ライフサイエンスコーパス: cytogenetics

1 ernational Staging System score, and adverse cytogenetics.

2 or the effects of other covariates including cytogenetics.

3 onal heterogeneity in AML based on metaphase cytogenetics.

4 to levels seen in patients without high-risk cytogenetics.

5 well as patients with favorable and adverse cytogenetics.

6 ovo AML when adjusted for disease status and cytogenetics.

7 ree survival even in patients with high-risk cytogenetics.

8 more powerful model for prognostication than cytogenetics.

9 to overcome the poor prognosis of high-risk cytogenetics.

10 viability of B-ALL cell lines with high-risk cytogenetics.

11 er outcomes more reliably than serial marrow cytogenetics.

12 iated with worse patient outcome and adverse cytogenetics.

13 needed to overcome the barrier of high-risk cytogenetics.

14 nts (13%), of whom 92% had intermediate-risk cytogenetics.

15 eukemia (AML) and poor- or intermediate-risk cytogenetics.

16 patients with normal/noninformative routine cytogenetics.

17 between age, morphology, immunophenotype, or cytogenetics.

18 combining single-cell strand sequencing with cytogenetics.

19 orphism arrays (SNP-A) complementing routine cytogenetics.

20 , 2 with isolated del(5q) and 3 with complex cytogenetics.

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

22 ogic disorder (P = .002) but not with age or cytogenetics.

23 n, including 52% of the patients with normal cytogenetics.

24 5% WT1(mut) patients harbored favorable risk cytogenetics.

25 e of particular use in patients with adverse cytogenetics.

26 IDH1(+) patients (91%) had intermediate-risk cytogenetics.

27 ouble or triple hit status was determined by cytogenetics.

28 ent prognostication can be enhanced by tumor cytogenetics.

29 differ in the presence or absence of adverse cytogenetics.

30 was 33% and correlated strongly with adverse cytogenetics.

31 atients with either favorable or unfavorable cytogenetics.

32 all survival varied significantly by age and cytogenetics.

33 5), and 18 (62%) of 29 patients had abnormal cytogenetics.

34 with acute myeloid leukemia (AML) and normal cytogenetics.

35 no benefit on those with inv(16) or t(8;21) cytogenetics.

36 effective, even in patients with unfavorable cytogenetics.

37 ficantly, better for patients with favorable cytogenetics.

38 H) mutational status or high-risk interphase cytogenetics.

39 characterization of AML patients with normal cytogenetics.

40 dict outcome in patients with AML and normal cytogenetics.

41 tation, and for those with intermediate-risk cytogenetics.

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

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

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

45 ticularly evident in patients with high-risk cytogenetics.

46 mmendations, established through bone marrow cytogenetics.

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

48 the poor prognosis associated with high-risk cytogenetics.

49 s known prognostic factors including adverse cytogenetics.

50 particularly in those with intermediate-risk cytogenetics.

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

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

53 have dismal outcomes, independent of age and cytogenetics.

54 ternational Prognostic Scoring System (IPSS) cytogenetics.

55 Two thirds of patients had complex MN cytogenetics.

56 59 years of age and/or those with high-risk cytogenetics.

57 ups, including 5 of 14 patients with adverse cytogenetics.

58 ge and cytogenetic risk groups (adverse risk cytogenetics: 1-year adjusted RR, 1.47; 95% CI, 1.23 to

59 even in a subset of AML patients with normal cytogenetics (10 of 64, 16%).

60 CRC patients less frequently had unfavorable cytogenetics (15% versus 36%) and HCT-CI scores of 3 or

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

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

63 Cytogenetics 2.7 M Microarrays/CytoScan HD arrays allowe

64 : (1) age older than 35 years; (2) poor-risk cytogenetics; (3) t-AML not in remission or advanced t-M

65 Of 1058 patients with abnormal cytogenetics, 319 (30%) were MK MK(+).

66 ORR was 20% in patients with adverse cytogenetics; 32% in those age 70 years or older; 32% in

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

68 of NY-ESO-1 compared to patients with normal cytogenetics (60% versus 31%; P = .004).

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

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

71 in adults younger than 60 years with normal cytogenetics acute myeloid leukemia (AML).

