ライフサイエンスコーパス: cytogenetic

1 range, 40-76 years), and 35.5% had high-risk cytogenetics.

2 ous transplant, and (30 [62%]) had high-risk cytogenetics.

3 ticularly evident in patients with high-risk cytogenetics.

4 mmendations, established through bone marrow cytogenetics.

5 stem (CPSS) based on clinical parameters and cytogenetics.

6 the poor prognosis associated with high-risk cytogenetics.

7 s known prognostic factors including adverse cytogenetics.

8 particularly in those with intermediate-risk cytogenetics.

9 endent of known risk factors such as age and cytogenetics.

10 ation for kappa and lambda light chains, and cytogenetics.

11 have dismal outcomes, independent of age and cytogenetics.

12 combining single-cell strand sequencing with cytogenetics.

13 c features at diagnosis, including high-risk cytogenetics.

14 ouble or triple hit status was determined by cytogenetics.

15 and 57% and 72% for patients with high-risk cytogenetics.

16 apy was two (2-5), 38 patients had high-risk cytogenetics, 17 were unresponsive to all previous treat

17 s was 5, and 17 patients (89%) had high-risk cytogenetics (17p deletion and/or complex karyotype).

18 Cytogenetics 2.7 M Microarrays/CytoScan HD arrays allowe

19 as similar in the 92 patients with high-risk cytogenetics (34.8%), also deepened with further treatme

20 Cytogenetic aberrations at the single-cell level represe

21 We studied whether these cytogenetic aberrations can be used for risk group strat

22 an database is a powerful resource, and that cytogenetic aberrations captured by traditional approach

23 Cytogenetic aberrations detected by interphase fluoresce

24 study, we addressed the prognostic impact of cytogenetic aberrations for bortezomib-treated patients.

25 quencies and outcome parameters of recurrent cytogenetic aberrations in AMKL, samples and clinical da

26 The high-risk cytogenetic aberrations t(4;14), t(14;16), and del(17p13

27 Two recurrent cytogenetic aberrations, namely del(17p), affecting TP53

28 CLL) depends on different markers, including cytogenetic aberrations, oncogenic mutations, and mutati

29 impact of therapy on the prognostic role of cytogenetic aberrations.

30 cytogenetic results; 137 (25%) had high-risk cytogenetic abnormalities and 172 (32%) had 1q21 amplifi

31 ed on multivariable Cox regression analyses, cytogenetic abnormalities and mutations in RUNX1, NRAS,

32 risk" group, defined as those with high-risk cytogenetic abnormalities and/or 1q21 amplification (HR,

33 Certain cytogenetic abnormalities are known to adversely impact

34 ain-Fusion (LGF) model, which represents all cytogenetic abnormalities as combinations of loss, gain,

35 Patients with AML and MDS who had cytogenetic abnormalities associated with unfavorable ri

36 ), as well as after adjustment for poor-risk cytogenetic abnormalities at diagnosis and platelet coun

37 Risk for cytogenetic abnormalities based on features and size: sm

38 in chromosome 20q, or del(20q), are frequent cytogenetic abnormalities detected in hematologic malign

39 Patients with multiple adverse cytogenetic abnormalities do not benefit from these agen

40 The acquisition of the cytogenetic abnormalities hyperdiploidy or translocation

41 we aimed to reassess the prognostic value of cytogenetic abnormalities in a large series of 617 adult

42 t(16;16)(p13.1;q22), one of the most common cytogenetic abnormalities in AML, leads to expression of

43 B hyperexpression are found in patients with cytogenetic abnormalities presenting a unfavorable progn

44 ltiple myeloma based on cytogenetics Several cytogenetic abnormalities such as t(4;14), del(17/17p),

45 High-risk cytogenetic abnormalities were defined as del(17p), t(4;

46 Six cytogenetic abnormalities were identified as clinically

47 ression induces centrosome amplification and cytogenetic abnormalities, and (2) in Ph(+) CML, it syne

48 isease as well as in patients with high-risk cytogenetic abnormalities, defined as t(4;14), t(14;16),

49 The other cytogenetic abnormalities, including complex and monosom

50 t across subgroups with individual high-risk cytogenetic abnormalities, including patients with del(1

51 of leukemias frequently defined by recurrent cytogenetic abnormalities, including rearrangements invo

52 is a B-cell malignancy stratified in part by cytogenetic abnormalities, including the high-risk copy

53 The presence of certain high-risk cytogenetic abnormalities, such as translocations (4;14)

54 roves the poor PFS associated with high-risk cytogenetic abnormalities.

