ライフサイエンスコーパス: MDS

1 MDS also shares diagnostic borders with other diseases.

2 MDS and secondary AML cells harbor mutations in many of

3 MDS are characterized by anemia and transfusion requirem

4 MDS arises from hematopoietic stem cells (HSCs); therefo

5 MDS patients have recurrent bacterial infections and abn

6 MDS patients with shorter telomere length, who have infe

7 MDS spectra were correlative with altered states in the

8 MDS-T and MDS-AML patients show a reduction of the expre

9 MDS-UPDRS Part I total mean (SD) scores increased from b

10 and its variant myelodysplastic syndrome 1 (MDS)/EVI encode zinc-finger proteins that have been reco

11 retransplant recipient blood samples in 1514 MDS patients and evaluated the association of telomere l

12 Here, analyzing 1809 MDS patients, we infer clonal architecture by using a st

13 poietic neoplasm (4 MDS, 1 AML, 1 MPN, and 2 MDS/MPN) and 3 patients (1.1%) developed BM failure char

14 (2.9%) developed a hematopoietic neoplasm (4 MDS, 1 AML, 1 MPN, and 2 MDS/MPN) and 3 patients (1.1%)

15 n of abnormal myeloid progenitors in del(5q) MDS, and in rare cases drive the progression of other tu

16 reatment of choice for patients with del(5q) MDS, but half of the responding patients become resistan

17 cal chronic myeloid leukemia (aCML; n = 71), MDS/MPN with ring sideroblasts and thrombocytosis (MDS/M

18 showed that in most cases (69 of 86 [80%]), MDS-PA either persisted or remained absent in patients w

19 Here we report a MDS patient-derived xenotransplantation model in cytokin

20 Accumulating MDS gene products, including alternative oxidases (AOXs)

21 X41 mutations are relatively common in adult MDS/AML, often without known family history, arguing for

22 In contrast to adult MDS, little is known about the genomic landscape of pedi

23 In the context of population aging, MDS incidence is set to increase substantially, with exp

24 In a new study by Muto et al., MDS stem cells sparked with TRAF6-activated innate immun

25 d faithful disease representation across all MDS subtypes.

26 ce of MDS-associated phenotypic alterations (MDS-PA) in the bone marrow of 285 patients with MM enrol

27 ients with MDS before transforming into AML (MDS-T), and patients with AML evolving from MDS (MDS-AML

28 intriguing clinical activity of HMAs in AML/MDS patients with chromosome 7 deletions and other monos

29 monstrates clinical activity in relapsed AML/MDS without reversing biologic features of T-cell exhaus

30 eloid leukemia/myelodysplastic syndrome (AML/MDS) treatment, also by virtue of their activity in pati

31 Splenic uptake was higher in the AML/MDS group than in the lymphoma group (P <= 0.05) or the

32 genes and clonal architecture differed among MDS/MPN subtypes.

33 teractions between these subsystems using an MDS in the space of the BOLD signal.

34 d thrombocytosis (MDS/MPN-RS-T; n = 71), and MDS/MPN unclassifiable (MDS/MPN-U; n = 106).

35 as a mechanism for immune escape in AML and MDS.

36 ide signaling, using hematopoietic cells and MDS samples.

37 m the effectiveness of combining the EIS and MDS.

38 el, we show here that high levels of EVI and MDS/EVI are expressed in the intestine at the climax of

39 contrast to the established role of EVI and MDS/EVI in cancer development, their potential function

40 er 50 years was the biggest risk factor, and MDS/AML usually manifested with marrow hypoplasia and mo

41 Each miRNA can significantly predict MDS and MDS-T groups.

42 ntly worse scores in UPSIT, UMSARS, MoCA and MDS-UPDRS III than HC, while Het GBA displayed worse out

43 human CD117 mAb, AMG 191, deplete normal and MDS HSCs in vivo in xenograft mouse models.

44 ith distinct subclones within pre-MDS-SC and MDS-SC contributing to generation of MDS blasts or progr

45 ng is implicated in inflammatory synergy and MDS progression.

46 MDS-T and MDS-AML patients show a reduction of the expression of m

47 had a significant improvement in DT-TUG and MDS-UPDRS-III for up to 3 months.

48 et GBA displayed worse outcomes in UPSIT and MDS-UPDRS III compared with HC.

49 n premalignant hematologic diseases, such as MDS.

