ライフサイエンスコーパス: myelodysplastic syndrome

1 premalignant state (clonal hematopoiesis or myelodysplastic syndrome).

2 ultiple myeloma, acute myeloid leukemia, and myelodysplastic syndrome).

3 agnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome.

4 agnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome.

5 had acute myelogenous leukemia or high-risk myelodysplastic syndrome.

6 iated with immunodeficiency, lymphedema, and myelodysplastic syndrome.

7 nked to the erythroid lineage in 5q deletion myelodysplastic syndrome.

8 evolution of CH to acute myeloid leukemia or myelodysplastic syndrome.

9 lymphoma, myeloproliferative neoplasms, and myelodysplastic syndrome.

10 leukaemia and 51% (29-68) for patients with myelodysplastic syndrome.

11 e induction in normal blood or patients with myelodysplastic syndrome.

12 erformed at our center for acute leukemia or myelodysplastic syndrome.

13 s confirmed and 11 (46%) of 24 patients with myelodysplastic syndrome.

14 tations in genes known to be associated with myelodysplastic syndrome.

15 bid patients with acute myeloid leukaemia or myelodysplastic syndrome.

16 kaemia and 26 (72%) initially presented with myelodysplastic syndrome.

17 bid patients with acute myeloid leukaemia or myelodysplastic syndrome.

18 ating agents are needed for the treatment of myelodysplastic syndromes.

19 s a therapeutic opportunity for SF3B1-mutant myelodysplastic syndromes.

20 atients with intermediate-risk and high-risk myelodysplastic syndromes.

21 patients with intermediate-risk or high-risk myelodysplastic syndromes.

22 L), T-cell acute lymphoblastic leukemia, and myelodysplastic syndromes.

23 precision-medicine concepts in leukemia and myelodysplastic syndromes.

24 fit patients with acute myeloid leukemia or myelodysplastic syndromes.

25 C in patients with acute myeloid leukemia or myelodysplastic syndromes.

26 ients with intact immune systems, such as in myelodysplastic syndromes.

27 t in patients with anaemia due to lower-risk myelodysplastic syndromes.

28 andard treatment for patients with high-risk myelodysplastic syndromes.

29 s, congenital dyserythropoietic anemias, and myelodysplastic syndromes.

30 utations likely contribute to development of myelodysplastic syndromes.

31 crucial to improve outcomes in patients with myelodysplastic syndromes.

32 ith poor survival in patients suffering from myelodysplastic syndromes.

33 2 (IDH2) occur in around 5% of patients with myelodysplastic syndromes.

34 ted with myeloproliferative neoplasms and/or myelodysplastic syndromes.

35 % of affected individuals progress to AML or myelodysplastic syndromes.

36 kappaB signalling, both relevant targets for myelodysplastic syndromes.

37 h has led to clinical trials in leukemia and myelodysplastic syndromes.

38 itabine bioavailability for the treatment of myelodysplastic syndromes.

39 ral integration site 1 (EVI) and its variant myelodysplastic syndrome 1 (MDS)/EVI encode zinc-finger

40 1.19), chronic myeloid leukemia (1.54), and myelodysplastic syndrome (1.30).

41 rative diseases, 18; Hodgkin disease, 2; and myelodysplastic syndrome, 2).

42 One patient developed myelodysplastic syndrome 28 months after receiving radio

43 g tested in phase 2 studies in patients with myelodysplastic syndrome, acute myeloid leukaemia, and m

44 rome, whereas acquired mutations are seen in myelodysplastic syndrome, acute myeloid leukemia, and in

45 ilty on outcomes for blood cancers including myelodysplastic syndromes, acute leukemia, non-Hodgkin l

46 orted a 0.27% 8-year cumulative incidence of myelodysplastic syndrome/acute myelogenous leukemia.

