ライフサイエンスコーパス: MRD

1 MRD after transplantation was a reliable marker for pred

2 MRD assessment can provide real-time information about t

3 MRD distributions of patients with distinct genetic subt

4 MRD level as a continuous variable determined by flow cy

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

6 MRD negativity correlated with both progression-free sur

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

8 MRD status and type of response (CR v CRp or CRi) should

9 MRD status at 3 months had better discrimination for ove

10 MRD status was an independent prognostic factor for time

11 MRD was evaluated by polymerase chain reaction analysis

12 MRD was measured by 6-color flow cytometry in 1 of 2 ref

13 MRD was measured by using standardized real-time quantit

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

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

16 MRD-negative status was strongly associated with prolong

17 level) and AALL0232 (high risk; with day 29 MRD <0.1% by FC) were evaluated by HTS and FC for event-

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

19 levels: MRD negative (<10(-5); n = 54, 34%), MRD positive (between <10(-4) and >/=10(-5); n = 20, 12%

20 Day 35 MRD status was available for 191 patients.

21 f induction, we log-transformed the absolute MRD value and examined its distribution across subgroups

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

23 50.7% of patients with IGHV-M achieved MRD-negativity posttreatment; of these, PFS was 79.8% at

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

25 The greatest impact of achieving MRD negativity was seen in patients receiving frontline

26 monstrate the long-term benefit of achieving MRD negativity, regardless of the therapeutic setting an

27 gression-free survival in patients achieving MRD negativity.

28 After multivariable adjustment, MRD-negative remission status remained statistically sig

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

30 An MRD-negative status was associated with significantly be

31 All 10 long-term survivors had an MRD response.

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

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

34 een <10(-4) and >/=10(-5); n = 20, 12%), and MRD positive (>/=10(-4); n = 88, 54%).

35 , between 3 and 30 residual cancer cells and MRD (undetectable with current methods) were non-invasiv

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

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

38 er significantly between MRD-negative CR and MRD-negative PR; however, PFS was longer for MRD-negativ

39 (CR), MRD-negative PR, MRD-positive CR, and MRD-positive PR experienced a median PFS from a landmark

40 een response (peripheral count recovery) and MRD at the time of morphologic remission.

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

42 d in both bulky lymphoma tumor xenograft and MRD animal models.

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

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

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

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

47 vel of residual disease was considered to be MRD positive.

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

49 PFS did not differ significantly between MRD-negative CR and MRD-negative PR; however, PFS was lo

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

51 Achieving BM MRD-negative complete remission (CR) is associated with

52 Achieving BM MRD-negative CR is a prerequisite for long-term unmainta

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

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

55 Studies that addressed EFS or OS by MRD status in patients with ALL were included; reviews,

56 how that similarly to transplant candidates, MRD monitoring is one of the most relevant prognostic fa

57 mber alterations (CNAs), in another 3 cases, MRD clonal PCs displayed all genetic alterations detecte

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

59 Fifteen patients with IGHV-M had 4-color MRD flow cytometry (sensitivity 0.01%) performed in peri

60 Conclusion MRD quantification allows for improved PFS prediction in

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

62 s with MRD-negative complete remission (CR), MRD-negative PR, MRD-positive CR, and MRD-positive PR ex

63 The Mississippi River Delta (MRD) has undergone tremendous land loss over the past ce

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

65 review available methodologies for detecting MRD and correlations with posttreatment outcomes.

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

67 lleagues utilized mismatch repair detection (MRD) technology to identify somatic mutations in primary

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

69 lapse-free survival (RFS; P = .002) than did MRD status at CR (P = .11 and P = .04, respectively).

70 with offspring of mothers on a regular diet (MRD) and transferable to germ-free mice.

