ライフサイエンスコーパス: minimal residual disease

1 treatment cytogenetics, and end-of-induction minimal residual disease.

2 ete marrow recovery) or negative bone marrow minimal residual disease.

3 g, risk stratification and quantification of minimal residual disease.

4 be more appropriate than (90)Y for treating minimal residual disease.

5 in group had results below the threshold for minimal residual disease.

6 used at earlier stages, such as for treating minimal residual disease.

7 ystems for early diagnosis and monitoring of minimal residual disease.

8 c technologies used for the determination of minimal residual disease.

9 on is warranted for patients with detectable minimal residual disease.

10 a remission sample containing drug-resistant minimal residual disease.

11 fy a rare leukemia population reminiscent of minimal residual disease.

12 ned prognostic among cases with intermediate minimal residual disease.

13 herapy is a marker of clinically significant minimal residual disease.

14 ery, and 61% had remission with undetectable minimal residual disease.

15 esponse, relapse, and methods of determining minimal residual disease.

16 orly understood population is referred to as minimal residual disease.

17 tigecycline to treat patients with CML with minimal residual disease.

18 in group had results below the threshold for minimal residual disease (0.01% marrow blasts) (78.4% vs

19 l group, had results below the threshold for minimal residual disease (1 tumor cell per 10(5) white c

20 survival compared with the 126 with negative minimal residual disease (72.7%, 42.5-88.8 vs 84.0%, 76.

21 ve that may be preferred in patients without minimal residual disease after induction chemotherapy.

22 he complete response status by improving the minimal residual disease after induction therapy is a ke

23 Minimal residual disease after primary definitive treatm

24 nt even among patients who were negative for minimal residual disease after remission induction thera

25 rs was 56% (95% CI 46-65) in those with high minimal residual disease and 72% (60-81) in patients wit

26 ng leukemia stem cells (LSCs), which sustain minimal residual disease and are responsible for CML rel

27 l therapies is a direction forward targeting minimal residual disease and bypass pathways early based

28 al implications in relation to assessment of minimal residual disease and development of alternative

29 otherapy is necessary to sufficiently reduce minimal residual disease and is associated with improved

30 t is expected that LSCs would be enriched in minimal residual disease and predictive of relapse.

31 -60), we modeled a postremission marrow with minimal residual disease and showed that the transplanta

32 provide key insights into the monitoring of minimal residual disease and the identification of thera

33 risk of infection, organized evaluations of minimal residual disease and treatment at relapse offer

34 This strategy could reduce minimal residual disease and/or allow for chemotherapy d

35 or all known relapse risk factors, including minimal residual disease, and 111 were significant even

36 isease response and resistance, for tracking minimal residual disease, and for cancer diagnosis.

37 ation of baseline genetics and assessment of minimal residual disease are expected to further improve

38 t negative uIFE predicted achieving negative minimal residual disease, as determined by flow cytometr

39 The presence of minimal residual disease, as determined by quantitation

40 stication and for estimating the presence of minimal residual disease, as well as the relevance of th

41 sample, approaching the sensitivity of some minimal residual disease assays.

42 be used to prognose patient outcome, monitor minimal residual disease, assess tumour resistance to th

43 on response to the prephase treatment and on minimal residual disease assessment is well established

44 aemia with late bone marrow relapses and low minimal residual disease at end of induction had favoura

45 ents with late bone marrow relapses and high minimal residual disease at the end of induction were al

46 ll transplantation, and 82 patients with low minimal residual disease at the end of induction were al

47 high-risk clinical features and/or elevated minimal residual disease at the end of remission inducti

48 nfirms the clinical significance of a novel, minimal residual disease-based algorithm to predict shor

49 w the repertoire of gene mutations useful in minimal residual disease-based prognostication in AML.

50 Patients with high minimal residual disease benefited from stem-cell transp

51 ndamentally change approaches for monitoring minimal residual disease burden.

