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 ic leukaemia, a childhood myeloproliferative/myelodysplastic disease caused by upregulated RAS signal

4 g, and ovarian cancer; myeloproliferative or myelodysplastic disorders; stage IV pancreatic cancer; o

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

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

7 llogeneic HSCT offers optimal eradication of myelodysplastic hematopoiesis when the procedure is perf

8 myeloid leukemia (aCML) is a rare subtype of myelodysplastic/myeloproliferative neoplasm (MDS/MPN) la

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

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

11 basis of myelodysplastic syndromes (MDS) and myelodysplastic/myeloproliferative neoplasms (MDS/MPN) h

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

13 Myelodysplastic/myeloproliferative neoplasms (MDS/MPNs),

14 eatment trials enrolling adult patients with myelodysplastic/myeloproliferative neoplasms (MDS/MPNs).

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

16 oliferative neoplasms and myeloproliferative-myelodysplastic overlap neoplasms.

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

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

19 quired aplastic anemia (AA) and hypocellular myelodysplastic syndrome (hMDS) is often difficult, espe

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

21 atic cohesin mutations have been reported in myelodysplastic syndrome (MDS) and acute myeloid leukemi

22 us deletions of chromosome 7 are frequent in myelodysplastic syndrome (MDS) and acute myeloid leukemi

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

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

25 ergence in their teens or young adulthood of 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 r of the hypoplastic anemia in patients with myelodysplastic syndrome (MDS) and chromosome 5q deletio

31 or outcomes in both AML and a mouse model of myelodysplastic syndrome (MDS) and leukemia.

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

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 Recurrently mutated genes in myelodysplastic syndrome (MDS) are pathogenic drivers an

36 diagnosis in patients suspected of having a myelodysplastic syndrome (MDS) can be challenging and co

37 plicing machinery are found in almost 50% of myelodysplastic syndrome (MDS) cases.

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

39 outcome of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) has been attributed to fa

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

41 Myelodysplastic syndrome (MDS) has long been presumed to

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

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

44 nting a set of potential miRNA biomarkers of myelodysplastic syndrome (MDS) in clinical EL samples (m

45 The myelodysplastic syndrome (MDS) is a clonal disorder char

46 The myelodysplastic syndrome (MDS) is a clonal hematologic d

47 Myelodysplastic syndrome (MDS) is clonal disorder charac

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

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

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

51 5q) transfusion-dependent low/intermediate-1 myelodysplastic syndrome (MDS) patients achieve an eryth

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

53 Only a minority of myelodysplastic syndrome (MDS) patients respond to hypom

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

55 Approximately one-third of patients with myelodysplastic syndrome (MDS) receiving allogeneic hema

56 Myelodysplastic syndrome (MDS) risk correlates with adva

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

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

59 Adults with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) typically remain hospital

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

61 lidomide is a highly effective treatment for myelodysplastic syndrome (MDS) with deletion of chromoso

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

63 Myelodysplastic syndrome (MDS), a hematopoietic stem cel

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

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

66 C2), are observed in ~\n10% of patients with myelodysplastic syndrome (MDS), but are rare in acute my

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

68 for up to 42 days and developed features of myelodysplastic syndrome (MDS), including dysplastic neu

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

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

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

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

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

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

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

76 ated on the X chromosome-are associated with myelodysplastic syndrome (MDS).

77 with a 20% risk of evolving into leukemia or myelodysplastic syndrome (MDS).

78 ted in the common deleted region for del(5q) myelodysplastic syndrome (MDS).

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

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

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

82 d for acute myeloid leukemia (AML, n = 138), myelodysplastic syndrome (n = 28), or acute lymphoblasti

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

84 yeloid leukaemia (t-AML) and therapy-related myelodysplastic syndrome (t-MDS) are well-recognized com

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

86 One patient developed myelodysplastic syndrome 28 months after receiving radio

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

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

89 ts were analyzed, including 97 patients with myelodysplastic syndrome and 52 patients with acute myel

90 lly and biologically active in patients with myelodysplastic syndrome and acute myeloid leukaemia.

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

92 between the disease in these mice and human myelodysplastic syndrome and AML.

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

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

95 zacitidine and lenalidomide for patient with myelodysplastic syndrome and have preliminary evidence t

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

97 iption factor RUNX1 is frequently mutated in myelodysplastic syndrome and leukemia.

98 ents met present WHO diagnostic criteria for myelodysplastic syndrome and other related myeloid neopl

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

100 Subtypes of myelodysplastic syndrome are characterized by different

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

102 leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome between 1999 and 2011 were incl

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

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

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

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

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

108 ute myeloid leukaemia and nine patients with myelodysplastic syndrome in the daily x 5 dose-escalatio

109 cute myeloid leukaemia and six patients with myelodysplastic syndrome in the once-weekly dose-escalat

110 ute myeloid leukaemia and four patients with myelodysplastic syndrome in the twice-weekly dose-escala

111 Myelodysplastic syndrome is a rare, chronic hematologica

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

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

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

115 rom nine North American medical centres with myelodysplastic syndrome or acute myeloid leukaemia that

116 Patients with myelodysplastic syndrome or acute myeloid leukaemia who

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

118 transplantation is curative in up to 40% of myelodysplastic syndrome patients.