47 y initiating event, in the transformation to myelodysplastic syndrome/acute myeloid leukemia in patie

48 ve been identified in patients with familial myelodysplastic syndrome/acute myeloid leukemia, monocyt

49 kbone of nonintensive acute myeloid leukemia/myelodysplastic syndrome (AML/MDS) treatment, also by vi

50 en identified in acute myeloid leukaemia and myelodysplastic syndrome among other cancers; however, i

51 The incidence of myelodysplastic syndrome and acute myeloid leukaemia acr

52 e adverse events, we first extracted data on myelodysplastic syndrome and acute myeloid leukaemia cas

53 clinical features of PARP inhibitor-related myelodysplastic syndrome and acute myeloid leukaemia cas

54 hibitors significantly increased the risk of myelodysplastic syndrome and acute myeloid leukaemia com

55 im of this study was to estimate the risk of myelodysplastic syndrome and acute myeloid leukaemia rel

56 harmacovigilance study of VigiBase, cases of myelodysplastic syndrome and acute myeloid leukaemia rel

57 The primary outcome was the summary risk of myelodysplastic syndrome and acute myeloid leukaemia rel

58 PARP inhibitors increased the risk of myelodysplastic syndrome and acute myeloid leukaemia ver

59 nd delayed adverse events including cases of myelodysplastic syndrome and acute myeloid leukaemia, fo

60 n of GATA2 expression has been implicated in myelodysplastic syndrome and acute myeloid leukemia (AML

61 ould be associated with an increased risk of myelodysplastic syndrome and acute myeloid leukemia, col

62 iation of CSNK1A1 mutations in patients with myelodysplastic syndrome and associated myeloid neoplasm

63 l processes associated with SF3B1 mutations (myelodysplastic syndrome and chronic lymphocytic leukemi

64 familial cases of acute myelogenous leukemia/myelodysplastic syndrome and in MonoMac syndrome.

65 Four patients with associated myelodysplastic syndrome and two who had received haemop

66 tidine and decitabine have shown efficacy in myelodysplastic syndromes and acute myeloid leukaemia, b

67 AZA is an approved drug for myelodysplastic syndromes and acute myeloid leukemia, an

68 are the most frequent class of mutations in myelodysplastic syndromes and are also common in clonal

69 s well-tolerated in patients with lower-risk myelodysplastic syndromes and severe thrombocytopenia an

70 rognostic Scoring System intermediate-1-risk myelodysplastic syndromes and severe thrombocytopenia.

71 in improving thrombocytopenia in lower-risk myelodysplastic syndromes and severe thrombocytopenia.

72 e for the treatment of anaemia in lower-risk myelodysplastic syndromes and so could therefore provide

73 tions in genes recurrently mutated in AML or myelodysplastic syndromes and were detectable at very lo

74 proach against 62 acute myeloid leukemia, 50 myelodysplastic syndrome, and 40 blood DNA samples from

75 iciency syndrome involving immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.

76 ies, including myeloproliferative neoplasms, myelodysplastic syndrome, and acute myeloid leukemia.

77 agnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome, and an Eastern Cooperative Onc

78 ed with large granular lymphocytic leukemic, myelodysplastic syndrome, and aplastic anemia.

79 dysplastic syndrome, modify surveillance for myelodysplastic syndrome, and possibly guide therapies,

80 d leukemia, acute lymphoblastic leukemia, or myelodysplastic syndrome, and their HLA-matched unrelate

81 in pathologies, including beta-thalassemia, myelodysplastic syndrome, and viral infection.

82 thropoiesis that resembles early-stage human myelodysplastic syndrome, and we sought to identify onco

83 ncies, such as myeloproliferative neoplasms, myelodysplastic syndromes, and acute myeloid leukemia, r

84 Myelodysplastic syndromes are characterised by ineffecti

85 To reveal the functional impact of myelodysplastic syndromes-associated mutations in SRSF2,

86 iting toxicities were noted in patients with myelodysplastic syndrome at 125 mg/m(2) daily x 5, thus

87 mission (blast counts <5% in bone marrow) or myelodysplastic syndrome (blast counts <20% in bone marr

88 ction of RNA-binding proteins contributes to myelodysplastic syndromes, cancer, and neuropathologies.

89 loid leukemia, chronic myeloid leukemia, and myelodysplastic syndrome cases, suggesting recognition o

90 atment of Refractory or Relapsed Leukemia or Myelodysplastic Syndrome) clinical trial (NCT02212561).