52 Minimal residual disease but not t(9;22) was associated

53 rate of complete remission with undetectable minimal residual disease by flow cytometry in both the b

54 (hazard ratio 17.3; P = .002) and persistent minimal residual disease by multiparameter flow cytometr

55 e main cause of resistance in myeloma is the minimal residual disease cells that are resistant to the

56 Studies of minimal residual disease confirmed durability of CLL era

57 Minimal residual disease detected during complete remiss

58 sera, providing personalized biomarkers for minimal residual disease detection and monitoring.

59 We suggest that more optimal use of minimal residual disease detection during first remissio

60 gated the prognostic impact of NPM1mut-based minimal residual disease detection from bone marrow for

61 f risk parameters, (2) molecular markers and minimal residual disease detection, (3) context of refer

62 R NGS assays for 1) clonality assessment, 2) minimal residual disease detection, and 3) repertoire an

63 acute myeloid leukemia and are suitable for minimal residual disease detection.

64 ere detected in 6 patients who had increased minimal residual disease during induction therapy, and a

65 The level of minimal residual disease during remission induction is t

66 Minimal residual disease evaluation and monitoring is de

67 ikely find considerable utility in assessing minimal residual disease following treatment and for ear

68 an exploit both the state of lymphopenia and minimal residual disease for generating antitumor immuni

69 Even genetic GR patients with minimal residual disease (>0.01%) at day 29 had an EFS i

70 three blocks of therapy, patients with high minimal residual disease (>=10(-4) cells) at the end of

71 rapeutic implications even in the context of minimal residual disease-guided treatment.

72 gression analyses revealed an association of minimal residual disease (hazard ratio 7.3; P < .001) an

73 NCAM1 is widely used as a marker of minimal residual disease; however, the biological functi

74 mbined use of genetic markers and detectable minimal residual disease identifies patients with chroni

75 ve polymerase-chain-reaction assay to detect minimal residual disease in 2569 samples obtained from 3

76 ed to establish the clinical significance of minimal residual disease in a prospective trial that use

77 atological cancer cells and for detection of minimal residual disease in a significant proportion of

78 ical setting, we apply the method to monitor minimal residual disease in acute lymphoblastic leukaemi

79 Integrin alpha6 has been implicated in minimal residual disease in ALL and in the migration of

80 hieved a complete response with undetectable minimal residual disease in bone marrow 2 months after t

81 A complete response and undetectable minimal residual disease in bone marrow 2 months after t

82 p to 2 years, and patients with undetectable minimal residual disease in bone marrow after 2 years we

83 A best response of undetectable minimal residual disease in bone marrow was achieved by

84 ortion of patients who achieved undetectable minimal residual disease in bone marrow with ibrutinib p

85 psed or refractory patients had undetectable minimal residual disease in both the blood and marrow.

86 Measuring minimal residual disease in cancer has applications for

87 Purpose Immunologic surveillance of minimal residual disease in chronic myelogenous leukemia

88 l interactions holds promise for eliminating minimal residual disease in MM.

89 single-agent venetoclcax fails to eradicate minimal residual disease in most patients.

90 ive to kinase inhibitors and responsible for minimal residual disease in treated patients.

91 nt recovery) and remission with undetectable minimal residual disease increased over time.

92 The importance of monitoring minimal residual disease is emphasized, with a discussio

93 Furthermore, detection of minimal residual disease is important for prognosis dete

94 l count is weaker and the rate of decline in minimal residual disease is slower in patients with T-li

95 e expression analyses from 207 children with minimal residual disease, is highly associated with poor

96 f three, and was stratified according to the minimal residual disease level achieved after first-line

97 x109/L, lack of extramedullary leukemia, and minimal residual disease level of <0.01% on remission in

98 For the 280 provisional low-risk patients, a minimal residual disease level of less than 1% on day 19

99 dicted a better outcome, irrespective of the minimal residual disease level on day 46.

100 Minimal residual disease level was measured by real-time

101 with late bone marrow relapses stratified by minimal residual disease level.