50 d with female sex (p=0.008), higher baseline MDS-UPDRS Part II scores (p<0.001) and more severe motor

51 At baseline, MDS patients showing a positive response after iron chel

52 a personal history of cytopenia years before MDS/AML diagnosis.

53 l describe the diagnostic boundaries between MDS, MDS/MPNs, sAML, clonal hematopoiesis of indetermina

54 The boundary between MDS and secondary acute myeloid leukemia (sAML) is arbit

55 in cell biology and maturation exist between MDS and AML secondary to MDS, these 2 diseases are genet

56 hermore, the host driver nodes identified by MDS are distributed throughout the pathways enabling eff

57 In one-half of the cases, MDS/AML patients showed a recurrent peripheral blood pat

58 enias, but not with bone marrow blast count, MDS treatment history, or history of prior cancer therap

59 High-risk DDX41 MDS/AML patients treated with intensive chemotherapy (n

60 ad an impact on the outcome of the different MDS/MPN subtypes, which may be relevant for clinical dec

61 >/=10 x 10(9) platelets per L) and disease (MDS vs AML).

62 features of the bone marrow failure disorder MDS.

63 diagnosis, 33 (11.6%) of 285 cases displayed MDS-PA.

64 binations that were associated with distinct MDS/MPN subtypes and that were mutually exclusive with m

65 In practice, measures that distinguish MDS from related disorders may be difficult to quantify

66 ole of diverse stem cell compartments during MDS progression to AML and have implications for current

67 potential as novel therapeutics to eradicate MDS HSCs and augment the curative effect of allogeneic H

68 In familial MDS/AML, mutations change the coding sequence of a gene

69 ions in single genes that instigate familial MDS/AML.

70 ic advances in our understanding of familial MDS/AML syndromes caused by germline mutations of hemato

71 as a possible disease-specific biomarker for MDS, and, mechanistically, as a driver of cardiovascular

72 artment and interrogated dominant clones for MDS-initiating cells.

73 cells exposed only to FeCl(3) and cells from MDS patients refractory to Deferasirox showed a specific

74 to clinical samples serially collected from MDS patients treated with decitabine, the method again d

75 Here, we analyzed RNA sequencing data from MDS patients and confirmed that SF3B1 mutants use aberra

76 erity of bradykinesia sub-score derived from MDS-UPDRS part III (r = -0.42; P = 0.02).

77 (MDS-T), and patients with AML evolving from MDS (MDS-AML).

78 We found that monocytes from MDS patients, irrespective of CD56 expression, have redu

79 , in both CD56(+) and CD56(-) monocytes from MDS patients, several abnormalities that may be related

80 analyze the nonhost sequences obtained from MDS.

81 clones can precede clinical progression from MDS by many months, suggesting that MDS with excess blas

82 Dendritic cells derived in vitro from MDS monocytes failed to develop dendritic projections an

83 ic disorder is rare, as a group, the genetic MDS disorders account for a significant subset of MDS in

84 e-matched mutation carriers who did not have MDS/AML.

85 like pseudokinase (MLKL) activation in human MDS samples.

86 For example, aplastic anemia and hypoplastic MDS can be difficult to distinguish in patients with pan

87 isorder Society - Unified PD Rating Scale-I (MDS-UPDRS-I) underwent open-label nabilone titration (0.

88 role of aberrant innate immune activation in MDS provides a new perspective for therapeutic developme

89 cused precision oncology approaches, both in MDS and possibly other cancers that evolve from premalig

90 overall response against malignant cells in MDS, and the current omission of immune status monitorin

91 imitations of precision-medicine concepts in MDS.

92 m cell subclones that were not detectable in MDS blasts became dominant upon AML progression.

93 ) change from predose to 30 min post-dose in MDS-UPDRS part 3 score at week 12 was -11.1 (SE 1.46, 95

94 ts the complexity of immune dysregulation in MDS pathophysiology and the fine balance between smolder

95 bset of S34F-dysregulated splicing events in MDS patients.

96 sistent with the absence of ice formation in MDS.

97 suggest that GLI1 activation is frequent in MDS during disease progression and inhibition of GLI1 is

98 erences in the frequency of mutated genes in MDS and secondary AML indicate that the order of mutatio

99 he engraftment of normal donor human HSCs in MDS xenograft mouse models, restoring normal human hemat

100 ic state have not been fully investigated in MDS or any other cancer type.