55 nto the effect of new drugs in patients with cytogenetic abnormalities.

56 groups, including in patients with high-risk cytogenetic abnormalities.

57 the high proportion of patients with adverse cytogenetic abnormalities.

58 a total of 53% of the patients had high-risk cytogenetic abnormalities.

59 ple myeloma (MM) outcome is driven mainly by cytogenetic abnormalities.

60 sume this is true regardless of accompanying cytogenetic abnormalities.

61 conducted to evaluate KRd vs Rd by baseline cytogenetics according to fluorescence in situ hybridiza

62 as many patients with high- or standard-risk cytogenetics achieved a complete response or better with

63 ncreasing melanoma size demonstrates greater cytogenetic alterations.

64 er and driver mutations and are enriched for cytogenetic alterations.

65 Cytogenetic analyses and DNA index were performed at COG

66 -genome sequencing, structural modelling and cytogenetic analyses of 17 different cancer types, inclu

67 rd downstream assays such as cytological and cytogenetic analyses that are more time consuming and co

68 It has long been clear by cytogenetic analyses, and recently confirmed by mutation

69 three inversions identified by our previous cytogenetic analyses.

70 Cytogenetic analysis and single-nucleotide polymorphism-

71 By applying comparative cytogenetic analysis and whole-chloroplast phylogenetics

72 years); 374 patients (94.7%) had genetic and cytogenetic analysis completed within 7 d and were centr

73 We concluded that cytogenetic analysis is a useful diagnostic and prognost

74 Cytogenetic analysis of mouse embryonic fibroblasts and

75 Comparative cytogenetic analysis of related species based on individ

76 Cytogenetic analysis revealed the presence of the Philad

77 g especially the results of biodosimetry via cytogenetic analysis using the FISH method.

78 PCR-based markers and cytogenetic analysis with genomic in situ hybridisation

79 uencing and centromere mapping combined with cytogenetic analysis, small molecule inhibitors, and gen

80 aneuploidy status at higher sensitivity than cytogenetic analysis.

81 ng driver mutations in 111 cancer genes with cytogenetic and clinical data, we defined AML genomic su

82 yeloma XI trial, for whom complete molecular cytogenetic and clinical outcome data were available.

83 Added contributions of cytogenetic and gene sequencing investigations were dete

84 Our cytogenetic and molecular assessments of 34 patients wit

85 ce of early NPM1m PB-MRD, independent of the cytogenetic and molecular context.

86 m (MPN) are characterized by a unique set of cytogenetic and molecular features distinct from de novo

87 of advanced age, high HCT-CI, very poor-risk cytogenetic and molecular features, and high IPSS-R scor

88 Given the high frequency of poor-risk cytogenetic and molecular features, malignant clones are

89 Accordingly, cytogenetic and molecular genetic analyses, such as conv

90 response are more likely to achieve improved cytogenetic and molecular responses with switching to ni

91 model incorporating comorbidities, age, and cytogenetic and molecular risks.

92 als.gov NCT03013998 ), which aims to provide cytogenetic and mutational data within 7 days (d) from s

93 alpha-WGD events shared by all Brassicaceae, cytogenetic and transcriptome analyses revealed two youn

94 ted overlap between proteomics data and both cytogenetics and genetic mutations.

95 Further understanding of melanoma cytogenetics and molecular pathways have helped to recog

96 Molecular cytogenetics and next-generation sequencing were used to

97 Patients with poor-risk cytogenetics and those at least 75 years old had CR + CR

98 isk ALL (defined as the absence of high-risk cytogenetics and undetectable minimal residual disease o

99 % of this cohort, and associated with normal cytogenetics and unmutated IGHV.

100 for KRd vs Rd were 79.2% vs 59.6% (high-risk cytogenetics) and 91.2% vs 73.5% (standard-risk cytogene

101 ostic categories as well as against genetic, cytogenetic, and cellular phenotypes of specimens from t

102 classes associated with typical mutational, cytogenetic, and gene expression patterns.

103 Phylogenetic, cytogenetic, and genomic analyses implied that the nonna

104 be an evolutionary dead end, morphological, cytogenetic, and genomic data suggest that bdelloid roti

105 kflows involving morphology, flow cytometry, cytogenetic, and molecular genetic analyses.