102 on day 19 compared with patients with lower minimal residual disease levels (69.2%, 95% CI 49.6-82.4

103 ly two of the 11 patients who had decreasing minimal residual disease levels between the end of induc

104 on between event-free survival and patients' minimal residual disease levels during remission inducti

105 Minimal residual disease levels during remission inducti

106 lish treatment intensity was based mainly on minimal residual disease levels measured on days 19 and

107 th provisional low-risk ALL and 1% or higher minimal residual disease levels on day 19 but negative m

108 cantly worse for patients with 1% or greater minimal residual disease levels on day 19 compared with

109 mmunotherapy, were eligible if they had high minimal residual disease levels or intermediate levels c

110 age, race/ethnicity, initial WBC, and day-29 minimal residual disease < 0.1%, CSF blast, regardless o

111 sidual disease levels on day 19 but negative minimal residual disease (<0.01%) on day 46 were treated

112 stem-cell transplantation and those with low minimal residual disease (<10(-4) cells) at the end of i

113 e implementation of risk stratification with minimal residual disease measurement and how to treat hi

114 in a prospective trial that used sequential minimal residual disease measurements to guide treatment

115 Rates of undetectable minimal residual disease (median 3 x 10-6 sensitivity) i

116 ensitivity by multiparameter flow cytometric minimal residual disease (MFC-MRD) detection has prognos

117 of liquid biopsies to meet the challenges of minimal residual disease monitoring after curative inten

118 Sequential minimal residual disease monitoring after remission indu

119 th longer RFS in patients with postinduction minimal residual disease (MRD) >/=10(-3) (hazard ratio,

120 complete response (CRu) without evidence for minimal residual disease (MRD) 6 months after applicatio

121 Persistence or recurrence of minimal residual disease (MRD) after chemotherapy result

122 PET) positivity pretransplant and detectable minimal residual disease (MRD) after transplant.

123 Both presence of minimal residual disease (MRD) and achievement of comple

124 Purpose Minimal residual disease (MRD) and genetic abnormalities

125 initial WBC count, genetic aberrations, and minimal residual disease (MRD) are used for risk stratif

126 determine the role of end-of-induction (EOI) minimal residual disease (MRD) assessment in the identif

127 h only 1 induction course and had at least 1 minimal residual disease (MRD) assessment; 25 patients u

128 l trial for elderly patients with MM who had minimal residual disease (MRD) assessments 9 months afte

129 rabine plus a tyrosine kinase inhibitor, had minimal residual disease (MRD) assessments for BCR-ABL1

130 Purpose To determine the value of minimal residual disease (MRD) assessments, together wit

131 Genetic abnormalities and the level of minimal residual disease (MRD) at day 22 of initial remi

132 lated mortality, response to prednisone, and minimal residual disease (MRD) at end of induction thera

133 In addition, persistence of minimal residual disease (MRD) at the end of induction o

134 Our objective was to evaluate minimal residual disease (MRD) at the end of induction t

135 97/99 and UKALL 2003), 10 were positive for minimal residual disease (MRD) at the end of induction,

136 It is well recognized that the presence of minimal residual disease (MRD) at the time of transplant

137 n patients with acute leukemia, detection of minimal residual disease (MRD) before allogeneic hematop

138 ry data show that patients with undetectable minimal residual disease (MRD) before HCT and those with

139 is issue of Blood by Leung et al, detectable minimal residual disease (MRD) before hematopoietic stem

140 Minimal residual disease (MRD) before myeloablative hema

141 Positive detection of minimal residual disease (MRD) by multichannel flow cyto

142 Overall response rate (ORR) and minimal residual disease (MRD) by next-generation sequen

143 Quantification of minimal residual disease (MRD) by real-time PCR directed

144 Monitoring minimal residual disease (MRD) by using real-time quanti

145 of patients with unsatisfactory reduction of minimal residual disease (MRD) can be improved by alloge

146 We assessed the prognostic value of minimal residual disease (MRD) detection in multiple mye

147 Minimal residual disease (MRD) detection is standard of

148 We asked whether minimal residual disease (MRD) determined by RUNX1/RUNX1

149 and 27% (VTDC) of patients were negative for minimal residual disease (MRD) during induction and post

150 he last decade, patients with persistence of minimal residual disease (MRD) during intensive therapy

151 The persistence of minimal residual disease (MRD) during therapy is the str

152 complete remission (CR) without evidence of minimal residual disease (MRD) had markedly better DFS (

