ライフサイエンスコーパス: MDS

1 MDS and acute myeloid leukemia patient samples harboring

2 MDS stem and progenitor cells are characterized by key f

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

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

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

6 (2.9%) developed a hematopoietic neoplasm (4 MDS, 1 AML, 1 MPN, and 2 MDS/MPN) and 3 patients (1.1%)

7 Overall, we identified 57 MDS patients with germline GATA2 mutations.

8 responsiveness of LEN-resistant non-del(5q) MDS cells and AML cells, providing an explanation for th

9 next-generation sequencing in 94 non-del(5q) MDS patients randomized in the GFM-Len-Epo-08 clinical t

10 n of the phenotypic diversity of non-del(5q) MDS remains unclear.

11 ata link Rps14 haploinsufficiency in del(5q) MDS to activation of the innate immune system and induct

12 superior responses of patients with del(5q) MDS to LEN treatment.

13 encoded by a gene (CAST) deleted in del(5q) MDS, correlated with LEN responsiveness in patients with

14 LEN responsiveness in patients with del(5q) MDS.

15 associated myelodysplastic syndrome (del(5q)-MDS), other targets likely exist.

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

17 Our data show that, in contrast to adult MDS, Ras/MAPK pathway mutations are common in pediatric

18 4) treatment in adult patients with advanced MDS or AML.

19 eing explored as therapeutic targets against MDS HSPCs.

20 cognition emerges as a molecular theme among MDS-relevant mutations of pre-mRNA splicing factors.

21 hematopoietic cells lacking Atg7 develop an MDS-like syndrome.

22 tworks that mediate LEN responsiveness in an MDS cell line, MDSL.

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

24 R = 1.49; 95% CI, 1.19-1.88; P = .0005), and MDS (RR = 1.31; 95% CI, 1.09-1.57; P = .003).

25 min walk ES=0.20 (95% CI -0.44 to 0.45) and MDS-UPDRS III ES=-0.30 (95% CI 0.07 to 0.54)) in favour

26 Patients with AML and MDS who had cytogenetic abnormalities associated with un

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

28 ate cancer immunogenicity via TEs in AML and MDS.

29 cerebral organoids derived from control and MDS-induced pluripotent stem cells (iPSCs) using time-la

30 technology, we have knocked out both EVI and MDS/EVI and have shown that EVI and MDS/EVI are not esse

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

32 EVI and MDS/EVI and have shown that EVI and MDS/EVI are not essential for embryogenesis and premetam

33 EVI and MDS/EVI are required for adult intestinal stem cell form

34 alis On the other hand, knocking out EVI and MDS/EVI causes severe retardation in the growth and deve

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

36 er allogeneic HSCT for patients with MDS and MDS/AML.

37 ffective in patients with lower-risk MDS and MDS/MPN.

38 hematopoietic neoplasms (MDS, AML, MPN, and MDS/MPN) was calculated and adjusted for sex, age, and f

39 er Center Support Grant, and the MD Anderson MDS & AML Moon Shots Program.

40 n premalignant hematologic diseases, such as MDS.

41 d significant replication of higher baseline MDS-UPDRS motor score, male sex, and increased age, as w

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

43 There was a weak trend (P = 0.1) between MDS and large drusen; those in the highest category of M

44 (</=4 score), those in the highest category MDS adherence (>6 score) showed lower odds of nvAMD (odd

45 ns do not confer poor prognosis in childhood MDS.

46 gous for either SAMD9L mutation, 3 developed MDS upon loss of the mutated SAMD9L allele following int

47 cin-3, and CD123 have begun to differentiate MDS HSPCs from healthy counterparts.

48 >/=10 x 10(9) platelets per L) and disease (MDS vs AML).

49 rative neoplasms (MPN) overlapping diseases (MDS/MPN).

50 equivalent dose, sex, age, disease duration, MDS-UPDRS III score at the first assessment, duration of

51 e cellular mechanism by which LEN eliminates MDS clones remains elusive.