72 In conclusion, pretreatment cytogenetics adds to other prognostic factors in older A

73 Unfavorable cytogenetics adversely impacted relapse, DFS, and OS.

74 tient who underwent transplantation based on cytogenetics, age, and a relapse-free survival (RFS) tim

75 th reduced LFS included active disease, poor cytogenetics, age, year of hematopoietic stem-cell trans

76 omosomal abnormalities by FISH and metaphase cytogenetics allows risk stratification in multiple myel

77 1mut) in 303 patients with intermediate-risk cytogenetics AML treated with intensive chemotherapy.

78 In younger adults with normal cytogenetics AML, splenomegaly predicts a lower CR rate,

79 Using DNA sequencing and molecular cytogenetics, an initial analysis of the repetitive frac

80 largely based on pretreatment assessment of cytogenetics and a limited panel of molecular genetic ma

81 abnormalities of chromosomes 5 or 7, complex cytogenetics and a reduced response to chemotherapy.

82 n predict the outcome of treatment including cytogenetics and an increasing list of molecular feature

83 information additional to that obtained from cytogenetics and analyses of gene mutations and single g

84 s standard risk or high risk on the basis of cytogenetics and beta2-microglobulin concentrations.

85 tive trait loci, physical mapping, molecular cytogenetics and comparative genomics.

86 t was mediated by other risk factors such as cytogenetics and DS status (EFS 1.45 [0.88-2.39], P = .1

87 expression in AML is closely associated with cytogenetics and FLT3-ITD mutations.

88 nt risk stratification schemes incorporating cytogenetics and FLT3/ITD status, the presence of WT1 mu

89 Metaphases were studied by conventional cytogenetics and fluorescent-labeled DNA probes (fluores

90 review article by Pickard et al., entitled "Cytogenetics and gene discovery in psychiatric disorders

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

92 groups, including in patients with poor-risk cytogenetics and in those with a history of myelodysplas

93 ;16), chromosome 13 deletion by conventional cytogenetics and loss of 17p13 by interphase fluorescenc

94 achieving CR were more likely to have normal cytogenetics and lower methylation levels.

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

96 MicroRNAs (miRNAs) are associated with cytogenetics and molecular subtypes of acute myelogeneou

97 Molecular cytogenetics and next-generation sequencing were used to

98 the basis of recent study results involving cytogenetics and oncologic pathways of HCCs, novel drugs

99 ures have been described in association with cytogenetics and outcome in acute myeloid leukemia.

100 Both groups were balanced according to cytogenetics and performance status.

101 but were infrequent in patients with adverse cytogenetics and secondary AML.

102 osomal abnormalities with the use of routine cytogenetics and single nucleotide polymorphism arrays a

103 ittle is known about the association between cytogenetics and the characteristics of relapse (eg, tim

104 Using cytogenetics and the percentage of marrow blasts after t

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

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

107 % of this cohort, and associated with normal cytogenetics and unmutated IGHV.

108 in, which we identified through conventional cytogenetics and whole-transcriptome sequencing analysis

109 Metaphases were abnormal by cytogenetics and/or metaphase FISH in 61 (40%) patients.

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

111 range, 60 to 84 years), 30% had adverse-risk cytogenetics, and 36% had a WHO performance score >or= 2

112 el(5q), 1 had del(5q) and +8, 23 had complex cytogenetics, and 7 others had del(5q) identified locall

113 s (40%) contained alterations not found with cytogenetics, and 98% of these regions contained genes.

114 lterations that are not apparent by standard cytogenetics, and aberrant epigenetic regulation of gene

115 with acute myeloid leukemia (AML) and normal cytogenetics, and associated with a poor prognosis.

116 SCT v conventional chemotherapy), among age, cytogenetics, and bone marrow blasts after the first ind

117 ation of National Cancer Institute criteria, cytogenetics, and early morphological response to induct

118 of National Cancer Institute (NCI) criteria, cytogenetics, and early response to induction therapy, w

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

120 analysis, adjusting for the effects of age, cytogenetics, and FLT3/ITD, the independent prognostic e

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

122 al-blood and bone marrow counts, informative cytogenetics, and follow-up data.