106 yelofibrosis (PMF) that integrates clinical, cytogenetic, and mutation data.

107 integrate prognostically relevant clinical, cytogenetic, and mutation data.

108 Clinical, cytogenetic, and mutational data are used to classify pa

109 cy that were associated with select genetic, cytogenetic, and phenotypic disease subsets, warranting

110 white cell count at diagnosis, pretreatment cytogenetics, and end-of-induction minimal residual dise

111 tic subtype on the basis of immunophenotype, cytogenetics, and fluorescence in situ hybridization.

112 stem score, increased incidence of high-risk cytogenetics, and higher revised international staging s

113 M) patients with high-risk and standard-risk cytogenetics, and improves the poor PFS associated with

114 h, such as single-cell strand sequencing and cytogenetics, and represents a valuable resource toward

115 e masked hypodiploid patients, undetected by cytogenetics, and their associated copy number neutral l

116 risk groups, including patients with adverse cytogenetics, and was associated with longer response du

117 No cytogenetic anomalies were found in the infiltrate excep

118 otype and identified 5q deletion as an early cytogenetic anomaly.

119 legumes, we took an integrated molecular and cytogenetic approach to track occurrences of polyploidy

120 t documents how key refinements in molecular cytogenetic approaches, from simple fluorescence in situ

121 highlighting the limitations of conventional cytogenetic approaches.

122 ogenetics) and 91.2% vs 73.5% (standard-risk cytogenetics); approximately fivefold as many patients w

123 Previous myeloid disorder, age, and cytogenetics are crucial determinants of outcomes and sh

124 When adverse-risk cytogenetics are present, patients with NPM1(mut) share

125 Cytogenetic array and mutational analysis of the parenta

126 sis, and Philadelphia chromosome-positive by cytogenetic assessment, with Eastern Cooperative Oncolog

127 We applied uniform cytogenetic assessments in a large cohort of newly diagn

128 Patients with aggressive disease and/or poor cytogenetics at diagnosis relapsing within the first 2 y

129 s locations on chromosomes using a system of cytogenetic bands, each with a unique name and region on

130 uding all individuals recorded in the Danish Cytogenetic Central Register with a 22q11.2 deletion or

131 We sorted TERT-positive cells with cytogenetic changes and followed their growth.

132 In multiple myeloma, cytogenetic changes are important predictors of patient

133 For those sarcomas with complex cytogenetic changes that lack specific alterations, addi

134 actors, a classification based on underlying cytogenetic changes, and new treatment options.

135 ssion of AID marked pre-B-ALL lacking common cytogenetic changes.

136 cal improvement) as well as on molecular and cytogenetic characteristics reassessed at the moment of

137 In this study, we have assessed frequency, cytogenetic characteristics, prognostic impact, and unde

138 It has been shown that a new cytogenetic classification, included in the IPSS-R (cyto

139 De novo assembly of long reads and cytogenetics confirmed this species-specific collapse of

140 These studies mostly confirmed the cytogenetic data and subclassified patients according to

141 A novel in silico approach compares cytogenetic data between the Mitelman database and TCGA,

142 We analyzed cytogenetic data from 427 children with relapsed B-cell

143 Five of 7 relapsed patients (71%) with cytogenetic data had trisomy 8.

144 ry of Ceratopteris based on both genomic and cytogenetic data, and on repeat proportions similar to t

145 Eye Hospital Oncology Service Uveal Melanoma Cytogenetic Database (N = 1172), 128 patients fulfilled

146 not differ between groups when stratified by cytogenetics, de-novo versus secondary or therapy-relate

147 ese patients when characterized with adverse cytogenetics (deletion 17p and translocation [4;14]) in

148 Patients with good-risk cytogenetics demonstrated the fastest disease clearance,

149 ation in diagnosed carriers depend on age at cytogenetic diagnosis, possibly reflecting age-specific

150 eatment strategies have shown promise for HR cytogenetic diseases, such as proteasome inhibition in c

151 g all available quantitative evidence on the cytogenetic effects of benzene exposure on CAs and MN re

152 Patients with favourable-risk cytogenetics (eg, t[15;17] or core-binding factor AML) o

153 ods, accurately detects clinically important cytogenetic events, and allows for further interrogation

154 Cytogenetic evolution did not correlate with mutational

155 Clonal cytogenetic evolution with additional chromosomal abnorm

156 tients includes regular BM morphological and cytogenetic examinations.