101 he dominant alternatively spliced isoform in MDS and AML and is characterized by a longer isoform tha

102 MML, ASXL1-SETBP1 in aCML, and SF3B1-JAK2 in MDS/MPN-RS-T).

103 view of the current therapeutic landscape in MDS focusing on recent advances in clinical and translat

104 first time, aberrantly expressed lncRNAs in MDS and further prioritize biologically relevant lncRNAs

105 ected by acquisition of somatic mutations in MDS.

106 and we demonstrate increased necroptosis in MDS bone marrow.

107 vative therapeutic targeting of the niche in MDS.

108 f research and long-awaited opportunities in MDS research.

109 l for diagnostic and prognostic precision in MDS as well as in future correlative studies of treatmen

110 predisposition is increasingly recognized in MDS presenting at older ages as well.

111 d predict iron chelation therapy response in MDS.

112 ion of Toll-like receptor (TLR) signaling in MDS hematopoietic stem and progenitor cells (HSPCs), the

113 ation of chronic innate immune signalling in MDS and AML.

114 d is associated with oncogenic signalling in MDS and AML.

115 ive molecular disease monitoring strategy in MDS.

116 ical predictions of response to treatment in MDS.

117 a3 axis, possibly associating with increased MDS risk.

118 In response to inflammation, MDS HSPCs switched from canonical to noncanonical NF-kap

119 CT), often fail to ablate disease-initiating MDS HSCs, and thus have low curative potential and high

120 We investigated MDS patients' bone marrow CD56(+)/CD56(-) monocytes and

121 ividual patients, we differentiated isogenic MDS induced pluripotent stem cells harboring up to 4 suc

122 n was greater splenic uptake in the leukemia/MDS group than in the lymphoma or multiple myeloma group

123 T), and patients with AML evolving from MDS (MDS-AML).

124 cribe the diagnostic boundaries between MDS, MDS/MPNs, sAML, clonal hematopoiesis of indeterminate po

125 The mean MDS-UPDRS III score for the more affected side decreased

126 MISTRG MDS patient-derived xenografts (PDX) reproduce patients'

127 MISTRG MDS-PDX demonstrate the cytotoxic and differentiation po

128 MISTRG MDS-PDX replicate the original sample's genetic complexi

129 The MISTRG MDS-PDX model opens novel avenues of research and long-a

130 ith worse outcome at 6 years in UPSIT, MoCA, MDS-UPDRS III and BDI.

131 Importantly, the presence of monocytic MDS-PA at diagnosis anticipated greater risk of hematolo

132 gated the clinical significance of monocytic MDS-PA in a larger series of 1252 patients enrolled in 4

133 le pathway for the treatment of SF3B1-mutant MDS.

134 ude that the microenvironment of TP53 mutant MDS and sAML has an immune-privileged, evasive phenotype

135 e myeloid leukemia (AML) and myelodysplasia (MDS) but are associated with a high risk of disease rela

136 e myeloid leukemia (AML) and myelodysplasia (MDS) remain limited, and novel treatment strategies are

137 ked to many diseases such as myelodysplasia (MDS) and cancer.

138 yelodysplastic/myeloproliferative neoplasms (MDS/MPNs).

139 Noteworthy, MDS-associated mutations infrequently emerged after high

140 tly mutated gene is SF3B1, mutated in 17% of MDS patients.

141 have been elusive due to limited ability of MDS stem cells to engraft current immunodeficient murine

142 determinant for the competitive advantage of MDS HSPCs and for disease progression.

143 responsible for the competitive advantage of MDS HSPCs in an inflammatory milieu over normal HSPCs re

144 echanistic basis for the clonal dominance of MDS HSPCs and indicate that interfering with noncanonica

145 Dynamics of MDS-PA at diagnosis and after autologous transplant were

146 (HSCs); therefore, successful elimination of MDS HSCs is an important part of any curative therapy.

147 -SC and MDS-SC contributing to generation of MDS blasts or progression to AML, respectively.

148 Using a murine model of MDS we demonstrated that constitutive Hh/Gli1 activation

149 oid disease in a NUP98-HOXD13 mouse model of MDS, confirming its role in disease progression.

150 diagnosis, classification, and monitoring of MDS to secondary AML progression.

151 Here, we compare the performance of MDS and three ML algorithms (ANN, random forest [RF], an

152 ndicate that PCA improved the performance of MDS compared to traditional inputs.

153 ghts into the specific clinical phenotype of MDS.