153 se or better) and who could be evaluated for minimal residual disease (MRD) had MRD-negative status (

154 Minimal residual disease (MRD) has become an increasingl

155 Monitoring of minimal residual disease (MRD) has become routine clinic

156 In many retrospective studies, detection of minimal residual disease (MRD) has been shown to enable

157 Noninvasive monitoring of minimal residual disease (MRD) has led to significant ad

158 Minimal residual disease (MRD) helps to accurately asses

159 igh CRLF2 expression (IKZF1, JAK, IL7R), and minimal residual disease (MRD) in 1061 pediatric ALL pat

160 d ABL1 genes for the DNA-based monitoring of minimal residual disease (MRD) in 48 patients with child

161 The role of various methodologies to detect minimal residual disease (MRD) in AML is reviewed, as we

162 y procedure was stepwise designed to measure minimal residual disease (MRD) in B-cell precursor (BCP)

163 ycle-dependent Ara-C chemotherapy to produce minimal residual disease (MRD) in leukemic mice, we show

164 The value of minimal residual disease (MRD) in multiple myeloma (MM)

165 The detection of minimal residual disease (MRD) in myeloma using a 0.01%

166 udies have evaluated the prognostic value of minimal residual disease (MRD) in patients with multiple

167 Early response markers of minimal residual disease (MRD) in the BM that are also p

168 Persistent minimal residual disease (MRD) in the bone marrow as mea

169 mpact of postinduction NPM1-mutated ( NPM1m) minimal residual disease (MRD) in young adult patients (

170 itive bone marrow-based techniques to detect minimal residual disease (MRD) inside and outside the bo

171 Minimal residual disease (MRD) is an important prognosti

172 Assessment of minimal residual disease (MRD) is becoming standard diag

173 Minimal residual disease (MRD) is highly prognostic in p

174 articularly leukemias, the ability to detect minimal residual disease (MRD) is increasingly influenci

175 Measurement of minimal residual disease (MRD) is nowadays recognized as

176 Minimal residual disease (MRD) is the most sensitive and

177 With all patients off treatment, we report minimal residual disease (MRD) kinetics and updated outc

178 HR criteria were minimal residual disease (MRD) levels >/=10(-3) at day 7

179 We determined the clinical significance of minimal residual disease (MRD) levels as measured by flo

180 treated with risk-directed therapy based on minimal residual disease (MRD) levels during remission i

181 Minimal residual disease (MRD) levels during the first m

182 s include KIT and/or FLT3 gene mutations and minimal residual disease (MRD) levels, but their respect

183 s assessed by immunoglobulin/T-cell receptor minimal residual disease (MRD) levels.

184 in prolonging the survival of NSG mice in a minimal residual disease (MRD) model.

185 Data on minimal residual disease (MRD) monitoring in acute promy

186 Response can now be assessed by minimal residual disease (MRD) monitoring with flow cyto

187 nts achieved complete response, and 68% were minimal residual disease (MRD) negative by flow cytometr

188 d vs RVd (62.6% vs 45.4%; P = .0177), as did minimal residual disease (MRD) negativity (10-5 threshol

189 his combination's tolerability and impact on minimal residual disease (MRD) negativity because this e

190 The rate of minimal residual disease (MRD) negativity using modified

191 Minimal residual disease (MRD) negativity, defined as <1

192 e with SR-average disease with end-induction minimal residual disease (MRD) of 0.01% to < 0.1% had an

193 Persistence of chemoresistant minimal residual disease (MRD) plasma cells (PCs) is ass

194 We investigated whether minimal residual disease (MRD) positivity by qualitative

195 reased relapse risk in children with >/=0.1% minimal residual disease (MRD) pretransplant, and decrea

196 oblastic leukemia (T-ALL) is mainly based on minimal residual disease (MRD) quantification.