157 rediction based on conventional clinical and cytogenetic factors alone.

158 by previous lines of therapy (<=4 vs >4) and cytogenetic features to receive 2.5 mg/kg or 3.4 mg/kg b

159 not merely by association with other adverse cytogenetic features.

160 d prior HMA treatment, and 32% had poor-risk cytogenetic features.

161 One of the cytogenetic findings in AML is structurally highly abnor

162 and to balance them for known mutations and cytogenetic findings.

163 nalysis), genomic (analysis of variants) and cytogenetic (fluorescence in situ hybridization) approac

164 stigation illustrates the power of precision cytogenetics for annotation of the infertile genome, sug

165 repeat loci that we detected correlated with cytogenetic fragile sites.

166 etics and breeding of A. digitata, including cytogenetics, genetic diversity and reproductive biology

167 myeloid leukemia (AML) was decided combining cytogenetics/genetics and postconsolidation levels of mi

168 ontrol of cell survival, tissue polarity and cytogenetic gradient during the development of the tectu

169 g taxonomic and phylogenetic puzzle to which cytogenetics has contributed crucial data.

170 essive disease states, such as patients with cytogenetic high-risk disease or patients ineligible for

171 did patients with favorable and intermediate cytogenetics (HR, 0.51;P= .03 and HR, 0.68;P= .01, respe

172 ; P < .001), as well as those with high-risk cytogenetics (HR, 12.6; P = .01).

173 Targeted sequencing and array-based cytogenetics identified a driver mutation and/or structu

174 Conventional cytogenetics identifies some patients with rearrangement

175 combination of genetic segregation analysis, cytogenetics, immunocytology and 3D imaging to genetical

176 Median age was 74 years, with poor-risk cytogenetics in 49% of patients.

177 i provide an invaluable tool for comparative cytogenetics in closely related species.

178 t routine BM flow cytometry, morphology, and cytogenetics in patients who present with cytopenia(s) c

179 the International Staging System and adverse cytogenetics in the multivariate analysis.

180 ted with patient characteristics, mutations, cytogenetics, induction treatments, and measurable resid

181 els with (MIPSS70-plus) or without (MIPSS70) cytogenetic information were developed.

182 In the MIPSS70-plus model, which included cytogenetic information, four risk categories were delin

183 In this exciting era of "next-gen cytogenetics," integrating genomic sequencing into the p

184 etic classification, included in the IPSS-R (cytogenetic-IPSS-R [C-IPSS-R]), can better predict the o

185 17 (76%) were categorized with standard-risk cytogenetics (KRd, n = 147; Rd, n = 170).

186 tients (24%) were categorized with high-risk cytogenetics (KRd, n = 48; Rd, n = 52) and 317 (76%) wer

187 nt samples that were sent to the Mayo Clinic cytogenetics laboratory for FISH testing (n = 2,851; fro

188 erize the genome at the genetic or molecular cytogenetic level have been conducted.

189 ntegrating linkage and comparative maps with cytogenetic map analyses assigned two linkage groups to

190 rated approaches of genetic, comparative and cytogenetic map analyses.

191 A Spirodela cytogenetic map containing 96 BAC markers with an averag

192 ning of paddlefish chromosomes combined with cytogenetic mapping of ribosomal genes and Hox paralogs

193 Our assembly is concordant with cytogenetic maps and Sanger sequences of over 90 Y chrom

194 ur knowledge, the first partial and complete cytogenetic maps for selected representatives of clade E

195 ss across Platyrrhini makes it an attractive cytogenetic marker for Saimiri and other New World monke

196 s satellite DNAs are potentially informative cytogenetic markers because they display high evolutiona

197 The molecular and cytogenetic markers developed herein could be used to tr

198 A total of 47 PLUG markers and a set of cytogenetic markers specific for Ae. comosa chromosomes

199 tected by traditional clinical molecular and cytogenetic methods.

200 ogic evaluation with diagnostically relevant cytogenetic, molecular, and immunohistochemical testing

201 omal inversions can provide windows onto the cytogenetic, molecular, evolutionary and demographic his

202 vances over the last 30 years in immunology, cytogenetics, molecular biology, gene expression profili

203 s with MPN with eosinophilia and nonspecific cytogenetic/molecular abnormalities and/or increased mye

204 The augmented HCT-CI, age, and cytogenetic/molecular risks could be combined into an AM

205 model comprising augmented HCT-CI, age, and cytogenetic/molecular risks had even better predictive e

206 ociated with prediction of overall survival: cytogenetic/molecular status (P = 0.015), T-size categor

207 efined by the International System for human Cytogenetic Nomenclature (ISCN).