154 to prospectively screen for the presence of MDS-associated phenotypic alterations (MDS-PA) in the bo

155 oth miR-15/16 clusters in the progression of MDS into AML and in AML pathogenesis.

156 As progression of MDS to AML in humans provides a biological system to det

157 We show that episomal reprogramming of MDS patient samples generates induced pluripotent stem c

158 The cell-intrinsic response of MDS HSPCs, which involves signaling through the noncanon

159 Bulk and single-cell-targeted sequencing of MDS recurrently mutated genes in CD34+ progenitors (and

160 Altogether, our series of MDS/AML families offer novel insights into the etiology

161 ich can be of use in the clinical setting of MDS/MPN.

162 s of misfolded proteins in the two stages of MDS that are most affected by oxidative stress: low-risk

163 cientific insights gleaned from the study of MDS predisposition syndromes.

164 review, we outline advances in the study of MDS to secondary AML progression, with a focus on the ge

165 isorders account for a significant subset of MDS in children and young adults.

166 61% and 39%, respectively, and two-thirds of MDS/AML patients died of pulmonary fibrosis and/or hepat

167 antibody agents not only in the treatment of MDS but also for the multitude of other HSC-driven blood

168 trioxide (ATO) have demonstrated synergy on MDS treatment, but the treatment can cause significant s

169 e, 59 years) with high-risk AML (n = 164) or MDS (n = 80) were randomly assigned 1:1 to a fludarabine

170 relapsed after allo-SCT for AML (n = 24) or MDS (n = 5) were treated with sequential AZA (75 mg/m(2)

171 in adults transplanted for high-risk AML or MDS regardless of pretransplant MRD status.

172 e findings reveal a novel role of EVI and/or MDS/EVI in regulating the formation and/or proliferation

173 ults with low- or intermediate 1-risk MDS or MDS/myeloproliferative neoplasm (MPN), including chronic

174 les that mimicked the ones observed in other MDS/MPN subtypes and that had an impact on the outcome o

175 oiesis and eradicating aggressive pathologic MDS cells.

176 own about the genomic landscape of pediatric MDS.

177 functionally defined pre-MDS stem cells (pre-MDS-SC), had a significantly higher subclonal complexity

178 ophenotypically and functionally defined pre-MDS stem cells (pre-MDS-SC), had a significantly higher

179 volution, with distinct subclones within pre-MDS-SC and MDS-SC contributing to generation of MDS blas

180 Each miRNA can significantly predict MDS and MDS-T groups.

181 ncanonical NF-kappaB signaling could prevent MDS progression.

182 relatively narrow cancer spectrum, primarily MDS and AML.

183 t methylation and DNMTi treatment of primary MDS stroma enhanced its ability to support erythroid dif

184 IL17RA, PRF1 and SEC23B), reported in prior MDS/AML or inherited bone marrow failure series (DNAH9,

185 with automated corneal nerve quantification, MDS-UPDRS III, Hoehn and Yahr scale, Montreal Cognitive

186 ed a significant worsening in UMSARS, RBDsq, MDS-UPDRS III and BDI scores at the 6-year follow-up com

187 Adults with low- or intermediate 1-risk MDS or MDS/myeloproliferative neoplasm (MPN), including

188 passing preleukemia, low-risk MDS, high-risk MDS, and secondary AML.

189 on of disease [acute leukemia or higher risk MDS] vs absence of hematological improvement) as well as

190 se stages encompassing preleukemia, low-risk MDS, high-risk MDS, and secondary AML.

191 hort of patients with non-del(5q) lower-risk MDS treated with ESAs, none of the most commonly used se

192 I1, of Hedgehog (Hh) signaling, in poor-risk MDS/AML.

193 ve applied a marginal distribution sampling (MDS) algorithm, a standard gap-filling method for other

194 ty-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor score (i.e., part III) for the more aff

195 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS) part 3 (motor) score at week 12, analysed on

196 ty-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) parts II and III.

197 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS).

198 ty-Unified Parkinson's Disease Rating Scale (MDS-UPDRS-III), and electrophysiological evaluation of c

199 nalysis (PCA) and multi-dimensional scaling (MDS) to compare network activity profiles of conolidine/

200 ed by means of the multidimensional scaling (MDS) clustering and visualization algorithm.