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

120 .6%) with marrow failure and 11 (24.4%) with myelodysplastic syndrome underwent HCT using matched unr

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

122 in patients with acute myeloid leukaemia and myelodysplastic syndrome was initially established at 50

123 mia and thrombocytopenia, and a diagnosis of myelodysplastic syndrome was made.

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

125 18 to 65 years of age with acute leukemia or myelodysplastic syndrome who underwent myeloablative HLA

126 ents with non-APL acute myeloid leukemia and myelodysplastic syndrome who were treated on a previousl

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

128 participants were previously untreated with myelodysplastic syndrome with an International Prognosti

129 sed or refractory acute myeloid leukaemia or myelodysplastic syndrome with bone marrow blasts more th

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

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

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

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

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

135 in patients with DNMT3A mutations, including myelodysplastic syndrome, acute myeloid leukemia, primar

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

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

138 treatment-related adverse events (pneumonia, myelodysplastic syndrome, and acute renal failure) and t

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

140 orders of red cell imbalance such as anemia, myelodysplastic syndrome, and polycythemia vera.

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

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

143 ms of the disease in patients diagnosed with myelodysplastic syndrome, as well as the assessment of t

144 y: 28 with acute myeloid leukaemia, six with myelodysplastic syndrome, five with chronic myeloid leuk

145 In del(5q) myelodysplastic syndrome, lenalidomide induces the degra

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

147 1206 adults with untreated AML or high-risk myelodysplastic syndrome, mostly younger than 60 years o

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

149 ome, secondary acute myeloid leukaemia after myelodysplastic syndrome, or de-novo acute myeloid leuka

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

151 9) for patients with acute myeloid leukemia, myelodysplastic syndrome, or non-Hodgkin lymphoma, the t

152 mbocytopenia in adult patients with advanced myelodysplastic syndrome, secondary acute myeloid leukae

153 improves survival in patients with high-risk myelodysplastic syndrome, the overall response remains a

154 geted screening for CSNK1A1 mutations and 20 myelodysplastic syndrome-associated mutations in 245 add

155 We detected coexisting myelodysplastic syndrome-related gene mutations in patie

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

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

158 in patients with acute myeloid leukaemia or myelodysplastic syndrome.

159 iated with immunodeficiency, lymphedema, and myelodysplastic syndrome.

160 and patients with secondary AML or high-risk myelodysplastic syndrome.

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

162 tion remains the only curative treatment for myelodysplastic syndrome.

163 groups according to the diagnosed subtype of myelodysplastic syndrome.

164 lymphoma, myeloproliferative neoplasms, and myelodysplastic syndrome.

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

166 Chronic myelomonocytic leukemia (CMML) is a myelodysplastic syndrome/ myeloproliferative neoplasm wh

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

168 cterized by lymphedema and predisposition to myelodysplastic syndrome/acute myeloid leukemia (MDS/AML

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

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

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

172 s, and diagnoses were acute leukemias (51%), myelodysplastic syndrome/myeloproliferative neoplasm (19

173 JMML is categorized as an overlap myelodysplastic syndrome/myeloproliferative neoplasm (MD

174 The prognosis of myelodysplastic syndromes (MDS) after allogeneic stem ce

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

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

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

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

179 Myelodysplastic syndromes (MDS) and acute myeloid leukem

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

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

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

183 entiation, as well as in the pathogenesis of myelodysplastic syndromes (MDS) and leukemia.

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

185 Our knowledge of the genetic basis of myelodysplastic syndromes (MDS) and myelodysplastic/myel

186 Myelodysplastic syndromes (MDS) and myeloproliferative n

187 A common deleted region (CDR) in both myelodysplastic syndromes (MDS) and myeloproliferative n

188 ost common structural abnormality in primary myelodysplastic syndromes (MDS) and therapy-related myel

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

190 Myelodysplastic syndromes (MDS) are a group of neoplasms

191 Myelodysplastic syndromes (MDS) are a heterogeneous grou

192 Acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are associated with dise

193 Myelodysplastic syndromes (MDS) are clonal disorders of

194 Myelodysplastic syndromes (MDS) are clonal hematopoietic

195 Myelodysplastic syndromes (MDS) are common hematologic d

196 Although myelodysplastic syndromes (MDS) are defined by cytopenia

197 Higher-risk myelodysplastic syndromes (MDS) are defined by patients

198 Myelodysplastic syndromes (MDS) are driven by complex ge

199 Once thought to be rare disorders, the myelodysplastic syndromes (MDS) are now recognized as am

200 Myelodysplastic syndromes (MDS) are stem cell disorders

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

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

203 Myelodysplastic syndromes (MDS) are uncommon in children

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

207 g chronic myelomonocytic leukemia (CMML) and myelodysplastic syndromes (MDS) in human.

