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

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

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

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

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

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

6 ned prognostic among cases with intermediate minimal residual disease.

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

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

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

10 y be a potential biomarker for monitoring of minimal residual disease.

11 tioning chemotherapy and low tumor burden or minimal residual disease.

12 r therapeutic manipulation and monitoring of minimal residual disease.

13 ghly investigated for its potential to fight minimal residual disease.

14 newly diagnosed EGFRvIII-expressing GBM with minimal residual disease.

15 t may have clinical utility in patients with minimal residual disease.

16 wing promise for treatment of both bulky and minimal residual disease.

17 of fresh bone marrow aspirate approximating minimal residual disease.

18 B-cell lymphoma with the goal of eradicating minimal residual disease.

19 e targets for therapy, and the monitoring of minimal residual disease.

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

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

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

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

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

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

26 sion (89% v 80%, respectively; P = .137) and minimal residual disease (29% v 25%, respectively; P = .

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

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

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

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

31 ased on presenting features and the level of minimal residual disease after remission-induction treat

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

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

34 ession studies, as well as investigations of minimal residual disease and host pharmacogenomics, offe

35 these mechanisms in the hope of eradicating minimal residual disease and improving survival in AML.

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

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

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

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

40 ffer the best chance of achieving a state of minimal residual disease and, thus, minimize tumor-induc

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

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

43 now to achieve complete remission, eradicate minimal residual disease, and improve survival.

44 highly sensitive biomarkers for detection of minimal residual disease, and prognostic tools.

45 progression or metastases, the detection of minimal residual disease, and response to various therap

46 In parallel, methods of monitoring minimal residual disease are evolving.

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

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

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

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

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

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

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

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

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

56 an attractive approach for the treatment of minimal residual disease because the short path lengths

57 ndamentally change approaches for monitoring minimal residual disease burden.

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

59 plerixafor may be observed in a situation of minimal residual disease, but caution is warranted when

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

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

62 Studies of minimal residual disease confirmed durability of CLL era

63 plete remission by morphologic criteria have minimal residual disease demonstrable by either flow cyt

64 Minimal residual disease detected during complete remiss

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

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

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

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

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

70 ll ALL, the t(4;11)(MLL-AF4), and detectable minimal residual disease during or at the end of remissi

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

72 Minimal residual disease evaluation and monitoring is de

73 The minimal residual disease foci that beget breast cancer r

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

75 blast cells at diagnosis and a high level of minimal residual disease (> or = 1%) after 6 weeks of re

76 e intermediate group with postinduction high minimal residual disease (>/=10(-4) cells) received an a

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

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

79 Biomarkers in breast cancer to monitor minimal residual disease have remained elusive.

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

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

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

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

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

85 with chemotherapy resulted in no detectable minimal residual disease in a xenograft model of primary

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

87 and a magnetic needle for the evaluation of minimal residual disease in CD34-positive acute leukemia

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

89 d developed an RT-PCR-based assay to monitor minimal residual disease in HCL.

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

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

92 Identification of minimal residual disease in patients achieving a complet

93 The genomic profiles of cfDNA infer dormancy/minimal residual disease in the majority of patients on

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

95 ts as consolidation therapy for treatment of minimal residual disease, in preparation for stem cell t

96 Evaluation for minimal residual disease included flow cytometry and a h

97 Recent investigations into the biology of minimal residual disease indicate that many early relaps

98 gnancy for which the accurate measurement of minimal residual disease is critical to determining prog

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

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

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

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

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

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

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

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

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

108 Minimal residual disease levels during remission inducti

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

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

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

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

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

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

115 mediate-risk patients with postinduction low minimal residual disease (<10(-4) cells) continued chemo

116 of JAK2 gene mutation by real-time PCR as a minimal residual disease marker after transplant.

117 ne marrow microenvironment and its impact on minimal residual disease may ultimately prevent relapse.

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

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

120 Sequential minimal residual disease monitoring after remission indu

121 exploring refinements in current methods of minimal residual disease monitoring is relevant.

122 ical useful tool for clonality detection and minimal residual disease monitoring.

123 erging role of gene expression profiling and minimal residual disease monitoring.