52 EQoL-MDS was a single-blind, randomised, controlled, phase 2

53 pean Working Group of MDS in Childhood (EWOG-MDS) conducted in Germany over a period of 15 years.

54 al primary MDS patients registered with EWOG-MDS were studied.

55 Finally, MDS mouse model treated with BTNPs showed better restora

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

57 sk and lower risk subjects were compared for MDS-UPDRS part III score (and derivations of this) to id

58 cytes are found, but diagnostic criteria for MDS or other hematologic diseases are not fulfilled, a c

59 ing HLA-matched and -mismatched allo HCT for MDS.

60 hematopoietic stem-cell transplantation for MDS may inform prognostic stratification and the selecti

61 ed on adopting treatment strategies used for MDS and MPN.

62 tion, which could be of prognostic value for MDS/MPN patients.

63 m asymptomatic clonal hematopoiesis to frank MDS, and, ultimately, to secondary AML.

64 ectories (n = 39) in patients suffering from MDS (n = 52) and chronic myelomonocytic leukemia-1 (n =

65 expands and maintains a more activated (G1) MDS HSPC.

66 [SD] age, 72.3 [15.6] years), 55 (64.0%) had MDS, 21 (24.4%) had de novo AML, and 10 (11.6%) had AML

67 ) or placebo (n=47); similar proportions had MDS (50 [51%] patients to eltrombopag, 22 (47%) patients

68 Patients with a very high MDS transplantation risk score, based on combination of

69 lso seen in a stage-specific manner in human MDS samples as well as in murine models of the disease.

70 r, previously shown to be increased in human MDS, were increased in NHD13 mice.

71 ur mouse model applicable for studying human MDS/AML diseases.

72 These novel findings may help to identify MDS patients with a high risk of disease progression who

73 d Parkinson's Disease Rating Scale Part III (MDS-UPDRS III) score at the last assessment as the outco

74 ntribute to the tumor suppressor activity in MDS and AML.

75 equisite steps for induction of apoptosis in MDS cells and in acute myeloid leukemia (AML) cells.

76 Here, we study the BMME in MDS in vivo using a transgenic murine model of MDS with

77 ideal to interrogate the role of the BMME in MDS.

78 ression (as assessed by the annual change in MDS-UPDRS score) into the final models of treatment effe

79 genomic heterogeneity of malignant clones in MDS.

80 imitations of precision-medicine concepts in MDS.

81 ing to guide clinical treatment decisions in MDS.

82 were associated with a more rapid decline in MDS-UPDRS III score.

83 signaling pathways has been demonstrated in MDS HSPCs and is being targeted therapeutically in precl

84 id dysplasia, mimicking dyserythropoiesis in MDS.

85 of H2AX contributes to dyserythropoiesis in MDS.

86 ugh CRBN and IKZF1, has cytotoxic effects in MDS and AML that depend on a calcium- and calpain-depend

87 he alarmin S100A9 that is found in excess in MDS HSPCs and bone marrow plasma.

88 ates with UPDRS part III scores (increase in MDS-UPDRS per doubling of odds 0.52, 95% CI 0.31 to 0.72

89 Also, dyserythropoiesis was increased in MDS patients with the deletion of chromosome 11q23, wher

90 major contributor to cell-free DNA levels in MDS patients as a result of ineffective hematopoiesis.

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

92 The median number of aKIR genes was lower in MDS patients than healthy controls (2 vs 3 genes; P = .0

93 Overall, we identify a role for MSI2 in MDS representing a therapeutic target in this disease.

94 on reflects the phenotype of the mutation in MDS and may be a therapeutic target in MDS.

95 estions about the role of these mutations in MDS development and maintenance remain.

96 mphomyeloid HSC origin of SF3B1 mutations in MDS-RS patients and provide a novel in vivo platform for

97 the unique enrichment of these mutations in MDS.

98 ng System by enumerating blasts from NECs in MDS-E and in the overall MDS population reclassified app

99 y kinase p38 MAPK (which is overactivated in MDS).

100 in (Ub) ligase activity, is overexpressed in MDS hematopoietic stem/progenitor cells (HSPCs).