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

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

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

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

75 ase inhibitor, had minimal residual disease (MRD) assessments for BCR-ABL1 by quantitative polymerase

76 rmine the value of minimal residual disease (MRD) assessments, together with the evaluation of clinic

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

78 were positive for minimal residual disease (MRD) at the end of induction, and 7 relapsed 18 to 59 mo

79 at the presence of minimal residual disease (MRD) at the time of transplantation is associated with a

80 itive detection of minimal residual disease (MRD) by multichannel flow cytometry (MFC) prior to hemat

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

82 and eliminate microscopic residual disease (MRD) causes lethal recurrence and metastases, and the re

83 ometry (FC) for measurable residual disease (MRD) detection at the end of induction chemotherapy in p

84 ith persistence of minimal residual disease (MRD) during intensive therapy still have a poor prognosi

85 Monitoring of minimal residual disease (MRD) has become routine clinical practice in frontline t

86 sive monitoring of minimal residual disease (MRD) has led to significant advances in personalized man

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

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

89 The value of minimal residual disease (MRD) in multiple myeloma (MM) has been more frequently i

90 The detection of minimal residual disease (MRD) in myeloma using a 0.01% threshold (10(-4)) after t

91 rognostic value of minimal residual disease (MRD) in patients with multiple myeloma (MM).

92 esponse markers of minimal residual disease (MRD) in the BM that are also predictive of survival coul

93 1-mutated ( NPM1m) minimal residual disease (MRD) in young adult patients (age, 18 to 60 years) with

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

95 Assessment of minimal residual disease (MRD) is becoming standard diagnostic care for potentiall

96 Minimal residual disease (MRD) is highly prognostic in pediatric B-precursor acute

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

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

99 Minimal residual disease (MRD) levels during the first months predict outcome and

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

101 lity and impact on minimal residual disease (MRD) negativity because this end point has been associat

102 Minimal residual disease (MRD) negativity, defined as <1 chronic lymphocytic leuke

103 of chemoresistant minimal residual disease (MRD) plasma cells (PCs) is associated with inferior surv

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

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

106 tients (69%) had a minimal residual disease (MRD) response (<10(-4) blasts), including 22 CR/CRh resp

107 a good response on minimal residual disease (MRD) testing after induction therapy.

108 methods can detect minimal residual disease (MRD) to a sensitivity of >/=1:10,000 (10(-4)).

109 Minimal residual disease (MRD) was assessed posttreatment by a polymerase chain re

110 adult patients at minimal residual disease (MRD).

111 otherapy targeting minimal residual disease (MRD).

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

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

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

115 This article shows that poor early MRD response, in contrast to conventional ALL risk facto

116 ent, intraoperatively detects and eliminates MRD in the surgical bed.

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

118 Conclusion Integration of EOI MRD level with morphology identifies induction failure m

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

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

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

122 65% vs 10% and 10-year OS of 70% vs 30% for MRD-negative vs MRD-positive patients, respectively.

123 in both groups (86% +/- 2% vs 58% +/- 4% for MRD-negative vs positive C-MTX subjects; 88% +/- 2% vs 6

124 than for MRD-positive CR ( P = .048) and for MRD-positive CR compared with MRD-positive PR ( P = .002

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

126 3.1; P = .04), with significant benefit for MRD-negative patients (median TTP not reached, 70% OS at

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

128 MRD-negative PR; however, PFS was longer for MRD-negative PR than for MRD-positive CR ( P = .048) and

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

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

131 PFS was longer for MRD-negative PR than for MRD-positive CR ( P = .048) and for MRD-positive CR comp

132 Furthermore, MRD negativity significantly improved TTP of patients >7

133 Patients who are not good MRD responders however, achieve better outcomes with all

134 This effect of pre-HCT MRD prompted us to compare outcomes in consecutive patie

135 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

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

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

138 In MRD-based standard-risk patients, the 5-year event-free

139 Technical advances in MRD detection methods in recent years have led to reduce

140 hat alpha-emitters are highly efficacious in MRD settings, where isolated cells and small tumor clust

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

142 easure of human malnutrition, was greater in MRD areas.

143 icted bushmeat extraction was also higher in MRD areas.

144 ive AML compared with 22% in 235 patients in MRD-negative remission.

145 relapse estimates were 67% in 76 patients in MRD-positive morphologic remission and 65% in 48 patient

146 similarities in outcomes between patients in MRD-positive morphologic remission and those with active

147 compare outcomes in consecutive patients in MRD-positive remission with patients with active AML who

148 Our results suggest that in MRD areas, forest wildlife rational use for better human

149 hemotherapy and stem cell transplantation in MRD-based high-risk patients resulted in a significantly

150 esent at diagnosis that were undetectable in MRD clonal PCs, but also a selected number of genetic al

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

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

153 icate that post-therapy parameters including MRD status and response are important independent progno

154 for those with MRD 0.01% to 0.1%; increasing MRD amounts was associated with progressively worse outc

155 Subjects with end-induction MRD <0.01% had a 5-year event-free survival (EFS) of 87%

156 with fewer than 30 patients or insufficient MRD description were excluded.

