ライフサイエンスコーパス: myeloproliferative neoplasm

1 ed CALR mutation status in familial cases of myeloproliferative neoplasm.

2 a phenotype resembling the nonacute phase of myeloproliferative neoplasm.

3 myelodysplastic syndrome or myelodysplastic/myeloproliferative neoplasm.

4 model results in progenitor expansion and a myeloproliferative neoplasm.

5 acids G60_A66dup in a child with an atypical myeloproliferative neoplasm.

6 contributes to impaired megakaryopoiesis in myeloproliferative neoplasms.

7 nant erythroid precursors from patients with myeloproliferative neoplasms.

8 om patients with chronic myeloid leukemia or myeloproliferative neoplasms.

9 cogenic activation of TpoR and lead to human myeloproliferative neoplasms.

10 d the development of bone marrow failure and myeloproliferative neoplasms.

11 sm of fibrotic transformation in MPL-mutated myeloproliferative neoplasms.

12 g of samples obtained from 151 patients with myeloproliferative neoplasms.

13 re phenotypic drivers in the pathogenesis of myeloproliferative neoplasms.

14 te megakaryoblastic leukemia and a subset of myeloproliferative neoplasms.

15 evelopment of post-PV myelofibrosis in human myeloproliferative neoplasms.

16 s to the pathogenesis and clinical course of myeloproliferative neoplasms.

17 eatment of PV and other JAK2V617F-associated myeloproliferative neoplasms.

18 Twenty-eight patients (52%) had myeloproliferative neoplasms.

19 r understanding of the pathogenetic basis of myeloproliferative neoplasms.

20 signaling and can lead to the development of myeloproliferative neoplasms.

21 tant etiologic factor for the development of myeloproliferative neoplasms.

22 (PMF) and polycythemia vera (PV) are chronic myeloproliferative neoplasms.

23 elopment of hematopoietic diseases including myeloproliferative neoplasms.

24 ement of this pathway in the pathogenesis of myeloproliferative neoplasms.

25 he relevance of screen hits for treatment of myeloproliferative neoplasms.

26 he pathogenic mutant CALR-MPL interaction in myeloproliferative neoplasms.

27 atures of both myelodysplastic syndromes and myeloproliferative neoplasms.

28 cells, and clonal evolution in patients with myeloproliferative neoplasms.

29 of PDGFRB are uncommon Philadelphia-negative myeloproliferative neoplasms.

30 te leukemias (51%), myelodysplastic syndrome/myeloproliferative neoplasm (19%), and lymphoproliferati

31 most commonly in those with myelodysplastic/myeloproliferative neoplasms (27 out of 219 individuals,

32 The age at which a patient presented with a myeloproliferative neoplasm, acquisition of JAK2 V617F h

33 fusion that causes a form of leukemia called myeloproliferative neoplasm, also localizes to centriola

34 t mutant females develop a highly aggressive myeloproliferative neoplasm and myelodysplastic syndrome

35 Lnk mutations have been identified in human myeloproliferative neoplasms and acute leukemia.

36 rosis (PMF) constitute the BCR-ABL1-negative myeloproliferative neoplasms and are characterized by mu

37 tive in preclinical models of JAK2-dependent myeloproliferative neoplasms and B cell acute lymphoblas

38 t tool for the further study of neutrophilic myeloproliferative neoplasms and implicates the clinical

39 ing mutations in NRAS are prevalent in human myeloproliferative neoplasms and leukaemia.

40 tic drivers that are known to occur in other myeloproliferative neoplasms and myeloproliferative-myel

41 and differentiation may entail the onset of myeloproliferative neoplasms and other preleukemic disor

42 d the Notch pathway as a tumor suppressor in myeloproliferative neoplasms and several solid tumors.

43 t yet comprehensive review of the biology of myeloproliferative neoplasms and therapeutic options wit

44 functional abnormalities distinct from other myeloproliferative neoplasms and these abnormalities are

45 r in patients with myelodysplastic syndrome, myeloproliferative neoplasms, and acute myeloid leukemia

46 ancies, including myelodysplastic syndromes, myeloproliferative neoplasms, and chronic myelomonocytic

47 oma, non-Hodgkin lymphoma, Hodgkin lymphoma, myeloproliferative neoplasms, and myelodysplastic syndro

48 The myeloproliferative neoplasms are a group of haematologic

49 Myeloproliferative neoplasms are clonal disorders charac

50 Myeloproliferative neoplasms are hematological malignanc

51 being classified as neoplastic diseases, the myeloproliferative neoplasms are often characterized by

52 Major causes of morbidity and mortality in myeloproliferative neoplasms are represented by arterial

53 ssential thrombocythemia (ET), 2 subtypes of myeloproliferative neoplasms, are associated with an ide