101 blasts (RAEB)-2 diagnosis is not possible in MDS-E, as patients with 10% to < 20% BM blasts from TNCs

102 y role of the BMME to disease progression in MDS and support a therapeutic strategy whereby manipulat

103 emia and stem cell function, but its role in MDS is unknown.

104 ive molecular disease monitoring strategy in MDS.

105 risk disease and reduced overall survival in MDS and AML patients.

106 nature that correlates with poor survival in MDS patients.

107 expression correlates with poor survival in MDS.

108 on in MDS and may be a therapeutic target in MDS.

109 azacitidine is the mainstay of treatment in MDS, only half of all patients respond.

110 rantly hypermethylated and underexpressed in MDS stroma.

111 Increasing MDS was associated with reduced odds of nvAMD in unadjus

112 a transcriptomic signature similar to known MDS/AML stem-like cell profiles.

113 ic (SALL4B Tg) mouse model with pre-leukemic MDS-like symptoms that transform to AML over time.

114 Compared with the lowest MDS adherence (</=4 score), those in the highest categor

115 ic cells, and we surmised that the malignant MDS genome would be a major contributor to cell-free DNA

116 N), myelodysplastic syndrome (MDS), or mixed MDS/MPN overlap syndrome (including chronic myelomonocyt

117 features of a pediatric unclassifiable mixed MDS/MPN and mimics many clinical manifestations of JMML

118 c-haploinsufficient mice (Apc(del/+) ) model MDS induced by an aberrant BM microenvironment.

119 ia (AML), myeloproliferative neoplasm (MPN), MDS/MPN, or otherwise unexplained cytopenia (for >6 mo).

120 expression profiling of HSPCs from the MSI2 MDS mice identifies a signature that correlates with poo

121 (K700E) myeloid progenitors and SF3B1-mutant MDS patient samples demonstrate aberrant 3' splice-site

122 on into immune-deficient mice, SF3B1 mutated MDS-RS HSCs differentiated into characteristic ring side

123 and therapeutically exploring SF3B1 mutated MDS-RS.

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

125 ound in 10% of patients with myelodysplasia (MDS) and 30% of patients with acute myeloid leukemia (AM

126 myelodysplastic/myeloproliferative neoplasm (MDS/MPN).

127 expected number of hematopoietic neoplasms (MDS, AML, MPN, and MDS/MPN) was calculated and adjusted

128 As previously observed, MDS and AML were the most common malignancies, often of

129 from NECs improves prognostic assessment of MDS.

130 Whether the genetic basis of MDS influences the outcome of allogeneic hematopoietic s

131 ture in CD34(+) cells from advanced cases of MDS, where it associated with adverse prognosis.

132 rge drusen; those in the highest category of MDS had 20% reduced odds compared with those in the lowe

133 D9/SAMD9L mutations represent a new class of MDS predisposition.

134 is sufficient to prevent the development of MDS in Apc(del/+) mice and that altered canonical WNT si

135 of WNT signaling prevents the development of MDS in Apc(del/+) mice.

136 shortened lifespan due to the development of MDS-like disease or myeloid leukaemia.

137 In this study, to investigate the effects of MDS on human progenitor subtypes that control neuronal o

138 nical vignettes showing specific features of MDS and AML in FA patients, this paper summarizes our pr

139 HSPCs) and reverses the clinical features of MDS.

140 f patients with the ring sideroblast form of MDS and a favorable prognosis.

141 B1 in stromal cells from a high frequency of MDS/AML patients, a finding that together with our resul

142 ive studies of the European Working Group of MDS in Childhood (EWOG-MDS) conducted in Germany over a

143 cteristic ring sideroblasts, the hallmark of MDS-RS.

144 ontribute to the phenotypic heterogeneity of MDS.

