ライフサイエンスコーパス: cytogenetics

1 more powerful model for prognostication than cytogenetics.

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

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

4 er outcomes more reliably than serial marrow cytogenetics.

5 iated with worse patient outcome and adverse cytogenetics.

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

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

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

9 patients with normal/noninformative routine cytogenetics.

10 between age, morphology, immunophenotype, or cytogenetics.

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

12 , 2 with isolated del(5q) and 3 with complex cytogenetics.

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

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

15 5% WT1(mut) patients harbored favorable risk cytogenetics.

16 e of particular use in patients with adverse cytogenetics.

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

18 ent prognostication can be enhanced by tumor cytogenetics.

19 differ in the presence or absence of adverse cytogenetics.

20 was 33% and correlated strongly with adverse cytogenetics.

21 atients with either favorable or unfavorable cytogenetics.

22 all survival varied significantly by age and cytogenetics.

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

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

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

26 effective, even in patients with unfavorable cytogenetics.

27 ficantly, better for patients with favorable cytogenetics.

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

29 mmendations, established through bone marrow cytogenetics.

30 characterization of AML patients with normal cytogenetics.

31 dict outcome in patients with AML and normal cytogenetics.

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

33 5) chromosomal translocation by conventional cytogenetics.

34 an important risk factor in AML with normal cytogenetics.

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

36 the poor prognosis associated with high-risk cytogenetics.

37 s known prognostic factors including adverse cytogenetics.

38 particularly in those with intermediate-risk cytogenetics.

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

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

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

42 have dismal outcomes, independent of age and cytogenetics.

43 ternational Prognostic Scoring System (IPSS) cytogenetics.

44 Two thirds of patients had complex MN cytogenetics.

45 59 years of age and/or those with high-risk cytogenetics.

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

47 ernational Staging System score, and adverse cytogenetics.

48 or the effects of other covariates including cytogenetics.

49 onal heterogeneity in AML based on metaphase cytogenetics.

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

51 well as patients with favorable and adverse cytogenetics.

52 ticularly evident in patients with high-risk cytogenetics.

53 ovo AML when adjusted for disease status and cytogenetics.

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

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

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

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

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

59 Cytogenetics 2.7 M Microarrays/CytoScan HD arrays allowe

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

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

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

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

64 rall survival (OS) than patients with normal cytogenetics (9.9 months vs 15.4 months; P =.006).

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

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

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

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

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

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

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

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

73 1mut) in 303 patients with intermediate-risk cytogenetics AML treated with intensive chemotherapy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 conversion to tumorigenicity using molecular cytogenetics and microarray technology.

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

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

93 Molecular cytogenetics and next-generation sequencing were used to

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

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

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

97 Both cytogenetics and RT-PCR detect most such patients, altho

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

99 RT-PCR should not replace cytogenetics and should not be used as the only diagnost

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

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

102 Using cytogenetics and the percentage of marrow blasts after t

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

104 % of this cohort, and associated with normal cytogenetics and unmutated IGHV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 rcentage of marrow erythroid cells, abnormal cytogenetics, and high levels of serum lactate dehydroge

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

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

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

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

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

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

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

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

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

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

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

133 letions are more complex than anticipated by cytogenetics, as revealed at the molecular level by our

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 Normal cytogenetics (CN) constitutes the single largest group,

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

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

151 Marrow cytogenetics data were reviewed.

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

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

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

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

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

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

158 High-risk cytogenetics did not impact outcomes.

159 Nonprioritized cytogenetics distinguished t(8;21) and inv(16)/t(16;16)

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

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

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

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

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

165 ts with high-risk features including adverse cytogenetics, failure to achieve remission with the firs

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

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

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

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

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

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

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

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

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

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

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

177 Cytogenetics had little influence on the overall outcome

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

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

180 marrow blast counts assessed by morphology, cytogenetics, hematologic parameters, and International

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

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

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

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

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

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

187 Diagnostic cytogenetics identifies patients with a higher rate of r

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

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

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

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

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

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

194 These data suggest that interphase cytogenetics in CLL may be predictive of a response to r

195 strated complete concordance between LOH and cytogenetics in detecting residual disease in 15 samples

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

197 GCT origin was confirmed by molecular cytogenetics in five patients.

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

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

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

201 etic strategies (linkage, association and/or cytogenetics) in the identification of candidate genes f

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

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

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

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

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

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

208 for favorable, intermediate, and unfavorable cytogenetics is 88% (95% CI, 59% to 97%), 48% (95% CI, 2

209 Pretreatment cytogenetics is a known predictor of outcome in hematolo

210 ertained independently of complex karyotype, cytogenetics is among the most useful factors predicting

211 Cytogenetics is the primary outcome predictor in acute m

212 17 (76%) were categorized with standard-risk cytogenetics (KRd, n = 147; Rd, n = 170).

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

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

215 ed the diagnostic repertoire of the clinical cytogenetics laboratory.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 Marrow cytogenetics, obtained in three of six cases at diagnosi

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

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

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

234 (<50 years) and patients without unfavorable cytogenetics or aFLT3-ITD mutation.

235 Evaluable cytogenetics or fluorescence in situ hybridization studi

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

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

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

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

240 0.0018), male gender (p = 0.019), high risk cytogenetics (p = 0.002), higher IDO-1 mRNA (p = 0.005),

241 ic Scoring System score (P =.009), poor-risk cytogenetics (P =.03), and treatment-related etiology (P

242 differ significantly from those with normal cytogenetics (P =.36).

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

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

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

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

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

248 However, no correlation was observed with cytogenetics, remission attainment, or overall survival

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

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

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

252 Cytogenetics revealed a normal female karyotype; molecul

253 cell count at diagnosis, B or T lineage, or cytogenetics revealed no differences in genotype frequen

254 6.5-12.5), similar to that of "unfavorable" cytogenetics risk groups (8.3 months; 95% CI, 6.8-9.5.)

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

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

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

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

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

260 Interphase cytogenetics studies demonstrated abnormal clonal FISH s

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

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

263 Cytogenetics supported this hypothesis, showing only rar

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

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

266 ned from individuals referred for diagnostic cytogenetics testing.

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

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

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

270 ospective studies in PCNHL should define the cytogenetics, the basis for cutaneous tropism, the progn

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

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

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

274 analyses confirmed the major contribution of cytogenetics to the probability of attaining CR, CIR, an

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

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

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

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

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

280 Cytogenetics was the only pretreatment characteristic pr

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

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

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

284 Day-100 cytogenetics were evaluated in surviving patients who en

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

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

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

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

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

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

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

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

293 emia, in 86 de novo AML patients with normal cytogenetics who were uniformly treated on Cancer and Le

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

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

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

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

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

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

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