201 We used inverse multidimensional scaling (MDS) to measure the extent to which arrangements of obje

202 nt Analysis (PCA), Multidimensional Scaling (MDS), and t-distributed Stochastic Neighbor Embedding (t

203 % of PNH patients go on to develop secondary MDS/AML by 10 years of follow-up.

204 ost-AA and post-PNH progression to secondary MDS/AML and provide practical guidance for approaching p

205 ors associated with progression to secondary MDS/AML include longer duration of disease, increased te

206 ly unbiased metagenomic RNA deep sequencing (MDS) to identify pathogens causing conjunctivitis.

207 emonstrates that the minimum dominating set (MDS) method better accounts for how the biological infor

208 odysplastic syndrome with ring sideroblasts (MDS-RS).

209 Molecular dynamic simulation (MDS) analysis predicts that ATM-3507 integrates into the

210 ry (CNT) and molecular dynamics simulations (MDS), we show that a network of closely spaced pores is

211 age, 2.1 +/- 0.6; Movement Disorder Society [MDS]-revised Unified Parkinson Disease Rating Scale [UPD

212 show that Microwave Dielectric Spectroscopy (MDS) can be used to determine the hydration state of the

213 ssion of mitochondrial dysfunction stimulon (MDS) genes regulated by ANAC013 and ANAC017.

214 inson's Disease Rating Scale motor subscale (MDS-UPDRS III) and Beck Depression Inventory (BDI).

215 en predisposing to myelodysplastic syndrome (MDS) and acute myelogenous leukemia.

216 n and evolution of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are driven by geno

217 t are prevalent in Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), and the most comm

218 risk of secondary myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

219 ic inflammation in myelodysplastic syndrome (MDS) and cell-intrinsic dysregulation of Toll-like recep

220 ficient amounts in myelodysplastic syndrome (MDS) and myeloproliferative neoplasm (MPN).

221 leukemia (AML) and myelodysplastic syndrome (MDS) families with 49 harboring germline variants in 16

222 ) development from myelodysplastic syndrome (MDS) has advanced significantly as a result of next-gene

223 Myelodysplastic syndrome (MDS) is characterized by bone marrow failure and a stron

224 Risk of developing myelodysplastic syndrome (MDS) is significantly increased in both multiple myeloma

225 /16 clusters in 93 myelodysplastic syndrome (MDS) patients divided in three subgroups: patients with

226 high-risk cases of myelodysplastic syndrome (MDS) showed far greater suppression of TEs than low-risk

227 Myelodysplastic syndrome (MDS) typically presents in older adults with the acquisi

228 Myelodysplastic syndrome (MDS) was most common, followed by acute myeloid leukemia

229 cur in a subset of myelodysplastic syndrome (MDS) with del(5q) karyotype.

230 the human disorder myelodysplastic syndrome (MDS), and we demonstrate increased necroptosis in MDS bo

231 for patients with myelodysplastic syndrome (MDS), but long-term survival is limited by the risk of t

232 ted necroptosis in myelodysplastic syndrome (MDS)-like disease in mice and detect increased RIPK1 exp

233 eukaemia (AML) and myelodysplastic syndrome (MDS).

234 s in patients with myelodysplastic syndrome (MDS).

235 rs associated with myelodysplastic syndrome (MDS).

236 andard of care for myelodysplastic syndrome (MDS).

237 out a diagnosis of myelodysplastic syndrome (MDS).

238 been implicated in myelodysplastic syndrome (MDS); however, its role in disease progression is unclea

239 ons are common in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but the oncogeni

240 Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are diseases of ab

241 rious subtypes of myelodysplastic syndromes (MDS) and healthy donors.

242 ng of genomics in myelodysplastic syndromes (MDS) and leukemias and the limitations of precision-medi

243 uently mutated in myelodysplastic syndromes (MDS) and many cancers.

244 in patients with myelodysplastic syndromes (MDS) and secondary AML (sAML).

245 Myelodysplastic syndromes (MDS) are a heterogeneous group of hematopoietic stem cel

246 Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis and

247 Myelodysplastic syndromes (MDS) are clonal diseases defined by clinical, morphologi

248 Myelodysplastic syndromes (MDS) are haematopoietic malignancies that are characteri

249 Myelodysplastic syndromes (MDS) arise in older adults through stepwise acquisitions

250 geneous nature of myelodysplastic syndromes (MDS) demands a complex and personalized variety of thera

251 eukemia (CML) and myelodysplastic syndromes (MDS) either sensitive or resistant to their respective t

252 Myelodysplastic syndromes (MDS) frequently progress to acute myeloid leukemia (AML)

253 inical studies of Myelodysplastic Syndromes (MDS) have been elusive due to limited ability of MDS ste

254 1/2- or high-risk myelodysplastic syndromes (MDS) or chronic myelomonocytic leukemia (CMML) were rand

255 The myelodysplastic syndromes (MDS) represent a group of clonal disorders that result i

256 enomic variant in myelodysplastic syndromes (MDS)(1).