157 h-risk B-ALL study AALL0232, we investigated MRD in subjects randomized in a 2 x 2 factorial design t

158 fy 3 patient groups according to MRD levels: MRD negative (<10(-5); n = 54, 34%), MRD positive (betwe

159 en 1996 and 2007, and received a bone marrow MRD assessment at the end of treatment according to the

160 001), especially early after HCT (day 30 MFC-MRD positive relapse rate, 35%; NGS-MRD positive relapse

161 high risk for relapse, but many pre-HCT MFC-MRD negative patients also relapse, and the predictive p

162 s also relapse, and the predictive power MFC-MRD early post-HCT is poor.

163 on was better at predicting relapse than MFC-MRD (P < .0001), especially early after HCT (day 30 MFC-

164 Thus, characterization of the minor MRD subclone may represent a unique model to understand

165 ltiparameter-flow cytometry (MFC) to monitor MRD in 162 transplant-ineligible MM patients enrolled in

166 Although HD-MTX was superior to C-MTX, MRD retained prognostic significance in both groups (86%

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

168 Newer MRD detection methods that use next-generation sequencin

169 y 30 MFC-MRD positive relapse rate, 35%; NGS-MRD positive relapse rate, 67%; P = .004).

170 Post-HCT NGS-MRD detection was better at predicting relapse than MFC-

171 Post-HCT NGS-MRD is highly predictive of relapse and survival, sugges

172 Absence of detectable IgH-V(D)J NGS-MRD pre-HCT defines good-risk patients potentially eligi

173 and addressed the question of whether NPM1m MRD may be used as a predictive factor of allogeneic ste

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

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

176 The accuracy of MRD measurements in predicting relapse was investigated

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

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

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

180 old with ALL were stratified on the basis of MRD levels after the first and second course of chemothe

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

182 es (n = 1273) provided data on the impact of MRD on PFS, and 12 studies (n = 1100) on OS.

183 The impact of MRD status on PFS and OS was assessed by pooling data fr

184 Finally, we discuss the importance of MRD-negative status as a surrogate marker for longer PFS

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

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

187 atients with intermediate and high levels of MRD improved with therapy intensification.

188 (medium risk) and high (high risk) levels of MRD.

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

190 Here, we compared the antigenic profile of MRD vs diagnostic clonal PCs in 40 elderly MM patients e

191 Genetic profiling of MRD vs diagnostic PCs was performed in 12 patients; 3 of

192 is tolerable and demonstrates high rates of MRD negativity in NDMM, translating into longer progress

193 for each unit increase in the (log) ratio of MRD(-) rates between arms, the log of the PFS hazard rat

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

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

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

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

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

199 We discuss the potential utility of MRD to direct individualized therapy.

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

201 However, the long-term prognostic value of MRD status in other therapeutic settings remains unclear

202 (LTP) in the ventral tegmental area (VTA) of MRD, but not MHFD offspring.

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

204 their prognostic effect was much lower once MRD and response were taken into account, the univariabl

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

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

207 ference for patients with MRD-negative PR or MRD-positive CR ( P = 0.612 and P = 0.853, respectively)

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

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

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

211 the difference between treatment arms in PB-MRD response rates increased, a reduction in the risk of

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

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

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

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

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

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

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

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

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

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

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

223 2 decades, which demonstrate that persistent MRD by multiparameter flow cytometry, polymerase chain r

224 ted OR, 0.64; P = .04), poorer postoperative MRD (adjusted OR, 0.32; P < .001), treatment with fronta

225 ve complete remission (CR), MRD-negative PR, MRD-positive CR, and MRD-positive PR experienced a media

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

227 sted OR, 4.92; P = .02), poorer preoperative MRD (adjusted OR, 0.64; P = .04), poorer postoperative M

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

229 fit from therapeutic strategies that release MRD cells from the niche.

230 achieve remission by day 29, or who remained MRD positive (>0.5%) at week 14.

231 can rapidly and precisely detect and remove MRD in simple intraoperative procedures.