123 tors, including age, white blood cell count, cytogenetics, and gene mutations, into survival analysis

124 rognostic factors, including age, WBC count, cytogenetics, and gene mutations, into survival analysis

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

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

127 Lack of remission at alloBMT, adverse cytogenetics, and low allograft nucleated cell dose were

128 importance of RBC transfusion dependency and cytogenetics, and offers a simple and powerful CPSS for

129 L correlate with known morphologic features, cytogenetics, and outcome.

130 in addition to proliferation rate, pre-ASCT cytogenetics, and performance status.

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

132 reasing marrow blast percentage, unfavorable cytogenetics, and salvage not including allogeneic stem

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

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

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

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

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

138 spectively, suggesting the potential role of cytogenetics as a risk factor applicable at any time in

139 rognostic factor for OS or RFS, highlighting cytogenetics as the most important prognostic factor in

140 uantitative polymerase chain reaction and/or cytogenetics at 3, 6, and 12 months.

141 P < .001) compared with patients with normal cytogenetics at CR (n = 183); 3-year RFS was 15% and 45%

142 normal cytogenetics at diagnosis, and normal cytogenetics at CR (NCR; n = 103) were compared with tho

143 ls determined the prognostic significance of cytogenetics at CR, adjusting for other covariates.

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

145 Patients with abnormal cytogenetics at diagnosis, and normal cytogenetics at CR

146 103) were compared with those with abnormal cytogenetics both at diagnosis and at CR (ACR; n = 15) f

147 ineage dysplasia correlates with unfavorable cytogenetics but has no independent impact on prognosis.

148 verall survival of patients with unfavorable cytogenetics but without MK was 13% in contrast to a 4-y

149 Some prognostic factors (interphase cytogenetics) but not others (immunoglobulin heavy-chain

150 ic abnormalities before treatment had normal cytogenetics by 1 year after treatment.

151 The presence of baseline high-risk cytogenetics by FISH (hazard ratio 17.3; P = .002) and p

152 rospective studies have identified poor-risk cytogenetics, chemotherapy resistance, comorbidities fro

153 iable-region mutation status, CD38 or ZAP-70 cytogenetics, clinical stage) were significantly associa

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

155 The increased incidence of unfavorable cytogenetics contributed to their poorer outcome, and, w

156 ase, circulating myeloblasts, platelets, and cytogenetics could further stratify MDS/MPN-U but not aC

157 Marrow cytogenetics data were reviewed.

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

159 FLT3-ITD AML, mouse blasts exhibited normal cytogenetics, decreased Mll-WT-to-Mll-PTD ratio, loss of

160 ical stage (HR = 2.75, P = .0025), poor risk cytogenetics (del 17p, HR = 2.38; del11q, HR = 2.36, P =

161 sence of hypodiploidy, del(13q) by metaphase cytogenetics, del(17p), IgH translocations [t(4;14), or

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

163 es with a donor-recipient sex mismatch, FISH cytogenetics demonstrated that the plasma cells were of

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

165 High-risk cytogenetics did not impact outcomes.

166 The percentage of patients with favorable cytogenetics dropped from 17% in those younger than age

167 patients with AML at higher risk with normal cytogenetics [e.g., FLT3-internal tandem duplication (IT

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

169 vs those whose disease remained stable) and cytogenetics [eg, del(5q)]; and (2) molecular criteria r

170 mpared to a control group of AML with normal cytogenetics; ERG and ETS2 also ranked among the most hi

171 Cytogenetics evidenced t(9;22)/(Ph(+)) (20%), 11q23/MLL

172 latelet counts, intermediate-risk and normal cytogenetics, FLT3 internal tandem duplication, and NPM1

173 tcome differences were observed according to cytogenetics, FLT3 mutational status, age, or performanc

174 However, among adults with normal cytogenetics, FLT3/ITD was present in 90% of SNP-positiv

175 Here, using cytogenetics, fluorescence in situ hybridization (FISH),

176 by higher-resolution CGH, paternity testing, cytogenetics, fluorescence in situ hybridization, and mi

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

178 n (FISH) is more sensitive than conventional cytogenetics for recognizing chromosomal changes.