197 Minimal residual disease (MRD) refers to the presence of

198 This minimal residual disease (MRD) remains a major challenge

199 Twenty-five patients (69%) had a minimal residual disease (MRD) response (<10(-4) blasts)

200 shown whether stratification of treatment by minimal residual disease (MRD) response improves outcome

201 Minimal residual disease (MRD) response was defined as <

202 Major secondary end points included minimal residual disease (MRD) response, rate of allogen

203 s currently the standard technique to define minimal residual disease (MRD) status outside the bone m

204 ons remain regarding the predictive value of minimal residual disease (MRD) status, durability of res

205 PFS, overall survival (OS), peripheral-blood minimal residual disease (MRD) status, genomic complexit

206 (alloSCT) if they achieve a good response on minimal residual disease (MRD) testing after induction t

207 Martinez-Lopez et al suggests that by using minimal residual disease (MRD) testing by sequencing, we

208 hain reaction (PCR)-based methods can detect minimal residual disease (MRD) to a sensitivity of >/=1:

209 ne response elicited by the progression from minimal residual disease (MRD) to actively growing recur

210 Minimal residual disease (MRD) was assessed posttreatmen

211 Minimal residual disease (MRD) was determined centrally

212 Marrow minimal residual disease (MRD) was measured by quantitat

213 The primary endpoint was detection of minimal residual disease (MRD) within 1 yr after ASCT at

214 We assessed the prognostic value of minimal residual disease (MRD) within the ML17638 phase

215 eated with a CD28-based CAR T cell achieving minimal residual disease (MRD)(-) status, consolidative

216 , 40.6% of patients were in CR with negative minimal residual disease (MRD), 40.6% were in CR MRD-pos

217 complete remission (CR) rates often include minimal residual disease (MRD), leading to relapse and r

218 (iwCLL) criteria was 83%, and 61% achieved a minimal residual disease (MRD)-negative marrow response

219 negative posttreatment and evaluate rates of minimal residual disease (MRD)-negative status and progr

220 imab (FCR) begs the question of the value of minimal residual disease (MRD)-negative status as a trea

221 nued presence of tumor cells, referred to as minimal residual disease (MRD).

222 solated from pediatric and adult patients at minimal residual disease (MRD).

223 y effective for radioimmunotherapy targeting minimal residual disease (MRD).

224 tations at diagnosis and provide a marker of minimal residual disease (MRD).

225 ALL), was recently approved for treatment of minimal residual disease (MRD).

226 ics/genetics and postconsolidation levels of minimal residual disease (MRD).

227 Fifteen patients had pretreatment minimal residual disease (MRD; <5% blasts in bone marrow

228 dpoint was overall survival in patients with minimal residual disease (MRD; enhancing tumour <2 cm(2)

229 Measurable (minimal) residual disease (MRD) after allo-HCT may be us

230 ction of subclinical levels of leukemia (ie, minimal residual disease, MRD) using MFC or molecular-ba

231 tial to eliminate DTPs and therefore prevent minimal residual disease, mutational drug resistance, an

232 Five out of 6 patients in CR were also minimal residual disease negative (MRD-).

233 omposite complete responses, 5 of which were minimal residual disease negative by flow cytometry.

234 nic lymphocytic leukaemia who do not achieve minimal residual disease negative disease state followin

235 lity of response and 4 patients converted to minimal residual disease negative status.

236 The overall intent-to-treat minimal residual disease-negative (MRD(-)) remission rat

237 chemotherapy came the first observation that minimal residual disease-negative (MRD-negative) complet

238 igen receptor (CAR) have produced impressive minimal residual disease-negative (MRD-negative) complet

239 table in 36% of patients, who, compared with minimal residual disease-negative cases, had a significa

240 e (88 vs 78%, P = .036), and the bone marrow minimal residual disease-negative complete remission rat

241 there was no apparent detrimental effect on minimal residual disease-negative complete remission rat

242 ukemia, with four of five patients obtaining minimal residual disease-negative CR.

243 nders ceased all therapy; among these all 11 minimal residual disease-negative responders remain prog

244 Minimal residual disease-negative status after treatment

245 36%) patients evaluated by ClonoSeq achieved minimal residual disease negativity with CLL <1/10 000 w

246 Group has defined new response categories of minimal residual disease negativity, with or without ima

247 nts); 50% of patients who responded achieved minimal residual disease negativity.