208 adults with acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS) is challenging because o

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

210 The diagnosis of patients with myelodysplastic syndromes (MDS) is largely dependent on

211 eased autoantibody reactivity in plasma from Myelodysplastic Syndromes (MDS) patients may provide nov

212 The diagnosis of myelodysplastic syndromes (MDS) remains problematic due

213 e factor (SF) genes occur more frequently in myelodysplastic syndromes (MDS) than in acute myeloid le

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

215 otypes resembling those found in early-stage myelodysplastic syndromes (MDS), including ineffective e

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

217 occur in approximately 11% of patients with myelodysplastic syndromes (MDS), the most common adult m

218 In low- to intermediate-risk myelodysplastic syndromes (MDS), we establish the existe

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

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

221 is the predominant clinical manifestation of myelodysplastic syndromes (MDS).

222 a somatic cytogenetic abnormality present in myelodysplastic syndromes (MDS).

223 ogenesis of age-related disorders, including myelodysplastic syndromes (MDS).

224 effective erythropoiesis in a mouse model of myelodysplastic syndromes (MDS).

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

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

227 al killer (NK) lymphoid deficiency; familial myelodysplastic syndromes (MDS)/acute myeloid leukemia (

228 Familial clustering of myelodysplastic syndromes (MDSs) and acute myeloid leuke

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

230 Myelodysplastic syndromes (MDSs) are a group of hematopo

231 Myelodysplastic syndromes (MDSs) are a group of heteroge

232 Myelodysplastic syndromes (MDSs) are hematopoietic stem

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

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

235 mDia1, a chromosome 5q gene, contributes to myelodysplastic syndromes (MDSs) by increasing innate im

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

237 The myelodysplastic syndromes (MDSs) include a spectrum of s

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

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

240 Therapy-related acute myeloid leukemia and myelodysplastic syndromes (t-AML/MDS) represent severe l

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

242 and lenalidomide in patients with high-risk myelodysplastic syndromes and acute myeloid leukaemia.

243 of chromosome 7 and 7q [-7/del(7q)] occur in myelodysplastic syndromes and acute myeloid leukemia (AM

244 gnancies and has been studied extensively in myelodysplastic syndromes and acute myeloid leukemia.

245 ations are frequently found in patients with myelodysplastic syndromes and certain leukemias, but how

246 Myelodysplastic syndromes and chronic myelomonocytic leu

247 new therapeutic entries for the treatment of myelodysplastic syndromes and leukaemia.

248 n the pathogenesis of the stem cell disorder myelodysplastic syndromes and myeloid leukaemia.

249 gnancies sharing phenotypic features of both myelodysplastic syndromes and myeloproliferative neoplas

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

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

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

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

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

255 Myelodysplastic syndromes are characterised by ineffecti

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

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

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

259 The clinical presentation of myelodysplastic syndromes is highly variable and so accu

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

261 Myelodysplastic syndromes may also present with the morp

262 al Working Group (IWG) response criteria for myelodysplastic syndromes nor the IWG Myeloproliferative

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

264 In 38% of patients with myelodysplastic syndromes or acute myeloid leukaemia, in

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

266 Adults (>/=18 years) with myelodysplastic syndromes were consecutively enrolled wi

267 21, 2013, and Feb 12, 2015, 58 patients with myelodysplastic syndromes were enrolled in the 12 week b

268 Myelodysplastic syndromes were not rare (2.3%).

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

270 median survival, 328 days) characteristic of myelodysplastic syndromes with symptoms including anemia

271 with CMML (training cohort, Spanish Group of Myelodysplastic Syndromes) and to validate it in an inde

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

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

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

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

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

277 In myelodysplastic syndromes, SF3B1 mutations appear to be

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

279 In myelodysplastic syndromes, thrombocytopenia is associate

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

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

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

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

284 s, congenital dyserythropoietic anemias, and myelodysplastic syndromes.

285 utations likely contribute to development of myelodysplastic syndromes.

286 crucial to improve outcomes in patients with myelodysplastic syndromes.

287 ith poor survival in patients suffering from myelodysplastic syndromes.

288 precision-medicine concepts in leukemia and myelodysplastic syndromes.

289 l variables and outcome in 124 patients with myelodysplastic syndromes.

290 fit patients with acute myeloid leukemia or myelodysplastic syndromes.

291 gnostic indices in patients with higher-risk myelodysplastic syndromes.

292 30% blasts to focus mainly on patients with myelodysplastic syndromes.

293 itabine) have been approved for treatment of myelodysplastic syndromes.

294 mia and to prolong survival in patients with myelodysplastic syndromes.

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

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

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

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

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

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