ライフサイエンスコーパス: cytogenetic

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

2 mmendations, established through bone marrow cytogenetics.

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

4 the poor prognosis associated with high-risk cytogenetics.

5 s known prognostic factors including adverse cytogenetics.

6 particularly in those with intermediate-risk cytogenetics.

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

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

9 have dismal outcomes, independent of age and cytogenetics.

10 ternational Prognostic Scoring System (IPSS) cytogenetics.

11 Two thirds of patients had complex MN cytogenetics.

12 59 years of age and/or those with high-risk cytogenetics.

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

14 ernational Staging System score, and adverse cytogenetics.

15 or the effects of other covariates including cytogenetics.

16 onal heterogeneity in AML based on metaphase cytogenetics.

17 ticularly evident in patients with high-risk cytogenetics.

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

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

20 Cytogenetics 2.7 M Microarrays/CytoScan HD arrays allowe

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

22 Cytogenetic aberrations detected by interphase fluoresce

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

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

25 se burden at diagnosis, CD38 expression, and cytogenetic aberrations of prognostic significance.

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

27 pression in AML patient samples with various cytogenetic aberrations, confirm that KLF4 overexpressio

28 ave witnessed major advances in defining the cytogenetic aberrations, mutational landscape, epigeneti

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

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

31 All enrolled participants had high-risk cytogenetic abnormalities (deletion 17p, TP53 mutation,

32 2 years, relapse occurred in 2 patients, and cytogenetic abnormalities (including monosomy 7) were ob

33 e analyzed data on 113 patients with FA with cytogenetic abnormalities (n = 54), MDS (n = 45), or acu

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

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

36 C clone probably contributes to the frequent cytogenetic abnormalities and poor responses to chemothe

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

38 Patients of all ages with very-bad-risk cytogenetic abnormalities and/or FLT3-ITD (internal tand

39 t duration of response to therapy or adverse cytogenetic abnormalities are associated with a poor out

40 Certain cytogenetic abnormalities are known to adversely impact

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

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

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

44 The acquisition of the cytogenetic abnormalities hyperdiploidy or translocation

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

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

47 peractivation, centrosome amplification, and cytogenetic abnormalities in the bone marrow (BM).

48 onresponders and 2 responders, developed new cytogenetic abnormalities on eltrombopag, including 5 wi

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

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

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

52 transplantation is critically determined by cytogenetic abnormalities, as previously defined by Inte

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

54 The other cytogenetic abnormalities, including complex and monosom

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

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

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

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

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

60 the high proportion of patients with adverse cytogenetic abnormalities.

61 lecular basis, characterized by nonrecurrent cytogenetic abnormalities.

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

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

64 f chromosome 5q (del[5q]) is the most common cytogenetic abnormality in MDS.

65 e loss of chromosome 7q (del(7q)), a somatic cytogenetic abnormality present in myelodysplastic syndr

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

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

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

69 effect of 12 recurrently mutated genes and 4 cytogenetic alterations on gene expression, diagnostic c

70 s of X-rays and examined the copy number and cytogenetic alterations.

71 ncreasing melanoma size demonstrates greater cytogenetic alterations.

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

73 or inv[16]/t[16;16]) represents a favorable cytogenetic AML subgroup, 30% to 40% of these patients r

74 (AML) is the largest and most heterogeneous cytogenetic AML subgroup.

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

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

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

78 risk stratification involving molecular and cytogenetic analyses.

79 By applying comparative cytogenetic analysis and whole-chloroplast phylogenetics

80 Our cytogenetic analysis identified 16 polymorphic inversion

81 By integrating mutational and cytogenetic analysis in 1274 CLL samples and using both

82 Cytogenetic analysis of mouse embryonic fibroblasts and

83 Cytogenetic analysis revealed the presence of the Philad

84 Pollen typing, segregation and cytogenetic analysis showed decreased numbers of crossov

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

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

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

88 Added contributions of cytogenetic and gene sequencing investigations were dete

89 Here, we used molecular, cytogenetic and genomic approaches to analyse rRNA gene

90 Cytogenetic and molecular characteristics are becoming m

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

92 review the clinical significance of various cytogenetic and molecular features of the disease, and w

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

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

95 This analysis explores the impact of early cytogenetic and molecular responses on the outcomes of p

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

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

98 We used genomic, cytogenetic and transcriptional analysis, coupled with n

99 tween the roles of each of the 3 drugs, both cytogenetic and transcriptional findings are similar to

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

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

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

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

104 Molecular cytogenetics and next-generation sequencing were used to

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

106 % of this cohort, and associated with normal cytogenetics and unmutated IGHV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 ital anomalies after exclusion of genetic or cytogenetic anomalies was not significantly different be

125 No cytogenetic anomalies were found in the infiltrate excep

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

127 highlighting the limitations of conventional cytogenetic approaches.

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

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

130 Cytogenetic array and mutational analysis of the parenta

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

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

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

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

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

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

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

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

139 ecially apparent in patients with favourable cytogenetic characteristics (20.7%; OR 0.47, 0.31-0.73;

140 Patients with adverse cytogenetic characteristics did not benefit (2.2%; OR 0.

141 The molecular cytogenetic characteristics of sSMC delineated the karyo

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

143 on a cohort of patients enriched with these cytogenetic characteristics.

144 urvival benefit for patients without adverse cytogenetic characteristics.

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

146 risk of relapse (p = 0.03) independently of cytogenetic classification in multivariate analysis.

