival in patients with a MRD of >=10(-2)vs those with a MRD of <10(-2) 3.33 [95%

20 tients with a MRD of >=10(-2)vs those with a MRD of <10(-2) 3.33 [95% CI 1.46-7.56], p=0.0039).

21 The value of having achieved MRD negativity is substantial in both pediatric and adul

22 apy and were evaluable for response achieved MRD-negative CR by high-resolution flow cytometry.

23 In patients who achieved MRD-negative CR by flow cytometry, absence of the index

24 ficantly better in the patients who achieved MRD-negative CR compared with those who did not (median

25 Achieving MRD-free CR of HCL after first-line cladribine is greatl

26 The EFS hazard ratio (HR) for achieving MRD negativity is 0.23 (95% Bayesian credible interval [

27 tly greater proportion of patients achieving MRD negativity at EOT (56% vs 41%; P = .01).

28 multivariable modeling in patients achieving MRD-negative CR showed that lower prelymphodepletion lac

29 Genetic mutations and GC affected MRD rates and PFS.

30 ion, the fully standardized EuroFlow BCP-ALL MRD strategy is applicable in >98% of patients with sens

31 d as a novel genetic high-risk marker in all MRD response groups in late relapsed BCP-ALL.

32 In exploratory analyses, although MRD impacted survival, a fourth course had no effect in

33 Models of AML MRD also showed benefit for MAC over RIC for those who t

34 An MRD-negative status was associated with significantly be

35 The majority of SCD patients lack an MRD, but outcomes following alternative donor HCT contin

36 ingle threshold for assigning patients to an MRD risk group does not reflect the response kinetics of

37 MRD-positive and -negative patients using an MRD threshold of 0.01%.

38 In multivariate analyses, MRD positivity was consistently revealed to be a poor pr

39 count >/=200 x 10(9)/L, gHiR classifier, and MRD >/=10(-4) demonstrated a 5-year CIR of 46%, whereas

40 C count <200 x 10(9)/L, gLoR classifier, and MRD <10(-4) had a very low risk of relapse, with a 5-yea

41 MM is highly heterogeneous, and MRD persistence may reflect survival of isolated single

42 KRd with ASCT achieved high rates of sCR and MRD-negative disease at the end of KRd consolidation.

43 ons on how to best implement MRD testing and MRD-directed therapy after allo-HCT are lacking.

44 terms of patient population, treatment, and MRD assessment methods.

45 ion with independent prognostic value in any MRD-based response subgroup.

46 rug using an intermediate end point, such as MRD, would require confirmation using traditional effica

47 ptive Biotechnologies Corporation) to assess MRD in 62 patients, all of whom had BM U-MRD by multicol

48 nd do not assimilate genetics when assigning MRD risk, which reduces predictive accuracy.

49 ive polymerase chain reaction (RQ-PCR)-based MRD detection via antigen-receptor rearrangements.

50 Comparison with RQ-PCR-based MRD data showed a clear positive relation between the pe

51 valuable patients, 40 (89%) were found to be MRD negative, and the MRD-positive patients experienced

52 ative to <=10-5, which is concerning because MRD-negative status predicts significantly longer surviv

53 apy, roughly 75% of MM patients never become MRD-negative to <=10-5, which is concerning because MRD-

54 There was no evidence of interaction between MRD status and conditioning regimen intensity for relaps

55 re precise quantitative relationship between MRD and PFS, and to support general applicability of MRD

56 4% (P < .0001, primary end point), and blood MRD-free rates 100% versus 50% (P < .0001), respectively

57 a 4-log reduction in NPM1m peripheral blood-MRD (PB-MRD) had a higher cumulative incidence of relaps

58 pharmacologic immunosuppression for the BuCy MRD, BuFlu MRD, BuCy MUD, and BuFlu MUD groups all were

59 ic immunosuppression for the BuCy MRD, BuFlu MRD, BuCy MUD, and BuFlu MUD groups all were 4.5 to 5 mo

60 disease model designed to reflect low-burden MRD, 3 studies demonstrated that single-dose 211At-CD38

61 g variables were the oncogenetic classifier, MRD, and white blood cell (WBC) count.

62 Rituximab can clear MRD, but long-term results are unknown and optimal timin

63 eatment during induction and were considered MRD positive for intent-to-treat analysis.