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

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

126 ral groups have demonstrated that monitoring minimal residual disease (MRD) after allo-HCT is feasibl

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

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

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

130 Purpose Minimal residual disease (MRD) and genetic abnormalities

131 ngle 7-day course of cladribine were without minimal residual disease (MRD) and potentially cured of

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

133 Minimal residual disease (MRD) as a marker of antileukem

134 All patients achieved a CR and minimal residual disease (MRD) assessed by consensus pri

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

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

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

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

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

140 last clearance at day 7 or 15 and persistent minimal residual disease (MRD) at day 28 of induction tr

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

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

143 97/99 and UKALL 2003), 10 were positive for minimal residual disease (MRD) at the end of induction,

144 Minimal residual disease (MRD) at the end of remission-i

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

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

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

148 Minimal residual disease (MRD) before myeloablative hema

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

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

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

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

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

154 To identify new markers for minimal residual disease (MRD) detection in acute lympho

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

156 Minimal residual disease (MRD) detection is standard of

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

158 s of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry du

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

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

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

162 Detection of increasing minimal residual disease (MRD) following HCT may permit

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

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

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

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

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

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

169 icant improvements in technologies to detect minimal residual disease (MRD) in acute myeloid leukemia

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

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

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

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

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

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

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

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

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

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

180 Minimal residual disease (MRD) is an important predictor

181 Minimal residual disease (MRD) is an important prognosti

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

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

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

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

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

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

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

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

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

191 dren with ALL and compared the findings with minimal residual disease (MRD) levels on days 19 and 46

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

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

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

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

196 The clinical value of serial minimal residual disease (MRD) monitoring in core bindin

197 ata concerning prospective use of sequential minimal residual disease (MRD) monitoring to identify mo

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

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

200 after FR, respectively; 15% of patients were minimal residual disease (MRD) negative.

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

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

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

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

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

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

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

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

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

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

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

212 Morphologic and minimal residual disease (MRD) responses were determined

213 diagnosed ALL and compared the findings with minimal residual disease (MRD) results obtained on day 1

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

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

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

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

218 eceptor gene rearrangements for detection of minimal residual disease (MRD) to identify children at h

219 Minimal residual disease (MRD) was assessed posttreatmen

220 Responses were recorded and BM minimal residual disease (MRD) was evaluated after the c

221 Minimal residual disease (MRD) was measured by flow cyto

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

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

224 , 40.6% of patients were in CR with negative minimal residual disease (MRD), 40.6% were in CR MRD-pos

225 re stringent degrees of CR or elimination of minimal residual disease (MRD), including multiparameter

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

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

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

229 the prognostic impact of pretransplantation minimal residual disease (MRD).

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

231 long-term single agents in an HNSCC model of minimal residual disease (MRD).

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

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

234 r (P = .001) and flow cytometric measures of minimal residual disease (MRD; P = .001) each provided i

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

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

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

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

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

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

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

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

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

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

245 Minimal residual disease-negative status after treatment

246 patients with higher Mcl-1 expression, both minimal residual disease-negative status and progression

247 36%) patients evaluated by ClonoSeq achieved minimal residual disease negativity with CLL <1/10 000 w

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

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

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

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

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

253 20% of the patients, including 5% who had no minimal residual disease on flow cytometry.

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

255 ore advanced disease; HR = 0.63; P = .03) or minimal residual disease (positive vs negative; HR = 2.1

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

257 Two with minimal residual disease-positive complete response prog

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

259 with pathologic complete response (RCB-0) or minimal residual disease (RCB-1).

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

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

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 for prolonged survival, with eradication of minimal residual disease seeming crucial to long-term di

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

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

269 ays after injection with leukemia to mimic a minimal residual disease state and achieved T cell-depen

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

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

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

273 enges to overcome therapeutic failure in the minimal residual disease status may relate to an incompl

274 Minimal residual disease status warrants consideration a

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

276 crease in WT1 mRNA expression as a marker of minimal residual disease, suggesting a vaccine-driven an

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

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

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

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

281 When the final pathology revealed pCR or minimal residual disease, the surgeons agreed that BCS i

282 Elimination of minimal residual disease through in-vivo purging of stem

283 Therefore, targeting minimal residual disease to prevent acquired resistance

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

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

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

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

288 Minimal residual disease was a protocol-specified explor

289 Minimal residual disease was also assessed.

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

291 Minimal residual disease was monitored by quantitative a

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

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

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

295 This study of minimal residual disease was undertaken in parallel, to

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

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

298 nt mutant forms of BCR-ABL, and to eliminate minimal residual disease with the goal of achieving tota

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

300 Given that the confirmation of pCR or minimal residual disease would change surgeons' recommen