91 but increased acute myeloid leukemia and/or myelodysplastic syndrome death rates (RR = 1.62; 95% CI:

92 ery-low-risk, low-risk, or intermediate-risk myelodysplastic syndromes (defined according to the Revi

93 iple myeloma (MM) and 5q deletion associated myelodysplastic syndrome (del(5q)-MDS), other targets li

94 cute myeloid leukemia and 1 patient with the myelodysplastic syndrome developing into acute myeloid l

95 as indication for the HSCT in 4 patients and myelodysplastic syndrome development in 1.

96 as done if available to confirm leukaemia or myelodysplastic syndrome diagnosis.

97 With the exception of selected patients with myelodysplastic syndromes, ESAs should not be offered to

98 Clinical Trial Group, and the International Myelodysplastic Syndromes Foundation developed recommend

99 ho underwent first HCT for acute leukemia or myelodysplastic syndrome from 2008 through 2012 were ana

100 atment of anaemia associated with lower-risk myelodysplastic syndromes; further studies are ongoing.

101 ents (grade 3 mental status changes, grade 4 myelodysplastic syndrome, grade 3 lung infection, and tw

102 id leukaemia and six of the 19 patients with myelodysplastic syndrome had a clinical response to trea

103 17 patients with myelodysplastic syndromes harbouring an IDH2 mutation (m

104 b monotherapy in a subgroup of patients with myelodysplastic syndromes harbouring mutations in IDH2 f

105 y acute myeloid leukemia (sAML) arising from myelodysplastic syndromes have a poor prognosis marked b

106 n recipients with acute myeloid leukemia and myelodysplastic syndrome (hazard ratio [HR], 0.09; 95% c

107 d or refractory acute myeloid leukaemia, and myelodysplastic syndromes; here we report the phase 2 re

108 r-engrafted CH, with 1 case progressing into myelodysplastic syndrome in both donor and recipient.

109 s were transient bone-marrow suppression and myelodysplastic syndrome in six patients who had not bee

110 s with available longitudinal data developed myelodysplastic syndrome in the setting of stable blood

111 ing use of CSFs in acute myeloid leukemia or myelodysplastic syndromes in adults.

112 group analysis of patients with IDH2-mutated myelodysplastic syndromes in the phase 1 dose-escalation

113 Patients with anemia and lower-risk myelodysplastic syndromes in whom erythropoiesis-stimula

114 Prior treatment of myelodysplastic syndrome, including hypomethylating agen

115 nduce responses in patients with mutant IDH2 myelodysplastic syndromes, including in those who have h

116 Testing for IDH2 mutations in myelodysplastic syndromes is essential for identifying p

117 The standard of care for myelodysplastic syndromes is hypomethylating agents such

118 ood cytopenias and myeloid neoplasms-such as myelodysplastic syndrome-is an area of active research,

119 r presenting for initial consultation at the myelodysplastic syndrome/leukemia, myeloma, or lymphoma

120 Myelodysplastic syndromes may also present with the morp

121 ed 426 children and adolescents with primary myelodysplastic syndrome (MDS) and 82 cases with seconda

122 tive hematopoiesis and often predisposing to myelodysplastic syndrome (MDS) and acute myelogenous leu

123 ntinuum ranging from clonal hematopoiesis to myelodysplastic syndrome (MDS) and acute myeloid leukemi

124 velopment of some myeloid disorders, such as myelodysplastic syndrome (MDS) and acute myeloid leukemi

125 ergence in their teens or young adulthood of myelodysplastic syndrome (MDS) and acute myeloid leukemi

126 ntified in most cancers but are prevalent in Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemi

127 sociated with an increased risk of secondary myelodysplastic syndrome (MDS) and acute myeloid leukemi

128 The initiation and evolution of myelodysplastic syndrome (MDS) and acute myeloid leukemi

129 and progenitor cells (HSPCs) from malignant myelodysplastic syndrome (MDS) and AML progenitors.