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

233 In resectable MRD, PNB-guided surgery prevented local recurrence and d

234 achieving at least a near-complete response, MRD negativity was found in 28 of 28 (100% [95% CI, 88%-

235 Results MRD was log normally distributed at the end of induction

236 ched and therapy reduction was declared safe.MRD-based medium-risk patients had a significantly highe

237 tance in patients with elderly MM, sensitive MRD monitoring might be particularly valuable in this pa

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

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

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

241 Superior MRD-negative rates after different induction regimens an

242 on-free survival (PFS) and overall survival; MRD status is the single best posttreatment predictor of

243 We propose that targeting MRD provides opportunity to realize this progress.

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

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

246 The MRD subclone showed significant downregulation of genes

247 The MRD techniques need to be sensitive (</=10(-4)), broadly

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

249 al selection could be already present at the MRD stage, where chemoresistant PCs show a singular phen

250 sis plus additional CNAs that emerged at the MRD stage, whereas in the remaining 6 patients, there we

251 alterations that became apparent only at the MRD stage.

252 Additional interventions targeted at the MRD-positive group may further improve outcome.

253 In contrast, 70% of animals in the MRD lymphoma model demonstrated complete eradication of

254 the effects were less pronounced than in the MRD setting.

255 (211)At-labeled 1F5 mAb were evident in the MRD setting.

256 In the MRD, hurricanes have been paradoxically identified as bo

257 , the phenotypic and genetic features of the MRD subclone have never been investigated.

258 ment supply for a major coastal basin of the MRD that assesses both fluvial and hurricane-induced con

259 n the GEM2010MAS65 study and showed that the MRD subclone is enriched in cells overexpressing integri

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

261 Therefore, MRD diagnostics becomes essential to assess treatment ef

262 e plus rituximab) were analyzed according to MRD assessed in peripheral blood at a threshold of 10(-4

263 us to identify 3 patient groups according to MRD levels: MRD negative (<10(-5); n = 54, 34%), MRD pos

264 eration MFC, immune profiling concomitant to MRD monitoring also contributed to identify patients wit

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

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

267 In the ALL-BFM-SCT 2003 trial, MRD was assessed in the bone marrow at days +30, +60, +9

268 o were selected on the basis of undetectable MRD levels, without jeopardizing the survival rate.

269 tially reduced in patients with undetectable MRD (standard risk) and intensified in patients with int

270 In unresectable MRD, PNB nanosurgery improved survival twofold compared

271 ort the use of treatment algorithms that use MRD- rather than morphology-based disease assessments.

272 10-year OS of 70% vs 30% for MRD-negative vs MRD-positive patients, respectively.

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

274 e remission rate (CRR) was 64%, and 36% were MRD negative.

275 All were MRD-negative.

276 Here we examine this hypothesis and whether MRD and response provide independent prognostic informat

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

278 , 2014, 745 patients were enrolled (405 with MRD, 338 with significant residual disease [SRD], and tw

279 , and similar poorer outcomes for cases with MRD levels between <10(-4) and >/=10(-5) vs >/=10(-4) (b

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

281 Compared with MRD-negative CR, only patients with MRD-positive PR had

282 well as lower risk of relapse compared with MRD-positive morphologic remission status or having acti

283 .048) and for MRD-positive CR compared with MRD-positive PR ( P = .002).

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

285 sk algorithms should integrate genetics with MRD to accurately identify patients with the lowest and

286 urvival (EFS) and overall survival (OS) with MRD status in pediatric and adult ALL using publications

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

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

289 Results Patients with MRD-negative complete remission (CR), MRD-negative PR, M

290 PFS (63 months) compared with patients with MRD-negative CR (61 months; P = .354), whereas patients

291 s no detectable difference for patients with MRD-negative PR or MRD-positive CR ( P = 0.612 and P = 0

292 Patients with MRD-negative PR who presented with residual splenomegaly

293 (61 months; P = .354), whereas patients with MRD-negative PR with lymphadenopathy showed a shorter PF

294 aly does not impact outcome in patients with MRD-negative PR.

295 red with MRD-negative CR, only patients with MRD-positive PR had a significantly shorter overall surv

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

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

298 p studies AALL0331 (standard risk [SR]; with MRD by FC at any level) and AALL0232 (high risk; with da

299 ) of 87% +/- 1% vs 74% +/- 4% for those with MRD 0.01% to 0.1%; increasing MRD amounts was associated

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