257 plasms, including myelodysplastic syndromes (MDS), are genetically heterogeneous disorders driven by

258 In patients with myelodysplastic syndromes (MDS), TP53 mutations are associated with high-risk disea

259 ong patients with myelodysplastic syndromes (MDS).

260 ogenic drivers of myelodysplastic syndromes (MDS).

261 yeloid malignancy myelodysplastic syndromes (MDS).

262 nditions, such as myelodysplastic syndromes (MDS).

263 (OT) acts in the mesolimbic dopamine system (MDS) to mediate the rewarding properties of social inter

264 ion from MDS by many months, suggesting that MDS with excess blasts could be viewed as an overlap bet

265 populations revealed that stem cells at the MDS stage, including immunophenotypically and functional

266 and neural activity within structures of the MDS in both males and females, and that this dose-respon

267 component of MS and the construction of the MDS prodromal probability score.

268 ary efficacy criterion was the change of the MDS-UPDRS-I between randomization and week 4.

269 At week 4, mean change of the MDS-UPDRS-I was 2.63 (95% confidence interval [CI] 1.53

270 chelation therapy can be effective in these MDS cases, but the molecular consequences of this treatm

271 N with ring sideroblasts and thrombocytosis (MDS/MPN-RS-T; n = 71), and MDS/MPN unclassifiable (MDS/M

272 e expression of miR-15a/-15b/-16 compared to MDS patients.

273 topoietic stem cell niche proves critical to MDS stem cell propagation and function in vivo.

274 es associated with genetic predisposition to MDS, discusses implications for clinical evaluation and

275 ation exist between MDS and AML secondary to MDS, these 2 diseases are genetically related.

276 yltransferase inhibitor widely used to treat MDS and AML, yet the impact of AZA on the cell-surface p

277 t in patients with TP53-mutant and wild-type MDS or sAML.

278 N-RS-T; n = 71), and MDS/MPN unclassifiable (MDS/MPN-U; n = 106).

279 yeloproliferative neoplasms, unclassifiable (MDS/MPN-U) are a group of rare and heterogeneous myeloid

280 the complex molecular mechanisms underlying MDS.

281 on of age-related somatic mutations, whereas MDS presenting in children and younger adults is more fr

282 ting germline DDX41 mutations in adults with MDS and AML.

283 aracterized cohort including 367 adults with MDS/MPN subtypes, including chronic myelomonocytic leuke

284 l hematopoiesis in 13 (50%) of 26 cases with MDS-PA vs 9 (22%) of 41 without MDS-PA; TET2 and NRAS we

285 ated the association of telomere length with MDS disease characteristics and transplantation outcomes

286 e used to improve outcomes for patients with MDS and secondary AML.

287 subgroups: patients with MDS, patients with MDS before transforming into AML (MDS-T), and patients w

288 We analyzed 3,324 patients with MDS for TP53 mutations and allelic imbalances and deline

289 n an unselected cohort of 1385 patients with MDS or AML.

290 busulfan-based RIC with MAC in patients with MDS or secondary acute myeloid leukemia.

291 ons in longitudinal samples of patients with MDS who progressed to AML.

292 ts divided in three subgroups: patients with MDS, patients with MDS before transforming into AML (MDS

293 For the majority of patients with MDS, treatment strategies are nonintensive and risk-adap

294 Based on MFC profiling, patients with MDS-PA have altered hematopoiesis and T regulatory cell

295 s in well-defined subgroups of patients with MDS.

296 Patients with MDS/MPN-U were the most heterogeneous and displayed diff

297 (grade 1-3), there was no relationship with MDS (P trend = 0.9).

298 6 cases with MDS-PA vs 9 (22%) of 41 without MDS-PA; TET2 and NRAS were the most frequently mutated g

299 remained absent in patients with or without MDS-PA at diagnosis, respectively.

300 hether adult short telomere patients without MDS/AML also had evidence of clonal hematopoiesis of ind