64 assessment (postinduction or consolidation), MRD detection method, phenotype/genotype (B cell, T cell

65 T-cell expansion were superior in the HD-Cy/MRD cohorts, as compared with the LD-Cy/morphologic coho

66 be critical to determine how best to deploy MRD testing in routine practice and whether MRD assessme

67 Low conversion to detectable MRD and sustained PFS after completion of 2 years of ven

68 e (MRD) before HCT and those with detectable MRD after HCT derive the strongest benefit from sorafeni

69 Among those with detectable MRD, low-level MRD (10(-4) to less than 10(-2)) predicte

70 describe the methods available for detecting MRD in patients with lymphoma and their relative advanta

71 Current risk algorithms dichotomize MRD data and do not assimilate genetics when assigning M

72 antly managed by methionine-restricted diet (MRD) to limit the production of Hcy.

73 BCR-ABL1 fusion in patients with discrepant MRD results.

74 Measurable (minimal) residual disease (MRD) after allo-HCT may be used as a predictor of impend

75 Purpose Minimal residual disease (MRD) and genetic abnormalities are important risk factor

76 eradication of measurable residual disease (MRD) and usually are taken indefinitely or until progres

77 the presence of measurable residual disease (MRD) assessed by flow cytometry before alloSCT as a stro

78 of-induction (EOI) minimal residual disease (MRD) assessment in the identification and stratification

79 ts with MM who had minimal residual disease (MRD) assessments 9 months after study enrollment.

80 s and the level of minimal residual disease (MRD) at day 22 of initial remission induction determined

81 to prednisone, and minimal residual disease (MRD) at end of induction therapy.

82 ve was to evaluate minimal residual disease (MRD) at the end of induction treatment with chemoimmunot

83 with undetectable minimal residual disease (MRD) before HCT and those with detectable MRD after HCT

84 ence of minimal/measurable residual disease (MRD) by molecular genetic and/or flow cytometric techniq

85 nse rate (ORR) and minimal residual disease (MRD) by next-generation sequencing were secondary end po

86 d be evaluated for minimal residual disease (MRD) had MRD-negative status (<=10(-4) nucleated cells).

87 Minimal residual disease (MRD) has become an increasingly prevalent and important

88 Assessing measurable residual disease (MRD) has become standard with many tumors, but the clini

89 Minimal residual disease (MRD) helps to accurately assess when children with late

90 ased monitoring of minimal residual disease (MRD) in 48 patients with childhood acute lymphoblastic l

91 esigned to measure minimal residual disease (MRD) in B-cell precursor (BCP) acute lymphoblastic leuke

92 chniques to detect minimal residual disease (MRD) inside and outside the bone marrow, helping to iden

93 ability to detect minimal residual disease (MRD) is increasingly influencing treatment paradigms.

94 eatment, we report minimal residual disease (MRD) kinetics and updated outcomes.

95 al significance of minimal residual disease (MRD) levels as measured by flow cytometry on day 28 of i

96 l of NSG mice in a minimal residual disease (MRD) model.

97 erformed serial measurable residual disease (MRD) monitoring in bone marrow (BM) and peripheral blood

98 P = .0177), as did minimal residual disease (MRD) negativity (10-5 threshold) rates in the intent-to-

99 The rate of minimal residual disease (MRD) negativity using modified ITT was 70% according to

100 with end-induction minimal residual disease (MRD) of 0.01% to < 0.1% had an inferior outcome compared

101 treatments, and measurable residual disease (MRD) postinduction.

102 Monitoring of measurable residual disease (MRD) provides prognostic information in patients with Nu

103 is mainly based on minimal residual disease (MRD) quantification.

104 Minimal residual disease (MRD) refers to the presence of disease in cases deemed t

105 Minimal residual disease (MRD) response was defined as < 1 tumor cell/10(4) bone m

106 AML measurable residual disease (MRD) status before alloHCT has been shown to be prognost

107 echnique to define minimal residual disease (MRD) status outside the bone marrow (BM) in patients wit

108 redictive value of minimal residual disease (MRD) status, durability of response, fixed treatment dur

109 , peripheral-blood minimal residual disease (MRD) status, genomic complexity (GC), and gene mutations

110 Minimal residual disease (MRD) was determined centrally using flow cytometry at tw

111 Pretransplant measurable residual disease (MRD) was monitored by flow cytometry (MFC-MRD) and corre

112 t was detection of minimal residual disease (MRD) within 1 yr after ASCT at the previously validated

113 R T cell achieving minimal residual disease (MRD)(-) status, consolidative allogeneic transplant lead

114 ates often include minimal residual disease (MRD), leading to relapse and repeated treatments.