54 brosis is a Philadelphia chromosome-negative myeloproliferative neoplasm associated with cytopenias,

55 Polycythemia vera (PV) is a chronic myeloproliferative neoplasm associated with JAK2 mutatio

56 Current drugs for myeloproliferative neoplasm-associated myelofibrosis, in

57 Our understanding of the genetic basis of myeloproliferative neoplasms began in 2005, when the JAK

58 Myeloproliferative neoplasm blast phase is associated wi

59 by other mutations that are less specific to myeloproliferative neoplasms but are prognostically rele

60 mutation into the murine Flt3 gene induces a myeloproliferative neoplasm, but not progression to acut

61 the Janus kinase 2 gene (JAK2) occur in many myeloproliferative neoplasms, but the molecular pathogen

62 e determined mutation order in patients with myeloproliferative neoplasms by genotyping hematopoietic

63 Our aim was to find new treatments for myeloproliferative neoplasms by identifying compounds th

64 Patients with myeloproliferative neoplasms carrying CALR mutations pre

65 Myelofibrosis is a chronic myeloproliferative neoplasm characterised by splenomegal

66 Myelofibrosis (MF) is a BCR-ABL-negative myeloproliferative neoplasm characterized by anemia, spl

67 Myelofibrosis (MF) is a BCR-ABL1-negative myeloproliferative neoplasm characterized by clonal myel

68 Chronic eosinophilic leukemia (CEL) is a myeloproliferative neoplasm characterized by expansion o

69 Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by megakaryocy

70 stem cells of primary myelofibrosis (PMF), a myeloproliferative neoplasm characterized by profound di

71 trophilic leukaemia (CNL) is recognized as a myeloproliferative neoplasm characterized by sustained n

72 inactive in polycythemia vera (PV) and other myeloproliferative neoplasms characterized by the expres

73 Further, as a subtype of the myelodysplastic/myeloproliferative neoplasms, CMML has a complex clinica

74 Health Organization (WHO) classification of myeloproliferative neoplasms defines 2 stages of primary

75 DS-like disease, which could progress to MDS/myeloproliferative neoplasm, demonstrating a haploinsuff

76 107 months (range, 13-362 months) after CML/myeloproliferative neoplasm diagnosis, 66 patients (4.6%

77 to centriolar satellites may be relevant to myeloproliferative neoplasm disease progression.

78 of erythroid precursors from patients with a myeloproliferative neoplasm due to a constitutively acti

79 ciency of L3MBTL1 contributes to some (20q-) myeloproliferative neoplasms, especially polycythemia ve

80 The classic myeloproliferative neoplasms--essential thrombocytosis,

81 onse criteria for myelofibrosis or for other myeloproliferative neoplasms fit such patients well.

82 atic Jak2 mutations in patients with chronic myeloproliferative neoplasms has led to significant inte

83 F mutation in most patients with Ph-negative myeloproliferative neoplasms has led to the development

84 Dysfunction was associated with a myeloproliferative neoplasm (hazard ratio, 8.18; 95% con

85 ts in Ldlr(-/-) mice and in a mouse model of myeloproliferative neoplasm in an ABCG4-dependent fashio

86 lomonocytic leukemia (JMML) is an aggressive myeloproliferative neoplasm in children characterized by

87 mes of 74 patients diagnosed with BCR-ABL(-) myeloproliferative neoplasms in blast phase receiving in

88 derived suppressor cells (MDSCs) that caused myeloproliferative neoplasms in mice.

89 thrombocytemia and primary myelofibrosis, 2 myeloproliferative neoplasms in which megakaryocytes (MK

90 ication of molecular lesions specific to the myeloproliferative neoplasms, in particular JAK2 V617F,

91 a role in the development and progression of myeloproliferative neoplasms including myelofibrosis (MF

92 Myeloproliferative neoplasms, including polycythemia ver

93 Philadelphia chromosome-negative myeloproliferative neoplasms, including polycythemia ver

94 nd treatment strategies in BCR-ABL1-negative myeloproliferative neoplasms, including polycythemia ver

95 As found in other myeloproliferative neoplasms, increased production of pr

96 ) BM cells, phenotypically distinct from the myeloproliferative neoplasm induced by FLT3-ITD using wi

97 Symptomatic burden in myeloproliferative neoplasms is present in most patients

98 Essential thrombocythemia, a myeloproliferative neoplasm, is associated with increase

99 monocytic leukemia (CMML), a myelodysplastic/myeloproliferative neoplasm, is characterized by monocyt

100 Primary myelofibrosis is the rarest of the myeloproliferative neoplasms, is the most obscure with r

101 Thus, PLC-beta3-deficient mice develop myeloproliferative neoplasm, like Lyn (Src family kinase

102 rized as an overlap myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN) by the World Healt

103 (aCML) is a rare subtype of myelodysplastic/myeloproliferative neoplasm (MDS/MPN) largely defined mo

104 n aggressive pediatric mixed myelodysplastic/myeloproliferative neoplasm (MDS/MPN).