145 AML, and 10 (11.6%) had AML and a history of MDS.

146 understanding of the molecular landscape of MDS, coupled with the emergence of cost- and time-effect

147 ouse model of MDS results in a rapid loss of MDS haematopoietic stem and progenitor cells (HSPCs) and

148 The majority of MDS patients have either clonal somatic karyotypic abnor

149 itional deletion of Msi2 in a mouse model of MDS results in a rapid loss of MDS haematopoietic stem a

150 S in vivo using a transgenic murine model of MDS with hematopoietic expression of the translocation p

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

152 thought to contribute to the pathogenesis of MDS and AML.

153 mutated genes central to the pathogenesis of MDS, which can be organized into a limited number of cel

154 atenin activation and disease progression of MDS.

155 ry of DAC and ATO for effective treatment of MDS.

156 ual inhibitor applicable to the treatment of MDS/AML.

157 udy, therefore, deepens our understanding of MDS cellular pathogenesis and highlights the broad utili

158 ent advances in our genetic understanding of MDS, with a particular focus on the emerging role for mu

159 re enrolled in the European Working Group on MDS consortium over a period of 15 years.

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

161 We enrolled 84 adult patients with AML or MDS in a single-institution trial of decitabine to ident

162 on for thrombocytopenic patients with AML or MDS who are ineligible for other treatment and who are n

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

164 d with the prognosis of patients with MDS or MDS/MPN, the role of ASXL1 in erythropoiesis remains unc

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

166 ce develop myelodysplastic syndrome (MDS) or MDS and myeloproliferative neoplasms (MPN) overlapping d

167 blasts from NECs in MDS-E and in the overall MDS population reclassified approximately 9% of lower-ri

168 centre, open-label, dose-finding study (PACE-MDS), with long-term extension, eligible patients were a

169 Although pediatric MDS is a very rare diagnosis, occurring in 0.8 to 4 case

170 Our data confirm that adult and pediatric MDS are separate diseases with disparate mechanisms, and

171 PK pathway mutations are common in pediatric MDS (45% of primary cohort), while mutations in RNA spli

172 he somatic and germline changes of pediatric MDS using whole exome sequencing, targeted amplicon sequ

173 own about the genomic landscape of pediatric MDS.

174 on germline defect predisposing to pediatric MDS with a very high prevalence in adolescents with mono

175 cording to karyotype, 108 additional primary MDS patients registered with EWOG-MDS were studied.

176 ed for 15% of advanced and 7% of all primary MDS cases, but were absent in children with MDS secondar

177 MD9 or SAMD9L were present in 17% of primary MDS patients, and these variants were routinely lost in

178 Notably, treatment of primary MDS specimens with this compound stimulated hematopoiesi

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

180 nd/or RNA-sequencing of 46 pediatric primary MDS patients.

181 med in an independent set of sorted, primary MDS-derived mesenchymal cells.

182 therapy-related MDS than those with primary MDS (15% vs. 3%, P<0.001).

183 ine GATA2 mutations in children with primary MDS was 7%, and 15% in those presenting with advanced di

184 ient in vivo on mice xenografted with SKM1-R MDS cell line.

185 +/-63% to +/-10% (tissue to background ratio MDS mean of 1.55, bias -0.05, limits of agreement -0.20

186 were absent in patients with therapy-related MDS or acquired aplastic anemia.

187 e common among patients with therapy-related MDS than those with primary MDS (15% vs. 3%, P<0.001).

188 ons a Hi-C dataset, performs high-resolution MDS separately on each partition, and then reassembles t

189 ssembles the partitions using low-resolution MDS.

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

191 Significantly enriched in high-risk MDS (in comparison to low-risk MDS), TP53, GATA2, KRAS,

192 s or older, with intermediate-2 or high-risk MDS or AML, with bone marrow blasts of 50% or less, and

193 d leukemia (sAML; in comparison to high-risk MDS), FLT3, PTPN11, WT1, IDH1, NPM1, IDH2 and NRAS mutat

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

195 randomly assigned patients with higher-risk MDS and chronic myelomonocytic leukemia (CMML) 1:1:1 to

196 Conclusion Patients with higher-risk MDS treated with azacitidine-based combinations had simi

197 in high-risk MDS (in comparison to low-risk MDS), TP53, GATA2, KRAS, RUNX1, STAG2, ASXL1, ZRSR2 and

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

199 fe and effective in patients with lower-risk MDS and MDS/MPN.