115 and 61% achieved a minimal residual disease (MRD)-negative marrow response by IGH sequencing.

116 evaluate rates of minimal residual disease (MRD)-negative status and progression-free survival (PFS)

117 d for treatment of minimal residual disease (MRD).

118 lidation levels of minimal residual disease (MRD).

119 ls, referred to as minimal residual disease (MRD).

120 s had pretreatment minimal residual disease (MRD; <5% blasts in bone marrow), and 10 patients had pre

121 l in patients with minimal residual disease (MRD; enhancing tumour <2 cm(2) post-chemoradiation by ce

122 was assessed as a marginal reflex distance (MRD) greater than 3 mm.

123 e excellent following matched-related donor (MRD) HCT, leading to significantly expanded application

124 val, a fourth course had no effect in either MRD-positive or MRD-negative patients.

125 pared its efficacy on a background of either MRD or normal methionine intake [regular diet (REG)] to

126 ll diameters, which is ideal for eliminating MRD if effectively targeted.

127 ients with M2 marrow (6 of 44) and a low EOI MRD level (< 0.01%) had 5-year EFS of 100%.

128 ition of c-FOS, DUSP1 and BCR-ABL eradicated MRD in multiple in vivo models, as well as in mice xenot

129 Of these, five patients experienced MRD-negative complete responses, and 1 had a partial res

130 crepant patients have worse outcomes than FC MRD-negative patients.

131 The IMWG flow MRD-negative response criterion is highly applicable and

132 he applicability and sensitivity of the flow MRD-negative criterion defined by the International Myel

133 ve patients (n = 125) was 92.7% vs 76.2% for MRD-positive patients (n = 21) (log-rank P = .011).

134 es were 72% and 84% for ITT, 85% and 91% for MRD-negative patients, and 57% and 72% for patients with

135 ts supporting the potential applications for MRD testing in the care of patients with lymphoma and st

136 se-negative rate of HTS improves upon FC for MRD detection in pediatric B-ALL by identifying a novel

137 we propose a refined practical guideline for MRD assessment in RUNX1-RUNX1T1+ AML.

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

139 n in patients with AML who test positive for MRD can prevent relapse and improve survival is unknown.

140 Ten-year survival for MRD grafts was 90%, as opposed to 79% for MUD grafts and

141 nt outcome; 5-year disease-free survival for MRD-negative patients (n = 125) was 92.7% vs 76.2% for M

142 Patients with both good (MRD < 10(-3)) and poor responses to induction treatment

143 uated for minimal residual disease (MRD) had MRD-negative status (<=10(-4) nucleated cells).

144 with low MRD positivity (HR, 0.50) and high MRD positivity (HR, 0.15).

145 ologic remission 2.3% (61 of 2,633) had high MRD (>/= 5%) and 5-year EFS of 47.0% (95% CI, 32.9 to 61

146 Higher MRD positivity rates were seen with BIRC3 and BRAF mutat

147 rove CCR or OS, even in patients with higher MRD, in whom it might have been predicted to provide mor

148 d using current chemotherapy and identifying MRD at 0.01% in up to one-third of patients who are miss

149 Longer follow-up will determine if MRD-free survival leads to less need for additional ther

150 e patients who are defined as having imaging MRD negativity.

151 sed recommendations on how to best implement MRD testing and MRD-directed therapy after allo-HCT are

152 -OS, 56% vs 96%; HR, 3.24; P = .0005) and in MRD-positive patients (2y-OS, 34% vs 100%; HR, 3.78; P =

153 n in NPM1mut TLs after 2 treatment cycles in MRD positive patients by the addition of GO led to a sig

154 Overall survival was also favorable in MRD-negative patients overall (HR, 0.57; 95% CI, 0.46-0.

155 both PFS and OS in Cox models that included MRD (as opposed to CR) for response assessment.

156 s with lymphoma and strategies for including MRD assessment in lymphoma clinical trials.