208 Currently, there is no tool to convert cytogenetic nomenclature into genomic coordinates.

209 Cytogenetic nomenclature is used to describe chromosomal

210 algorithm to parse International System for Cytogenetic Nomenclature notation for quantitative abnor

211 pping population was analysed utilising both cytogenetic observations and high-throughput genotyping

212 omosome evolution by classical and molecular cytogenetics of both parental species and hybrids.

213 Whole genome sequencing and cytogenetics of experimentally evolved populations revea

214 were (1) monosomy 3 and 8q amplification by cytogenetic or DecisionDx-UM Class 2 and (2) monosomy 3

215 enefit of intensive consolidation within the cytogenetic or FLT3-internal tandem duplication and NPM1

216 nally assessed in clinical diagnostics using cytogenetic or microarray testing.

217 Patients in the sunitinib group had worse cytogenetic or molecular features (monosomy 3 and 8q amp

218 hieved a long-term sustainable response at a cytogenetic or molecular level.

219 b interface allows users to upload molecular cytogenetic or processed single cell whole-genome sequen

220 (<50 years) and patients without unfavorable cytogenetics or aFLT3-ITD mutation.

221 0.0018), male gender (p = 0.019), high risk cytogenetics (p = 0.002), higher IDO-1 mRNA (p = 0.005),

222 The cytogenetic PI improves the classification of newly diag

223 with an intermediate-risk or favorable-risk cytogenetic profile (29 of 43 patients [67%] vs. 24 of 7

224 shown that patients with an unfavorable-risk cytogenetic profile and TP53 mutations who receive conve

225 tients with AML who had an intermediate-risk cytogenetic profile and who also received serial 10-day

226 To determine the risks for altered cytogenetic profile based on melanoma features and size.

227 gher among patients with an unfavorable-risk cytogenetic profile than among patients with an intermed

228 metastasis on the basis of individual tumor cytogenetic profile.

229 On the basis of personalized cytogenetic profiles, Kaplan-Meier estimates (1, 3, and

230 stasis strongly correlates with personalized cytogenetic profiles, with 5-year Kaplan-Meier estimates

231 among study patients with intermediate-risk cytogenetic profiles.

232 Cytogenetic profiling revealed that mis-segregated chrom

233 re a hallmark of human cancers, with complex cytogenetic rearrangements leading to genetic changes pe

234 diagnosis, possibly reflecting age-specific cytogenetic referral reasons.

235 The 15q11.2 BP1-BP2 cytogenetic region has been associated with learning and

236 In comparison with patients in complete cytogenetic remission, TKI-resistant LSC and progenitors

237 tes has been correlated with hematologic and cytogenetic remissions in patients with Philadelphia chr

238 ients with chromosome 13q deletion or normal cytogenetics represent the majority of chronic lymphocyt

239 reproductive biology. The objectives of our cytogenetic research were to determine the genome size,

240 racterization has largely been restricted to cytogenetic resolution.

241 tinib 400 mg once daily and had a suboptimal cytogenetic response according to 2009 ELN recommendatio

242 esults suggest that patients with suboptimal cytogenetic response are more likely to achieve improved

243 th e13a2, e14a2, and both achieving complete cytogenetic response at 3 and 6 months was 59%, 67%, and

244 The primary endpoint was complete cytogenetic response at 6 months in the intention-to-tre

245 Complete cytogenetic response at 6 months was achieved by 48 of 9

246 t any time, or for patients with no complete cytogenetic response at 6 months.

247 a clinically relevant mutation lost complete cytogenetic response compared with 15 (17%) of 86 patien

248 dose escalation for patients with suboptimal cytogenetic response on imatinib.

249 Cytogenetic response rates were 61% and 25% (P = .02), r

250 d leukaemia in chronic phase with suboptimal cytogenetic response remains undetermined.

251 d leukaemia in chronic phase with suboptimal cytogenetic response to imatinib according to the 2009 E

252 ient with a CSNK1A1 mutation showed complete cytogenetic response to lenalidomide.