130 etic mutations drive the pathogenesis of the myelodysplastic syndrome (MDS) and are closely associate

131 to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here w

132 ZRSR2 mutations are associated with myelodysplastic syndrome (MDS) and cause U12 splicing de

133 Despite evidence of chronic inflammation in myelodysplastic syndrome (MDS) and cell-intrinsic dysreg

134 as many as 72% of adolescents diagnosed with myelodysplastic syndrome (MDS) and monosomy 7 harbor ger

135 regulated below haploinsufficient amounts in myelodysplastic syndrome (MDS) and myeloproliferative ne

136 A splicing factors recur among patients with myelodysplastic syndrome (MDS) and related malignancies.

137 n families with multiple cases of late onset myelodysplastic syndrome (MDS) and/or acute myeloid leuk

138 ry anemia with ring sideroblasts (RARS) is a myelodysplastic syndrome (MDS) characterized by isolated

139 ohort of 86 acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) families with 49 harborin

140 cute myeloid leukemia (AML) development from myelodysplastic syndrome (MDS) has advanced significantl

141 esis in the deletion 5q (del(5q)) subtype of myelodysplastic syndrome (MDS) has been linked to hetero

142 ory anemia with ring sideroblasts subtype of myelodysplastic syndrome (MDS) have mutations in Splicin

143 Several monogenic causes of familial myelodysplastic syndrome (MDS) have recently been identi

144 Myelodysplastic syndrome (MDS) is characterized by bone

145 Myelodysplastic syndrome (MDS) is clonal disorder charac

146 Risk of developing myelodysplastic syndrome (MDS) is significantly increase

147 atients had a concomitant coded diagnosis of myelodysplastic syndrome (MDS) or acute myeloid leukemia

148 associated with predisposition to leukemia, myelodysplastic syndrome (MDS) or dyserythropoietic anem

149 ly, we reported that Asxl1(+/-) mice develop myelodysplastic syndrome (MDS) or MDS and myeloprolifera

150 5q) transfusion-dependent low/intermediate-1 myelodysplastic syndrome (MDS) patients achieve an eryth

151 is of bone marrow-derived stromal cells from myelodysplastic syndrome (MDS) patients and observed wid

152 the role of the two miR-15/16 clusters in 93 myelodysplastic syndrome (MDS) patients divided in three

153 most common class of genetic alterations in myelodysplastic syndrome (MDS) patients.

154 Similarly, high-risk cases of myelodysplastic syndrome (MDS) showed far greater suppre

155 pite the recent evidence of the existence of myelodysplastic syndrome (MDS) stem cells in 5q-MDS pati

156 Myelodysplastic syndrome (MDS) typically presents in old

157 Myelodysplastic syndrome (MDS) was most common, followed

158 nase 1 alpha (CK1alpha) occur in a subset of myelodysplastic syndrome (MDS) with del(5q) karyotype.

159 the high response rates of individuals with myelodysplastic syndrome (MDS) with deletion of chromoso

160 allogeneic transplantation in patients with myelodysplastic syndrome (MDS) within a randomized trial

161 Myelodysplastic syndrome (MDS), a hematopoietic stem cel

162 PHD was defined as diagnosis of myelodysplastic syndrome (MDS), acute myeloid leukemia (

163 ently in patients with clonal hematopoiesis, myelodysplastic syndrome (MDS), and acute myeloid leukem

164 fferentiation, resembling the human disorder myelodysplastic syndrome (MDS), and we demonstrate incre

165 ntially curative treatment for patients with myelodysplastic syndrome (MDS), but long-term survival i

166 Many underlying diseases, like myelodysplastic syndrome (MDS), develop preferentially i

167 In a subset of patients with non-del(5q) myelodysplastic syndrome (MDS), lenalidomide promotes er

168 ring as a myeloproliferative neoplasm (MPN), myelodysplastic syndrome (MDS), or mixed MDS/MPN overlap

169 ons of TET2 are frequently observed in human myelodysplastic syndrome (MDS), which is a clonal malign

170 Rip1 kinase (Ripk1)-mediated necroptosis in myelodysplastic syndrome (MDS)-like disease in mice and

171 of Asxl2 in mice leads to the development of myelodysplastic syndrome (MDS)-like disease.

172 ions of key splicing factors associated with myelodysplastic syndrome (MDS).

173 dine and decitabine are standard of care for myelodysplastic syndrome (MDS).

