ライフサイエンスコーパス: myelodysplastic

1 we show that elevation of angiopoietin-1 in myelodysplastic CD34(+) stem-like cells is associated wi

2 f poor prognostic factors, the management of myelodysplastic CMML is largely inspired from myelodyspl

3 elopmental aberrations, progressive BMF with myelodysplastic features, and increased susceptibility t

4 atients with progressive BMF associated with myelodysplastic features, immunodeficiency affecting B c

5 emia (JMML) is an aggressive pediatric mixed myelodysplastic/myeloproliferative neoplasm (MDS/MPN).

6 Chronic myelomonocytic leukemia (CMML) is a myelodysplastic/myeloproliferative neoplasm with variabl

7 with non-small cell lung cancer (NSCLC) and myelodysplastic/myeloproliferative neoplasms (MDS/MPN),

8 rs have been formally described, such as the myelodysplastic/myeloproliferative neoplasms (MDS/MPNs).

9 More than 90% of patients with myelodysplastic/myeloproliferative neoplasms (MDSs/MPNs)

10 Further, as a subtype of the myelodysplastic/myeloproliferative neoplasms, CMML has a

11 typical chronic myeloid leukemia (aCML), and myelodysplastic/myeloproliferative neoplasms, unclassifi

12 classified as an overlap myeloproliferative/myelodysplastic neoplasm by the World Health Organizatio

13 1.19), chronic myeloid leukemia (1.54), and myelodysplastic syndrome (1.30).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Myelodysplastic syndrome (MDS) is characterized by bone

42 Myelodysplastic syndrome (MDS) is clonal disorder charac

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

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

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

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

47 5q) transfusion-dependent low/intermediate-1 myelodysplastic syndrome (MDS) patients achieve an eryth

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

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

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

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

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

53 Myelodysplastic syndrome (MDS) typically presents in old

54 Myelodysplastic syndrome (MDS) was most common, followed

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 One patient developed myelodysplastic syndrome 28 months after receiving radio

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

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

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

87 The incidence of myelodysplastic syndrome and acute myeloid leukaemia acr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 18 (69%) of 26 patients with myelodysplastic syndrome received upfront therapy (14 ha

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

126 .6%) with marrow failure and 11 (24.4%) with myelodysplastic syndrome underwent HCT using matched unr

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

128 2222 patients with acute myeloid leukemia or myelodysplastic syndrome were analyzed.

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

130 18 to 65 years of age with acute leukemia or myelodysplastic syndrome who underwent myeloablative HLA

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

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

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

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

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

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

137 premalignant state (clonal hematopoiesis or myelodysplastic syndrome).

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

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

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

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

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

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

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

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

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

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

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

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

150 Prior treatment of myelodysplastic syndrome, including hypomethylating agen

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

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

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

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

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

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

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

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

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

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

161 iated with immunodeficiency, lymphedema, and myelodysplastic syndrome.

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

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

164 lymphoma, myeloproliferative neoplasms, and myelodysplastic syndrome.

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

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

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

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

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

170 bid patients with acute myeloid leukaemia or myelodysplastic syndrome.

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

172 bid patients with acute myeloid leukaemia or myelodysplastic syndrome.

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

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

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

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

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

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

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

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

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

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

183 Myelodysplastic syndromes (MDS) and acute myeloid leukem

184 Myelodysplastic syndromes (MDS) and acute myeloid leukem

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

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

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

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

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

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

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

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

193 Myelodysplastic syndromes (MDS) are a group of neoplasms

194 Myelodysplastic syndromes (MDS) are a heterogeneous grou

195 Myelodysplastic syndromes (MDS) are characterized by ine

196 Myelodysplastic syndromes (MDS) are clonal diseases defi

197 Myelodysplastic syndromes (MDS) are clonal disorders of

198 Myelodysplastic syndromes (MDS) are driven by complex ge

199 Myelodysplastic syndromes (MDS) are haematopoietic malig

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

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

202 Myelodysplastic syndromes (MDS) are uncommon in children

203 Myelodysplastic syndromes (MDS) arise in older adults th

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

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

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

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

208 Myelodysplastic syndromes (MDS) frequently progress to a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 Myelodysplastic syndromes (MDSs) are a group of hematopo

228 Myelodysplastic syndromes (MDSs) are hematopoietic stem

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

230 Myelodysplastic syndromes (MDSs) are stem cell disorders

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 Myelodysplastic syndromes are characterised by ineffecti

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

247 17 patients with myelodysplastic syndromes harbouring an IDH2 mutation (m

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

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

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

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

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

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

254 Myelodysplastic syndromes may also present with the morp

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

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

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

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

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

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

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

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

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

264 21, 2013, and Feb 12, 2015, 58 patients with myelodysplastic syndromes were enrolled in the 12 week b

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

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

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

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

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

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

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

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

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

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

275 In myelodysplastic syndromes, thrombocytopenia is associate

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

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

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

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

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

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

282 precision-medicine concepts in leukemia and myelodysplastic syndromes.

283 fit patients with acute myeloid leukemia or myelodysplastic syndromes.

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

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

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

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

288 s, congenital dyserythropoietic anemias, and myelodysplastic syndromes.

289 utations likely contribute to development of myelodysplastic syndromes.

290 crucial to improve outcomes in patients with myelodysplastic syndromes.

291 2 (IDH2) occur in around 5% of patients with myelodysplastic syndromes.

292 ted with myeloproliferative neoplasms and/or myelodysplastic syndromes.

293 % of affected individuals progress to AML or myelodysplastic syndromes.

294 kappaB signalling, both relevant targets for myelodysplastic syndromes.

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

296 itabine bioavailability for the treatment of myelodysplastic syndromes.

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

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

299 ntation is excluded, CMML is stratified into myelodysplastic (white blood cell count <13 x 10(9)/L) a

300 ng the two patients initially diagnosed with myelodysplastic who progressed- two (16%) received HSCT