179 c information complementing that gained from cytogenetics, gene mutations, and altered gene expressio

180 molecular studies on MGUS and SMM, involving cytogenetics, gene-expression profiling, and microRNA as

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

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

183 gorithm, generated by combining pretreatment cytogenetics/genetics and posttreatment MRD determinatio

184 Patients with high-risk cytogenetics had a shorter PFS and overall survival in t

185 nty-four percent of AML patients with normal cytogenetics had CNA, whereas 40% of patients with an ab

186 Cytogenetics had little influence on the overall outcome

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

188 Molecular markers in combinations with cytogenetics have improved the risk stratification and i

189 increased structural variants by array-based cytogenetics have provided potential objective markers o

190 Increasing age, male sex, high-risk cytogenetics, higher bone marrow blast count, and the ab

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

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

193 In this era of "next-generation cytogenetics" (i.e., an integration of traditional cytog

194 were compared with results from conventional cytogenetics; identification of monosomy 7 populations w

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

196 Diagnostic cytogenetics identifies patients with a higher rate of r

197 Conventional cytogenetics identifies some patients with rearrangement

198 es were not significantly different based on cytogenetics, IgVH mutational status, CD38 expression, o

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

200 New prognostic factors such as interphase cytogenetics, immunoglobulin heavy-chain gene mutational

201 ing CNAs that were not identified by routine cytogenetics in 20 patients (18%).

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

203 ated the relative prognostic significance of cytogenetics in 635 adult acute myeloid leukemia (AML) p

204 expression of HOXA-genes with poor prognosis cytogenetics in acute myeloid leukemia and mixed lineage

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

206 for AML with intermediate-risk and high-risk cytogenetics in first complete remission (CR1), from mat

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

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

209 hain gene rearrangements in six patients and cytogenetics in three patients.

210 aried applications of this resource to tumor cytogenetics, in combination with other molecular cytoge

211 rcome many of the limitations of traditional cytogenetics, including a need for cell culture.

212 mutated (> or = 98%) or high-risk interphase cytogenetics, including either del(17p) or del(11q), app

213 the proportion of patients with unfavorable cytogenetics increased from 35% in those younger than ag

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

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

216 tinctive chromosomes allow an integration of cytogenetics into mutagenesis screens and analyses.

217 Pretreatment cytogenetics is a known predictor of outcome in hematolo

218 Cytogenetics is the primary outcome predictor in acute m

219 17 (76%) were categorized with standard-risk cytogenetics (KRd, n = 147; Rd, n = 170).

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

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

222 ties who were referred to the Leeds Clinical Cytogenetics Laboratory.

223 estricted to patients with intermediate-risk cytogenetics lacking an FLT3/ITD or NPM1 mutation.

224 Bone marrow cytogenetics, marrow blast percentage, and cytopenias re

225 Metaphase cytogenetics (MC) detects an abnormal karyotype in only

226 chromosomal defects undetected by metaphase cytogenetics (MC) in hematologic cancers, offering super

227 ield stems from the application of metaphase cytogenetics (MC), but recently, novel molecular technol

228 Using metaphase cytogenetics (MC), chromosomal abnormalities are found i

229 As compared with conventional cytogenetics methods, digital karyotyping, array compara

230 Discoveries in cytogenetics, molecular biology, and genomics have revea

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

232 Although pretreatment covariates such as cytogenetics, monosomal karyotype, relapsed or refractor

233 p and in the subgroup with intermediate-risk cytogenetics, MRD was an independent prognostic factor.

234 , and the International Working Group on MDS Cytogenetics (n = 44) databases.

235 survival benefit for patients with favorable cytogenetics, no benefit for patients with poor-risk dis

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

237 Whole genome sequencing and cytogenetics of experimentally evolved populations revea

238 Cytogenetics of the malignant cells identified a t(4;14)

239 We examined the prognostic impact of cytogenetics on the outcome of 200 acute lymphoblastic l

240 of Ig V(H) mutational status and interphase cytogenetics on treatment outcome.

241 (<50 years) and patients without unfavorable cytogenetics or aFLT3-ITD mutation.