174 r in patients with vs without a diagnosis of myelodysplastic syndrome (MDS).

175 ctor U2AF35 are found in several cancers and myelodysplastic syndrome (MDS).

176 roleukemia, and when BM blasts are < 20%, as myelodysplastic syndrome (MDS).

177 wnregulation was associated with a subset of myelodysplastic syndrome (MDS).

178 leukaemia, acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS).

179 (LTL) on survival outcomes in patients with myelodysplastic syndrome (MDS).

180 leukemia, BCR-ABL1 negative (aCML) is a rare myelodysplastic syndrome (MDS)/myeloproliferative neopla

181 juvenile myelomonocytic leukemia (JMML) are myelodysplastic syndrome (MDS)/myeloproliferative neopla

182 Chronic inflammation has been implicated in myelodysplastic syndrome (MDS); however, its role in dis

183 hronic myeloid leukemia (CML, n = 1079); and myelodysplastic syndrome (MDS, n = 1197).

184 ening complication in patients with advanced myelodysplastic syndromes (MDS) and acute myeloid leukae

185 ve indicator of disease progression for both myelodysplastic syndromes (MDS) and acute myeloid leukae

186 Spliceosome mutations are common in myelodysplastic syndromes (MDS) and acute myeloid leukae

187 SALL4 is aberrantly expressed in human myelodysplastic syndromes (MDS) and acute myeloid leukem

188 l genes) are commonly found in patients with myelodysplastic syndromes (MDS) and acute myeloid leukem

189 Myelodysplastic syndromes (MDS) and acute myeloid leukem

190 Myelodysplastic syndromes (MDS) and acute myeloid leukem

191 opoietic stem cell transplantation (HSCT) in myelodysplastic syndromes (MDS) and chronic myelomonocyt

192 plasma of patients with various subtypes of myelodysplastic syndromes (MDS) and healthy donors.

193 progenitor cells (HSPCs) from patients with Myelodysplastic syndromes (MDS) and healthy donors.

194 of malignant clones in the hematopoiesis of myelodysplastic syndromes (MDS) and its impact on respon

195 iew the current understanding of genomics in myelodysplastic syndromes (MDS) and leukemias and the li

196 liceosomal protein, is frequently mutated in myelodysplastic syndromes (MDS) and many cancers.

197 key determinants of outcome in patients with myelodysplastic syndromes (MDS) and secondary AML (sAML)

198 Myelodysplastic syndromes (MDS) are a diverse group of b

199 Myelodysplastic syndromes (MDS) are a group of neoplasms

200 Myelodysplastic syndromes (MDS) are a heterogeneous grou

201 Myelodysplastic syndromes (MDS) are characterized by ine

202 Myelodysplastic syndromes (MDS) are clonal diseases defi

203 Myelodysplastic syndromes (MDS) are clonal disorders of

204 Myelodysplastic syndromes (MDS) are driven by complex ge

205 Myelodysplastic syndromes (MDS) are haematopoietic malig

206 emic patients with non-deleted 5q lower-risk myelodysplastic syndromes (MDS) are treated with erythro

207 atients with acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS) are unclear.

208 Myelodysplastic syndromes (MDS) are uncommon in children

209 Myelodysplastic syndromes (MDS) arise in older adults th

210 myelodysplasia as they aged, culminating in myelodysplastic syndromes (MDS) at 24 months of age, wit

211 mprove survival in patients with higher-risk myelodysplastic syndromes (MDS) but are less well-studie

212 The heterogeneous nature of myelodysplastic syndromes (MDS) demands a complex and pe

213 including chronic myeloid leukemia (CML) and myelodysplastic syndromes (MDS) either sensitive or resi

214 Myelodysplastic syndromes (MDS) frequently progress to a

215 Comprehensive preclinical studies of Myelodysplastic Syndromes (MDS) have been elusive due to

216 The genetic basis of myelodysplastic syndromes (MDS) is heterogeneous, and va

217 coring System intermediate-1/2- or high-risk myelodysplastic syndromes (MDS) or chronic myelomonocyti

218 The myelodysplastic syndromes (MDS) represent a group of clo

219 he most common structural genomic variant in myelodysplastic syndromes (MDS)(1).