157 es in low-disease-burden settings, including MRD.

158 andidates; 150 (44%) to AuSCT (115 FR, 35 IR MRD-negative) plus 27 IR patients (8%) with no leukemia-

159 located: 165 (48%) to AlloSCT (122 PR, 43 IR MRD-positive) plus 23 rescued after salvage therapy, for

160 on, AuSCT may still have a role in FR and IR MRD-negative categories.

161 5% in the PR category, 79% and 61% in the IR MRD-negative category, and 70% and 67% in the IR MRD-pos

162 In the IR MRD-positive category, AlloSCT prolongs OS and DFS to eq

163 negative category, and 70% and 67% in the IR MRD-positive category.

164 dicted improved PFS compared with high-level MRD (10(-2) or greater).

165 developed disease progression (11 high-level MRD, three low-level MRD).

166 Among those with detectable MRD, low-level MRD (10(-4) to less than 10(-2)) predicted improved PFS

167 Focusing on patients with low-level MRD before alloSCT, those with FLT3 internal tandem dupl

168 gression (11 high-level MRD, three low-level MRD).

169 sociated with superior PFS compared with low MRD positivity (HR, 0.50) and high MRD positivity (HR, 0

170 erior outcome compared with those with lower MRD and no improvement with IC (6-year CCR: SC, 77.5% +/

171 e (MRD) was monitored by flow cytometry (MFC-MRD) and correlated with outcome.

172 Detectable pretransplant MFC-MRD was associated with an increased CIR (2-year CIR 41.

173 y to patients who test positive in molecular MRD assays, which have far greater sensitivity.

174 and predictive markers along with monitoring MRD can guide the development of individualized, better-

175 ecular to morphologic relapse, necessitating MRD assessment at short intervals during this time perio

176 were also minimal residual disease negative (MRD-).

177 -to-treat minimal residual disease-negative (MRD(-)) remission rate for this phase 1 study was 89%.

178 mpressive minimal residual disease-negative (MRD-negative) complete remission (CR) rates in patients

179 els (TLs) and achievement of MRD negativity (MRD-) for impact on prognosis.

180 Newer MRD detection methods that use next-generation sequencin

181 d evaluated the prognostic impact of NPM1mut MRD and the effect of gemtuzumab ozogamicin (GO) on NPM1

182 .0081, hazard radio favoring CDAR, 0.094) of MRD-free CR.

183 Approximately 50% of MRD patients and 30% of MUD patients never required immu

184 of complete remission (CR) in the absence of MRD negativity was not associated with prolonged progres

185 1 transcript levels (TLs) and achievement of MRD negativity (MRD-) for impact on prognosis.

186 t TL log10 reduction >= 3 and achievement of MRD negativity in BM and PB were significantly associate

187 After completion of therapy, achievement of MRD- in both BM and PB was an independent, favorable pro

188 d recent studies suggest that achievement of MRD-negativity with blinatumomab improves outcomes in pa

189 PFS, and to support general applicability of MRD surrogacy for PFS across diverse patient characteris

190 any subtypes of lymphoma, the application of MRD assessment techniques, like flow cytometry or polyme

191 Assessing the association of MRD status following induction therapy in patients with

192 6 months later (delayed) after detection of MRD in blood.

193 tations and translocations, determination of MRD is complicated by the fact that many treated patient

194 n profiles can improve the discrimination of MRD-defined risk categories was unknown.

195 More detailed dissection of MRD response heterogeneity and the specific genetic aber

196 The primary end point was eradication of MRD after 12 months of combined therapy.

197 n patients with AML with genomic evidence of MRD before alloHCT can result in improved survival.

198 ment methods, including the incorporation of MRD assessment into clinical trials in patients with lym

199 ative evidence to support the integration of MRD assessment as an end point in clinical trials of MM.

200 he bone marrow aspirate), and high levels of MRD had an estimated 2-year overall survival (2y-OS) of

201 depending on the postconsolidation levels of MRD.

202 ith many tumors, but the clinical meaning of MRD in multiple myeloma (MM) remains uncertain, particul

203 f our study was to exploit the full power of MRD by examining it as a continuous variable and to inte

204 There was a high rate of MRD eradication that led to the cessation of therapy in

205 h low CRS severity, and led to high rates of MRD-negative response by IGH sequencing.