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

148 eatures of human OS; namely, histopathology, cytogenetic complexity, and metastatic potential.

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

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

151 n conclusion, the integration of genomic and cytogenetic data defines 2 subgroups with distinct respo

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

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

154 Marrow cytogenetics data were reviewed.

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

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

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

158 High-risk cytogenetics did not impact outcomes.

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

160 To account for the morphologic and cytogenetic diversity of these neoplasms, a well-annotat

161 Clonal cytogenetic evolution with additional chromosomal abnorm

162 tients includes regular BM morphological and cytogenetic examinations.

163 rediction based on conventional clinical and cytogenetic factors alone.

164 red the BM flow cytometric, morphologic, and cytogenetic features of 28 GATA2 patients with those of

165 not merely by association with other adverse cytogenetic features.

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

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

168 corresponding to methylation clusters and/or cytogenetic groups.

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

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

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

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

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

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

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

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

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

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

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

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

181 17 (76%) were categorized with standard-risk cytogenetics (KRd, n = 147; Rd, n = 170).

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

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

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

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

186 titive regions of the genome, produced using cytogenetic mapping to mitotic and polytene chromosomes,

187 deleterious effects, inferring physical and cytogenetic mapping, reporting related HapMap data, find

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

189 They were found as robust cytogenetic markers for karyotyping of meadow fescue and

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

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

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

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

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

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

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

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

198 A often antedated clinical disease, periodic cytogenetic monitoring is recommended.

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

200 sponded; no patients who achieved a complete cytogenetic (n = 13) or molecular (n = 8) remission lost

201 Herein, we present a system called Next-Gen Cytogenetic Nomenclature, which is concordant with the I

202 dant with the International System for Human Cytogenetic Nomenclature.

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

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

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

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

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

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

209 (<50 years) and patients without unfavorable cytogenetics or aFLT3-ITD mutation.

210 0.0018), male gender (p = 0.019), high risk cytogenetics (p = 0.002), higher IDO-1 mRNA (p = 0.005),

211 s that challenge the current concepts of the cytogenetic pathogenesis of uveal melanoma and demonstra

212 men, is active and well tolerated in adverse cytogenetic patients with early RRMM, particularly in th

213 Chromosome 5M(g) -specific SNPs and cytogenetic probe-based resources were developed and val

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

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

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

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

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

219 metastasis on the basis of individual tumor cytogenetic profile.

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

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

222 among study patients with intermediate-risk cytogenetic profiles.

223 , 2, and 4) into the well established Dohner cytogenetic prognostic model, we showed these, which col

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

225 0.1% to 1% IS, which corresponds to complete cytogenetic remission (8-year OS, 92% v 83%; P = .047).

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

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

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

229 racterization has largely been restricted to cytogenetic resolution.

230 e, dasatinib or nilotinib) achieved complete cytogenetic response (58 [87%] of 67 for imatinib 400 mg

231 Patients in complete cytogenetic response (CCyR) with detectable BCR-ABL1 aft

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

233 arting imatinib had higher rates of complete cytogenetic response and major molecular response at 12

234 We analysed long-term molecular and cytogenetic response and survival outcomes for four TKI

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

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

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

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

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

240 ble; the estimated rate of a sustained major cytogenetic response of at least 12 months was 91%.

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

242 to determine whether achievement of complete cytogenetic response or major molecular response had sim

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

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

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

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

247 iduals of all ages with a report of complete cytogenetic response to treatment or deeper within 1 yea

248 Median time to complete cytogenetic response was 3 vs 6 months with dasatinib vs

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

250 Molecular and cytogenetic responses at 3 and 6 months were highly pred

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

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

253 The main matching criteria were AML type, cytogenetic risk group, patient age, and time in first C

254 ciated with inferior survival across age and cytogenetic risk groups (adverse risk cytogenetics: 1-ye

255 vs 21%; P < .001) at 5 years, independent of cytogenetic risk groups and known molecular risk factors

256 Cytogenetic risk groups were predictive of outcome postr

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

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

259 Patients with intermediate cytogenetic risk profiles had similar findings.

260 , 1.25; 95% CI, 1.06 to 1.28), comprehensive cytogenetic risk score of poor or very poor (HR, 1.43; 9

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

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

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

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

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

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

267 ng to International Staging System stage and cytogenetic risk.

268 study, we assessed the impact of the IPSS-R cytogenetic score (C-IPSS-R) on the outcome of 367 MDS p

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

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

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

272 Cytogenetic studies demonstrated that MDSCs in patients

273 We recently initiated molecular cytogenetic studies of second-trimester human fetal ovar

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

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

276 4 mutations per patient varied according to cytogenetic subgroup, age, and history of previous hemat

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

278 Multiple cytogenetic subgroups have been described in adult Phila

279 Careful analysis of cytogenetic subgroups in trials comparing different trea

280 erized by under-representation of the common cytogenetic subgroups of childhood ALL and overrepresent

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

282 Correlation with cytogenetic subgroups showed that mutations were most fr

283 tion frequency of TP53, its association with cytogenetic subgroups, and its impact on survival in a l

284 8%, P = .02) but similar for all arms across cytogenetic subgroups, as was remission duration and ove

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

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

287 netics" (i.e., an integration of traditional cytogenetic techniques and next-generation sequencing),

288 ied by fluorescence in situ hybridization or cytogenetic testing, thus refining the spectrum of disor

289 ned from individuals referred for diagnostic cytogenetics testing.

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

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

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

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

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

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

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

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

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