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

201 f 1,698 patients with non-del(5q) lower-risk MDS treated with ESAs.

202 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor subscale (part 3) in the practically de

203 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Part I score and other validated NMS scales a

204 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS) part III, of 208 individuals who had previous

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

206 ty Unified Parkinson's Disease Rating Scale, MDS-UPDRS III), fitness, health and well-being measured.

207 JAY to the popular multidimensional scaling (MDS) approach for visualization of small data sets drawn

208 n approximation of multidimensional scaling (MDS) that partitions a Hi-C dataset, performs high-resol

209 eviously published Mediterranean Diet Score (MDS) was used to classify participants according to thei

210 screened >600 cases of primary or secondary MDS in children and adolescents who were enrolled in the

211 c syndrome (MDS) and 82 cases with secondary MDS enrolled in 2 consecutive prospective studies of the

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

213 ng, including molecular dynamic simulations (MDS).

214 ctable epilepsy, and Miller-Dieker syndrome (MDS) is the most severe form of the disease.

215 cents with primary myelodysplastic syndrome (MDS) and 82 cases with secondary MDS enrolled in 2 conse

216 l hematopoiesis to myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

217 disorders, such as myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

218 young adulthood of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

219 Cs) from malignant myelodysplastic syndrome (MDS) and AML progenitors.

220 athogenesis of the myelodysplastic syndrome (MDS) and are closely associated with clinical phenotype.

221 miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an e

222 re associated with myelodysplastic syndrome (MDS) and cause U12 splicing defects.

223 nts diagnosed with myelodysplastic syndrome (MDS) and monosomy 7 harbor germline mutations in GATA2.

224 mong patients with myelodysplastic syndrome (MDS) and related malignancies.

225 ases of late onset myelodysplastic syndrome (MDS) and/or acute myeloid leukemia (AML), suggesting tha

226 el(5q)) subtype of myelodysplastic syndrome (MDS) has been linked to heterozygous deletion of RPS14,

227 oblasts subtype of myelodysplastic syndrome (MDS) have mutations in Splicing Factor 3B, Subunit 1 (SF

228 causes of familial myelodysplastic syndrome (MDS) have recently been identified.

229 Myelodysplastic syndrome (MDS) is clonal disorder characterized by ineffective hem

230 coded diagnosis of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).

231 (+/-) mice develop myelodysplastic syndrome (MDS) or MDS and myeloproliferative neoplasms (MPN) overl

232 low/intermediate-1 myelodysplastic syndrome (MDS) patients achieve an erythroid response with lenalid

233 stromal cells from myelodysplastic syndrome (MDS) patients and observed widespread aberrant cytosine

234 tic alterations in myelodysplastic syndrome (MDS) patients.

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

236 f individuals with myelodysplastic syndrome (MDS) with deletion of chromosome 5q (del(5q)) to treatme

237 n in patients with myelodysplastic syndrome (MDS) within a randomized trial.

238 ed as diagnosis of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), myeloproliferative n

239 nal hematopoiesis, myelodysplastic syndrome (MDS), and acute myeloid leukemia (AML) and are associate

240 ing diseases, like myelodysplastic syndrome (MDS), develop preferentially in elderly individuals.

241 s with non-del(5q) myelodysplastic syndrome (MDS), lenalidomide promotes erythroid lineage competence

242 ve neoplasm (MPN), myelodysplastic syndrome (MDS), or mixed MDS/MPN overlap syndrome (including chron

243 the development of myelodysplastic syndrome (MDS)-like disease.

244 everal cancers and myelodysplastic syndrome (MDS).

245 asts are < 20%, as myelodysplastic syndrome (MDS).

246 e (aCML) is a rare myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) for which no curr

247 eukemia (JMML) are myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) overlap disorders

248 nts with advanced myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML).

249 gression for both myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML).

250 xpressed in human myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).

251 in patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).