206 cytogenetics, with prognostic superiority of MRD negativity versus CR particularly evident in patient

207 The survival of MRD stem or progenitor cells in the absence of oncogenic

208 onine intake [regular diet (REG)] to that of MRD alone.

209 nt across therapies, methods of and times of MRD assessment, cutoff levels, and disease subtypes.

210 size, patient age, follow-up time, timing of MRD assessment (postinduction or consolidation), MRD det

211 To evaluate the utility of MRD detection in patients with newly diagnosed MM.

212 Further validation of MRD assessment methods, including the incorporation of M

213 of tyrosine-kinase inhibitors) as well as on MRD testing.

214 include morphologic induction failure and/or MRD >/= 5% identified 3.9% (120 of 3,133 patients) of th

215 Induction failure (morphologic or MRD >/= 5%) occurred most frequently in T-ALL (10.1%; 39

216 urse had no effect in either MRD-positive or MRD-negative patients.

217 ith HTS identifying 55 (38.7%) more patients MRD positive at this threshold.

218 nger PFS, which establishes the impact of PB MRD on the benefit of fixed-duration, venetoclax-contain

219 Safety and peripheral blood (PB) MRD status-at cycle 4, 2 to 3 months after end of combin

220 PB-MRD levels were measured in 393, 337, and 474 patients f

221 icant interaction between ASCT effect and PB-MRD response ( P = .024 and .027 for disease-free surviv

222 ication (ITD), and a < 4-log reduction in PB-MRD were significantly associated with a higher relapse

223 lood cell count, and < 4-log reduction in PB-MRD, but not FLT3-ITD allelic ratio, remained of signifi

224 rved in those with a > 4-log reduction in PB-MRD, with a significant interaction between ASCT effect

225 ASCT in those with a < 4-log reduction in PB-MRD.

226 reduction in NPM1m peripheral blood-MRD (PB-MRD) had a higher cumulative incidence of relapse (subha

227 Moreover, NPM1m PB-MRD may be used as a predictive factor for ASCT indicati

228 ng prognostic significance of early NPM1m PB-MRD, independent of the cytogenetic and molecular contex

229 Our surrogacy model supports use of PB-MRD as a primary end point in randomized clinical trials

230 relationship between treatment effect on PB-MRD and treatment effect on PFS.

231 t effect on PFS using treatment effect on PB-MRD.

232 ice remained polymerase chain reaction (PCR)-MRD negative after treatment.

233 ional Staging System III status and positive MRD had dismal progression-free and overall survivals (m

234 significant differences in postconsolidation MRD-negative (<10(-6); 76% vs 75%; P = .9) and 2-year PF

235 al approach to MRD monitoring for preemptive MRD-triggered intervention, using patient scenarios to i

236 io [OR], 1.76; P = .04), better preoperative MRD (adjusted OR, 2.21; P < .001), and absence of Marcus

237 brogated the adverse impact of pretransplant MRD on CIR and overall survival.

238 -risk AML or MDS regardless of pretransplant MRD status.

239 is after myeloablative, HLA-matched related (MRD), or HLA-matched unrelated (MUD) donor T-cell-replet

240 hs median follow-up, 94% versus 12% remained MRD free.

241 ess, 12 patients in the delayed arm remained MRD free when restaged 6-104 (median, 78) months after l

242 Eligible studies reported MRD status and progression-free survival (PFS) or overal

243 -4 threshold and the need for more sensitive MRD evaluation.

244 pse rate that was associated with a specific MRD value or category varied significantly by genetic su

245 Integration of genetic subtype-specific MRD values allowed more refined risk group stratificatio

246 Comparing the results with standard MRD monitoring based on immunoglobulin/T-cell receptor (

247 Superior MRD-negative rates after different induction regimens an

248 8 subjects who achieved an initial sustained MRD-neg remission, remission durability correlated with

249 Conclusion Our results demonstrate that MRD-negative status surpasses the prognostic value of CR

250 of lymphoma subtypes, fueling the hope that MRD detection may soon be applicable in clinical practic

251 The MRD alone decreased plasma Hcy by 67% and corrected the

252 The MRD(-) remission rate was 93% in patients who received a

253 (89%) were found to be MRD negative, and the MRD-positive patients experienced early subsequent relap