220 Myeloid neoplasms, including myelodysplastic syndromes (MDS), are genetically heterog

221 e the most common mutations in patients with myelodysplastic syndromes (MDS), but their role in MDS p

222 subclasses of patients with acute leukemias, myelodysplastic syndromes (MDS), myeloproliferative neop

223 In patients with myelodysplastic syndromes (MDS), TP53 mutations are asso

224 elucidate differential roles of mutations in myelodysplastic syndromes (MDS), we investigated clonal

225 nt of all subtypes of the myeloid malignancy myelodysplastic syndromes (MDS).

226 premalignant hematologic conditions, such as myelodysplastic syndromes (MDS).

227 ctable in approximately 50% of patients with myelodysplastic syndromes (MDS).

228 standard, first-line therapy in higher-risk myelodysplastic syndromes (MDS).

229 n S34F-encoding mutation among patients with myelodysplastic syndromes (MDS).

230 were identified as key pathogenic drivers of myelodysplastic syndromes (MDS).

231 ine DDX41 mutations are involved in familial myelodysplastic syndromes (MDSs) and acute myeloid leuke

232 he U2 snRNP component SF3B1 are prominent in myelodysplastic syndromes (MDSs) and other cancers and h

233 Anemia of lower-risk myelodysplastic syndromes (MDSs) and primary myelofibros

234 Myelodysplastic syndromes (MDSs) are a group of hematopo

235 Myelodysplastic syndromes (MDSs) are hematopoietic stem

236 The diagnosis and monitoring of myelodysplastic syndromes (MDSs) are highly reliant on b

237 Myelodysplastic syndromes (MDSs) are stem cell disorders

238 Recent studies have demonstrated that myelodysplastic syndromes (MDSs) arise from a small popu

239 The heterogeneity of myelodysplastic syndromes (MDSs) has made evaluating pat

240 frequent class of mutations in patients with myelodysplastic syndromes (MDSs) in particular.

241 Despite genetic heterogeneity, myelodysplastic syndromes (MDSs) share features of cytol

242 tion of hematopoiesis and is dysregulated in myelodysplastic syndromes (MDSs), contributing to ineffe

243 marrow microenvironment (BMME) is altered in myelodysplastic syndromes (MDSs).

244 conditions could allow earlier diagnosis of myelodysplastic syndrome, modify surveillance for myelod

245 excess risk of acute myeloid leukemia and/or myelodysplastic syndrome mortality in radiologists who g

246 owever, 2 patients with -7 and 7q- developed myelodysplastic syndrome, most likely due to haploinsuff

247 lasms (MPN), these patients can present with myelodysplastic syndrome/MPN, as well as de novo or seco

248 heterodimer was unaffected by cancer-linked myelodysplastic syndrome mutants.

249 In this clinical trial, patients with myelodysplastic syndrome (n=25) received reduced decitab

250 In VigiBase, 178 cases of myelodysplastic syndrome (n=99) and acute myeloid leukae

251 the chemotherapy group (infection [n=1] and myelodysplastic syndrome [n=1]) compared with nine (3%)

252 (infection [n=1], febrile neutropenia [n=1], myelodysplastic syndrome [n=1], secondary malignancy [n=

253 py; the control group included patients with myelodysplastic syndromes not targeted by this warning.

254 ult patients with acute myeloid leukemia and myelodysplastic syndrome on induction therapy or allogen

255 nical features and outcomes of patients with myelodysplastic syndrome or acute myeloid leukaemia and

256 patients with Shwachman-Diamond syndrome and myelodysplastic syndrome or acute myeloid leukaemia owin

257 of Shwachman-Diamond syndrome who developed myelodysplastic syndrome or acute myeloid leukaemia were

258 patients with Shwachman-Diamond syndrome and myelodysplastic syndrome or acute myeloid leukaemia.

259 ble safety profile in patients with advanced myelodysplastic syndrome or acute myeloid leukaemia.