252 ntation (HSCT) in myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML).

253 rom patients with Myelodysplastic syndromes (MDS) and healthy donors.

254 hematopoiesis of myelodysplastic syndromes (MDS) and its impact on response to drug therapy remain p

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

256 Myelodysplastic syndromes (MDS) are a diverse group of bone marrow disorders and cl

257 Myelodysplastic syndromes (MDS) are clonal disorders of haematopoiesis characterise

258 Myelodysplastic syndromes (MDS) are driven by complex genetic and epigenetic altera

259 ted 5q lower-risk myelodysplastic syndromes (MDS) are treated with erythropoiesis-stimulating agents

260 leukemia (AML) or myelodysplastic syndromes (MDS) are unclear.

261 Myelodysplastic syndromes (MDS) are uncommon in children and have a poor prognosis.

262 with higher-risk myelodysplastic syndromes (MDS) but are less well-studied in lower-risk disease.

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

264 genetic basis of myelodysplastic syndromes (MDS) is heterogeneous, and various combinations of somat

265 acute leukemias, myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPNs), non-Hodgkin l

266 s of mutations in myelodysplastic syndromes (MDS), we investigated clonal dynamics using whole-exome

267 of patients with myelodysplastic syndromes (MDS).

268 py in higher-risk myelodysplastic syndromes (MDS).

269 nditions, such as myelodysplastic syndromes (MDS).

270 EEG/fMRI and multivariate dynamical systems (MDS) analysis to characterize network relationships betw

271 gether, these studies have demonstrated that MDS stem cells are functionally critical for the initiat

272 The MDS HSPCs remain dependent on MSI2 expression after dise

273 efect that was rescued when we corrected the MDS causative chromosomal deletion and severe apoptosis

274 apeutic strategy whereby manipulation of the MDS microenvironment may improve hematopoietic function

275 s used to investigate the association of the MDS score and AMD, taking account of potential confounde

276 eeks, off-medication scores on part 3 of the MDS-UPDRS had improved by 1.0 points (95% CI -2.6 to 0.7

277 Although these MDS-relevant mutations alter the splicing of a subset of

278 4.15 times smaller than those caused due to MDS.

279 ological presentation, and predisposition to MDS with -7/del(7q), whereas hematopoietic revertant mos

280 2 families with cytopenia, predisposition to MDS with chromosome 7 aberrations, immunodeficiency, and

281 ECs, 22% of patients with MDS-E and 12% with MDS from the whole series diagnosed within WHO categorie

282 We have used SF3b1 mutations associated with MDS to interrogate the role of the yeast ortholog, Hsh15

283 The association with MDS did not differ by Y204H risk allele (P = 0.89).

284 MDS cases, but were absent in children with MDS secondary to therapy or acquired aplastic anemia.

285 nism, and association of risk estimates with MDS-UPDRS III scores assessed.

286 ))-which commonly occurs in individuals with MDS and AML-in an inducible, hemizygous manner in hemato

287 etically defined subsets of individuals with MDS or AML.

288 ival after allogeneic HSCT for patients with MDS and MDS/AML.

289 ll survival after HSCT in both patients with MDS and patients with MDS/AML (P values ranging from .00

290 only curative treatment of FA patients with MDS or AML.

291 sociated with the prognosis of patients with MDS or MDS/MPN, the role of ASXL1 in erythropoiesis rema

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

293 all survival similar to MAC in patients with MDS or secondary acute myeloid leukemia.

294 fore transplantation from 1514 patients with MDS who were enrolled in the Center for International Bl

295 Among patients with MDS, detection of mutations in SF3B1 define a subgroup o

296 stematically from NECs, 22% of patients with MDS-E and 12% with MDS from the whole series diagnosed w

297 rogenitor cell compartments in patients with MDS-RS.

298 in both patients with MDS and patients with MDS/AML (P values ranging from .003 to .035).

299 In patients with MDS/AML, gene ontology (ie, secondary-type AML carrying

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

301 ng a cumulative observation time of 75 years MDS disease progression.