242 Evaluable cytogenetics or fluorescence in situ hybridization studi

243 -RARA fusion identified by routine metaphase cytogenetics or interphase fluorescence in situ hybridiz

244 ess likely to occur in patients with complex cytogenetics or TP53 mutations.

245 ars; P < .001), more likely with unfavorable cytogenetics (P < .001) and antecedent hematologic disor

246 (P = .029), older age (P = .047), and normal cytogenetics (P < .001).

247 0.0018), male gender (p = 0.019), high risk cytogenetics (p = 0.002), higher IDO-1 mRNA (p = 0.005),

248 rable in patients with favorable and adverse cytogenetics (PFS, P = .014 and P < .001, respectively)

249 riate analysis identified older age, adverse cytogenetics, poor performance status, elevated creatini

250 ping of the amplified region using molecular cytogenetics, positional cloning and genomic sequencing

251 G overexpression in AML patients with normal cytogenetics predicts an adverse clinical outcome and se

252 ased on SNPs may be confounded and molecular cytogenetics remains the only method to genotype these i

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

254 merican, found himself conducting unexpected cytogenetics research in Manzanar, a "relocation center,

255 e example of how research from the fields of cytogenetics, retroviral oncology, protein phosphorylati

256 Cytogenetics revealed a normal female karyotype; molecul

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

258 After adjusting for differences in age and cytogenetics risk, the hazard of mortality among all ant

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

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

261 However, a predefined analysis by cytogenetics showed highly significant interaction with

262 e efficiency and resolution of canine cancer cytogenetics studies by developing a small-scale genomic

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

264 ory disease and normal karyotype or low risk cytogenetics, such as hyperdiploidy.

265 Cytogenetics supported this hypothesis, showing only rar

266 ational Staging System 3 (ISS3), and adverse cytogenetics [t(4;14) and/or del(17p)].

267 both groups, with the exception of favorable cytogenetics [t(8;21), inv(16)/t(16;16), t(15;17)] at di

268 ned from individuals referred for diagnostic cytogenetics testing.

269 t show substantially better concordance with cytogenetics than do two other alignment procedures.

270 s, with prognostic information distinct from cytogenetics that correlated with remission attainment,

271 ML, t-CMML is associated with more high-risk cytogenetics that manifest as poor outcomes.

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

273 -exome sequencing, copy-number profiling and cytogenetics to analyse 84 myeloma samples.

274 FISH was a necessary adjunct to cytogenetics to detect t(4;14) and t(14;16) in metaphase

275 Here we used classical and molecular cytogenetics to test the ploidy level of T. barrerae and

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

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

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

279 its are seen for AML in CR1 with unfavorable cytogenetics using matched unrelated donors (URDs).

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

281 009), and evolution to monosomy 7 or complex cytogenetics was more common in the first quartile (18.8

282 Cytogenetics was the only pretreatment characteristic pr

283 Using cytogenetics, we profiled meiotic DNA double-strand brea

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

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

286 P-gp expression and cytogenetics were correlated, though independent prognos

287 Atypical megakaryocytes and abnormal cytogenetics were more common in GATA2 marrows.

288 Poor-risk cytogenetics were more common in P-gp(+) patients.

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

290 number losses are identified using metaphase cytogenetics, whereas detection of UPD is accomplished b

291 heavy chain gene (V(H)) mutation status and cytogenetics, which were tested in 533 and 579 cases, re

292 sizeable subset of patients with unfavorable cytogenetics who have a particularly poor prognosis.

293 considered for all patients with unfavorable cytogenetics who lack a suitable HLA-matched sibling don

294 s in patients with relapsed MM and high-risk cytogenetics who were undergoing allogeneic T cell-deple

295 FISH, karyotypic aberrations by conventional cytogenetics with novel mitogens identify a subset of ca

296 SNP-A complements traditional metaphase cytogenetics with the unique ability to delineate a prev

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

298 remission rate in patients with unfavorable cytogenetics without MK was 34% versus 18% with MK (P <

299 orkshop (n = 816), the Spanish Hematological Cytogenetics Working Group (n = 849), and the Internatio

300 acute myeloid leukemia (AML) and unfavorable cytogenetics would be evaluated during induction for a p

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