260 cludes true residual or early recurrent AML, myelodysplastic syndrome or CH that is ancestral to the

261 hemotherapy; secondary AML (progressed after myelodysplastic syndrome or chronic myelomonocytic leuka

262 -cell arteritis) or a hematologic condition (myelodysplastic syndrome or multiple myeloma) or both.

263 cute myeloid leukaemia arising from previous myelodysplastic syndrome or myeloproliferative neoplasm,

264 ) with previously treated or newly diagnosed myelodysplastic syndromes or chronic myelomonocytic leuk

265 nrolled patients aged 18 years or older with myelodysplastic syndromes or chronic myelomonocytic leuk

266 ng System-defined low or intermediate 1 risk myelodysplastic syndromes or non-proliferative chronic m

267 ed patients 18 years or older with high-risk myelodysplastic syndromes or oligoblastic acute myeloid

268 Selinexor showed responses in patients with myelodysplastic syndromes or oligoblastic acute myeloid

269 y and activity of selinexor in patients with myelodysplastic syndromes or oligoblastic acute myeloid

270 ications such as severe bone marrow failure, myelodysplastic syndrome, or acute myeloid leukemia.

271 osis and disease evolution to myelofibrosis, myelodysplastic syndrome, or acute myeloid leukemia.

272 had a haematological malignancy (leukaemia, myelodysplastic syndrome, or lymphoma), were between 16

273 leukaemia, chronic myelomonocytic leukaemia, myelodysplastic syndrome, or myelofibrosis who were refr

274 te-1-risk, intermediate-2-risk, or high-risk myelodysplastic syndromes, or chronic myelomonocytic leu

275 ative findings in acute myeloid leukemia and myelodysplastic syndrome patient samples, these data sug

276 um of how to appropriately define and follow myelodysplastic syndrome precursor states, such as clona

277 18 (69%) of 26 patients with myelodysplastic syndrome received upfront therapy (14 ha

278 G in patients with acute myeloid leukemia or myelodysplastic syndrome receiving myeloablative conditi

279 overall survival of patients with high-risk myelodysplastic syndromes refractory to hypomethylating

280 yelodysplastic CMML is largely inspired from myelodysplastic syndromes, relying on erythropoiesis-sti

281 In patients with newly diagnosed higher-risk myelodysplastic syndromes, self-reported fatigue severit

282 nital neutropenia (SCN) evolves to secondary myelodysplastic syndrome (sMDS) and/or secondary acute m

283 with acute myeloid leukemia (AML)/high-risk myelodysplastic syndromes, that is, idarubicine-cytarabi

284 In myelodysplastic syndromes, thrombocytopenia is associate

285 .6%) with marrow failure and 11 (24.4%) with myelodysplastic syndrome underwent HCT using matched unr

286 ), median overall survival for patients with myelodysplastic syndrome was 7.7 years (95% CI 0.8-not r

287 the maximum tolerated dose in patients with myelodysplastic syndrome was 90 mg/m(2) daily x 5.

288 2222 patients with acute myeloid leukemia or myelodysplastic syndrome were analyzed.

289 Patients with myelodysplastic syndromes were aged 18 years or older wi

290 21, 2013, and Feb 12, 2015, 58 patients with myelodysplastic syndromes were enrolled in the 12 week b

291 ight of ten with leukaemia and 25 of 26 with myelodysplastic syndrome) were known to have Shwachman-D

292 secutive patients with acute leukemia or the myelodysplastic syndrome who received a first myeloablat

293 18 to 65 years of age with acute leukemia or myelodysplastic syndrome who underwent myeloablative HLA

294 rug in phase 3 clinical trials for high-risk myelodysplastic syndrome whose molecular target had rema

295 Cdx2-transgenic mice develop myelodysplastic syndrome with progression to acute leuke

296 ) in older patients (>=60 years) with AML or myelodysplastic syndrome with refractory anemia with exc

297 ene SF3B1 are found in >80% of patients with myelodysplastic syndrome with ring sideroblasts (MDS-RS)

298 g best supportive care only in patients with myelodysplastic syndromes with excess blasts after failu

299 verity of anemia in patients with lower-risk myelodysplastic syndromes with ring sideroblasts who had

300 dine (decitabine) are commonly used to treat myelodysplastic syndromes, with or without a myeloprolif