253 For patients with a complete cytogenetic response, 13 (14%) of 93 patients screened h

254 ment with imatinib, and 82.8% had a complete cytogenetic response.

255 Of 722 randomized patients, 552 had cytogenetic results; 137 (25%) had high-risk cytogenetic

256 Cytogenetics revealed the loss of chromosome Y (LOY) in

257 newly diagnosed multiple myeloma, including cytogenetic risk and transplantation status subgroup ana

258 djusted for known prognostic factors such as cytogenetic risk and WBC count, neither the presence of

259 reatment to risk, we need to better define a cytogenetic risk classification.

260 By cytogenetic risk group, in standard-risk patients, 3-yea

261 in subgroup analyses of patients across all cytogenetic risk groups support further investigation of

262 Cytogenetic risk groups were predictive of outcome postr

263 We identified 3 distinct cytogenetic risk groups: low risk (no MYC aberration), i

264 Overall, the C-IPSS-R changed the IPSS cytogenetic risk only in 8% of cases but identified a ne

265 Thus, cytogenetic risk predominates over molecular risk in NPM

266 status, in those with favorable/intermediate cytogenetic risk profile, and in women.

267 , 1.25; 95% CI, 1.06 to 1.28), comprehensive cytogenetic risk score of poor or very poor (HR, 1.43; 9

268 Of 417 patients with known cytogenetic risk status, 100 patients (24%) were categor

269 n patients with relapsed MM, irrespective of cytogenetic risk status, and should be considered a stan

270 ced with respect to age, race, FLT3 subtype, cytogenetic risk, and blood counts but not with respect

271 and safety of IRd vs placebo-Rd according to cytogenetic risk, as assessed using fluorescence in situ

272 mide drugs, time from diagnosis to ASCT, and cytogenetic risk.

273 ng to International Staging System stage and cytogenetic risk.

274 lderly MM patients, irrespectively of age or cytogenetic risk.

275 for high-risk (HR) multiple myeloma based on cytogenetics Several cytogenetic abnormalities such as t

276 s fludarabine refractory or who have complex cytogenetics should have occult RT excluded before initi

277 DFT2 bears no detectable cytogenetic similarity to DFT1 and carries a Y chromosom

278 d novel, quantitative, and widely applicable cytogenetic strategies to elucidate the molecular bases

279 Cytogenetic studies demonstrated that MDSCs in patients

280 In some cases, cytogenetic studies of the dermal infiltrate were also p

281 of chromosome 21 (iAMP21) defines a distinct cytogenetic subgroup of childhood B-cell precursor acute

282 4 mutations per patient varied according to cytogenetic subgroup, age, and history of previous hemat

283 owing classification in 10 exclusive primary cytogenetic subgroups and in secondary subgroups, includ

284 Multiple cytogenetic subgroups have been described in adult Phila

285 Careful analysis of cytogenetic subgroups in trials comparing different trea

286 This improvement remained applicable for all cytogenetic subgroups other than del(17p).

287 8%, P = .02) but similar for all arms across cytogenetic subgroups, as was remission duration and ove

288 acebo-Rd in both high-risk and standard-risk cytogenetics subgroups: in high-risk patients, the hazar

289 Subsets including those with favorable cytogenetics, those lacking a mutation of FLT3 or NPM1,

290 evolution of risk profiling of AML from the cytogenetic to molecular era and describe the implicatio

291 rative Oncology Group performance status and cytogenetics, to receive ibrutinib plus obinutuzumab (or

292 ome sequencing (GS) is an enhanced and novel cytogenetic tool to define the contribution of chromosom

293 For patients with standard-risk cytogenetics, treatment with KRd led to a 10-month impro

294 For patients with high-risk cytogenetics, treatment with KRd resulted in a median PF

295 inical standard-risk patients with high-risk cytogenetics was equivalent to clinical high-risk patien

296 ents with good, intermediate-, and high-risk cytogenetics were 68%, 47%, and 26%, respectively (P < .

297 ith NPM1(mut)/FLT3-ITD(neg/low) AML, adverse cytogenetics were associated with lower complete remissi

298 Patients with unfavorable cytogenetics were shown to benefit from HD daunorubicin

299 by prior transplantation, disease stage, and cytogenetics, with prognostic superiority of MRD negativ

300 sought to determine whether MM with adverse cytogenetics would benefit more from Pom-Dex if exposed