248 64%) of 543 versus 236 (44%) of 542 achieved minimal residual disease-negativity (10(-5) sensitivity

249 Of provisional standard-risk patients with minimal residual disease of less than 1% on day 19, the

250 ss than 1% on day 19, the 15 with persistent minimal residual disease on day 46 seemed to have an inf

251 e of high-risk cytogenetics and undetectable minimal residual disease on days 33 and 78) were randoml

252 20% of the patients, including 5% who had no minimal residual disease on flow cytometry.

253 kemia cells or clinical response parameters (minimal residual disease, overall survival (OS), and tre

254 disease and 72% (60-81) in patients with low minimal residual disease (p=0.0078).

255 ed in pediatric and Ph(+) r/r, as well as in minimal residual disease-positive ALL, and might also of

256 Two with minimal residual disease-positive complete response prog

257 mission frequently relapse due to persistent minimal residual disease possibly supported, at least in

258 The pathologic complete response or minimal residual disease rate was 30% (n = 15 of 50) in

259 al disease status after remission induction, minimal residual disease re-emerged in four of 382 studi

260 On sequential monitoring of minimal residual disease, relapse was reliably predicted

261 nd point was pathologic complete response or minimal residual disease (residual tumor <= 5 mm).

262 y of single-agent blinatumomab with complete minimal residual disease response in children with relap

263 Major secondary end points included minimal residual disease response, rate of allogeneic he

264 88% of CR/CRh responders achieved a complete minimal residual disease response.

265 o cycles, 14 (52%) of whom achieved complete minimal residual disease response.

266 Complete remission without minimal residual disease seems a particularly useful sho

267 ibitors for treatment of MM, especially in a minimal residual disease setting.

268 Of patients attaining negative minimal residual disease status after remission inductio

269 adverse effect was not independent of age or minimal residual disease status and did not seem to be d

270 ppeared to vary according to the presence of minimal residual disease status before transplantation.

271 Minimal residual disease status warrants consideration a

272 ependent of International Staging System and minimal residual disease status.

273 The determination of minimal-residual-disease status was more informative.

274 At the regression site, there was minimal residual disease that was resistant to loss of M

275 Among patients without minimal residual disease, the hazard ratios were lower (

276 Among patients without minimal residual disease, the magnitude of these associa

277 linical practice, including the detection of minimal residual disease, the management of patients wit

278 that among patients with pretransplantation minimal residual disease, the probability of overall sur

279 Among patients with minimal residual disease, the risk of death was higher i

280 ALL) or NCI standard-risk B-ALL with defined minimal residual disease thresholds during induction wer

281 hosphamide to create a therapeutic window of minimal residual disease to favor host immune developmen

282 Therefore, targeting minimal residual disease to prevent acquired resistance

283 uestion of radioimmunotherapy efficacy in MM minimal residual disease treatment in mice with a low tu

284 hieve blood or bone marrow (BM) undetectable minimal residual disease (U-MRD) status after first-line

285 omplete remission (CR/CRi), and undetectable minimal residual disease (U-MRD) were analyzed for all p

286 CML patients who had sustained undetectable minimal residual disease (UMRD) by conventional quantita

287 oid leukemia (CML) who have had undetectable minimal residual disease (UMRD) for at least 2 years.

288 Rate of undetectable (<10(-4)) minimal residual disease (uMRD) in peripheral blood for

289 presence of DNMT3A(R882) mutations predicts minimal residual disease, underscoring their role in AML

290 Minimal residual disease was a protocol-specified explor

291 Minimal residual disease was also assessed.

292 Minimal residual disease was assessed by means of multic

293 Negative marrow minimal residual disease was attained in 20 (80%) of 25

294 ents achieved second complete remission, and minimal residual disease was evaluable in 192 (87%).

295 ), as was the percentage of patients in whom minimal residual disease was not detected (79% vs. 65%,

296 The risk of relapse among patients with minimal residual disease was significantly higher in the

297 The presence of minimal residual disease was the only independent progno

298 Additional measurements of minimal residual disease were made on weeks 17, 48, and

299 of 49 patients who achieved negative marrow minimal residual disease with acceptable safety.

300 ed a low incidence of complete responses and minimal residual disease, with residual T3- or lymph nod