254 However, the MRD increased anxiety and reduced bone mineral content i

255 On background of the MRD, OT-58 performed equally well with plasma Hcy entire

256 of relapse was directly proportional to the MRD level within each genetic risk group, absolute relap

257 r induction had reduced EFS (56%), and their MRD persisted until allo-HSCT more frequently than it di

258 re, I describe our institutional approach to MRD monitoring for preemptive MRD-triggered intervention

259 ation on patient characteristics, treatment, MRD assessment, and outcomes were extracted using a stan

260 After induction treatment, MRD-based treatment stratification resulted in excellent

261 a French Association 0702 (ALFA-0702) trial, MRD evaluation was available in 152 patients in first re

262 rall, 27% and 16% of the patients achieved U-MRD in blood and marrow, respectively.

263 ess MRD in 62 patients, all of whom had BM U-MRD by multicolor flow cytometry (sensitivity 10-4) at e

264 BM) undetectable minimal residual disease (U-MRD) status after first-line fludarabine, cyclophosphami

265 and undetectable minimal residual disease (U-MRD) were analyzed for all patients (n = 436) and for th

266 Only 27.4% of the 62 patients had U-MRD by NGS.

267 with mutated IGHV were more likely to have U-MRD by NGS at the end of treatment (EOT; 41% vs 13%, P =

268 Rate of U-MRD by NGS was lowest in BM (25%), compared with PBMC (5

269 superior for patients achieving CR/CRi or U-MRD in landmark analyses.

270 Patients with U-MRD at EOT had superior PFS vs MRD+ patients, regardless

271 No patient with U-MRD by NGS in BM or PBMC was MRD+ in plasma.

272 Undetectable MRD (uMRD) at end of combination therapy (EOCT) was asso

273 Attaining undetectable MRD overcame poor prognostic features at diagnosis, incl

274 , 205 (45%) of 458 patients had undetectable MRD after consolidation, and only 14 of them (7%) have e

275 Timing of undetectable MRD (after induction v intensification) had no impact on

276 intenance increased the rate of undetectable MRD by 17%.

277 ab achieved a higher rate of PB undetectable MRD (uMRD; less than 10(-4)) at EOCT (62% v 13%) with su

278 pendent analysis, patients with undetectable MRD had an 82% reduction in the risk of progression or d

279 fter 12 months of ibrutinib plus venetoclax, MRD negativity (fewer than one CLL cell in 10,000 leukoc

280 tients with U-MRD at EOT had superior PFS vs MRD+ patients, regardless of sample type assessed (BM, P

281 patient with U-MRD by NGS in BM or PBMC was MRD+ in plasma.

282 The primary end point was MRD at day 22.

283 with a complete response or better, 29% were MRD negative at a threshold of 10(-5) Among the 62 respo

284 For high-risk patients who were MRD negative, 5-year rates were 77% and 81%.

285 MRD testing in routine practice and whether MRD assessment can ultimately bring us closer to the goa

286 , 2014, 745 patients were enrolled (405 with MRD, 338 with significant residual disease [SRD], and tw

287 When combined with MRD and a WBC count >/=200 x 10(9)/L, it identifies a si

288 The risk of relapse was correlated with MRD kinetics, and each log reduction in disease level re

289 Importantly, among the 60% of patients with MRD <10(-4), 5-year CIR was 29% for gHiR patients and 4%

290 w for different proportions of patients with MRD in different studies, and analyzed using the Peto me

291 Patients with MRD may respond to therapies aiming to unleash or enhanc

292 Patients with MRD of 0.01% or greater at the end of induction had 5-ye

293 This is especially true for patients with MRD of 0.01% or greater at the end of induction.

294 Patients with MRD of 10(-2) or greater after induction had reduced EFS

295 Interestingly, patients with MRD of 10(-3) or greater before allo-HSCT (late nonrespo

296 more frequently than it did in patients with MRD of 10(-3) or greater to less than 10(-2) (P = .037).

297 erence in overall survival for patients with MRD: median overall survival was 20.1 months (95% CI 18.

298 ted concordance of 98% (97% for samples with MRD < 0.01%).

299 entification of 19.9% of SR patients without MRD at any detectable level who had excellent 5-year EFS

300 s from 397 patients; the 61 patients without MRD data discontinued treatment during induction and wer