105 splastic syndromes (MDS) and myelodysplastic/myeloproliferative neoplasms (MDS/MPN) has considerably

106 odysplastic syndromes (MDS), myelodysplastic/myeloproliferative neoplasms (MDS/MPN), or secondary acu

107 cell lung cancer (NSCLC) and myelodysplastic/myeloproliferative neoplasms (MDS/MPN), respectively.

108 pathologic features of mixed myelodysplastic/myeloproliferative neoplasms (MDS/MPNs) with progression

109 Myelodysplastic/myeloproliferative neoplasms (MDS/MPNs), including chron

110 nrolling adult patients with myelodysplastic/myeloproliferative neoplasms (MDS/MPNs).

111 (RARS-T), 2 distinct subtypes of MDS and MDS/myeloproliferative neoplasms (MDSs/MPNs).

112 -) and Apoe(-/-) mice or in a mouse model of myeloproliferative neoplasm mediated by Flt3-ITD mutatio

113 ere elevated in the plasmas of patients with myeloproliferative neoplasms (MF > polycythemia vera or

114 induction of erythrocytosis in a JAK2 V617F myeloproliferative neoplasm mouse model.

115 s present in the majority of patients with a myeloproliferative neoplasm (MPN) and is sufficient to r

116 LNK deficiency promotes myeloproliferative neoplasm (MPN) development in mice, a

117 ML) is a rare myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) for which no current s

118 The genetic landscape of classical myeloproliferative neoplasm (MPN) is in large part eluci

119 in receptor gene (MPL) in most patients with myeloproliferative neoplasm (MPN) led to the clinical de

120 ia (JMML) are myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) overlap disorders char

121 and germline genetic events responsible for myeloproliferative neoplasm (MPN) pathogenesis have been

122 ytokine receptor axis play a central role in myeloproliferative neoplasm (MPN) pathogenesis.

123 Myeloproliferative neoplasm (MPN) patients frequently sh

124 PY5R) is frequently detected in platelets of myeloproliferative neoplasm (MPN) patients, but not in p

125 molecular responses are not observed in most myeloproliferative neoplasm (MPN) patients.

126 ells by the JAK2V617F mutation recapitulates myeloproliferative neoplasm (MPN) phenotypes in mice, es

127 Myeloproliferative neoplasm (MPN) symptoms are troubleso

128 yelomonocytic leukemia (JMML), an aggressive myeloproliferative neoplasm (MPN) that is refractory to

129 murine hematopoietic cells promotes an acute myeloproliferative neoplasm (MPN) that recapitulates man

130 id leukemia (AML) may follow a JAK2-positive myeloproliferative neoplasm (MPN), although the mechanis

131 d for the treatment of myelofibrosis, a rare myeloproliferative neoplasm (MPN), but clinical trials a

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

133 yndrome (MDS), acute myeloid leukemia (AML), myeloproliferative neoplasm (MPN), MDS/MPN, or otherwise

134 eloid neoplasm, most commonly occurring as a myeloproliferative neoplasm (MPN), myelodysplastic syndr

135 ombosis is common in patients suffering from myeloproliferative neoplasm (MPN), whereas bleeding is l

136 titution of bone marrow cells, and a chronic myeloproliferative neoplasm (MPN).

137 t/ITD) "knockin" mice develop a slowly fatal myeloproliferative neoplasm (MPN).

138 7F mutation is found in most patients with a myeloproliferative neoplasm (MPN).

139 myelomonocytic leukaemia (JMML), a childhood myeloproliferative neoplasm (MPN).

140 in both myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN) affects the long arm

141 Myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN) are hematologically d

142 hrombocythemia and primary myelofibrosis are myeloproliferative neoplasms (MPN) characterized by mult

143 AT-activating mutations in BCR-ABL1-negative myeloproliferative neoplasms (MPN) has led to the develo

144 Clonal proliferation in myeloproliferative neoplasms (MPN) is driven by somatic

145 overy of JAK2/MPL mutations in patients with myeloproliferative neoplasms (MPN) led to clinical devel

146 op myelodysplastic syndrome (MDS) or MDS and myeloproliferative neoplasms (MPN) overlapping diseases

147 ified somatic alterations in the majority of myeloproliferative neoplasms (MPN) patients, including J

148 ation, the cellular and molecular biology of myeloproliferative neoplasms (MPN) remains incompletely

149 he oncogenetic events that transform chronic myeloproliferative neoplasms (MPN) to acute myeloid leuk

150 Cases of myeloproliferative neoplasms (MPN) with TET2 mutations s

151 evolution in the management of patients with myeloproliferative neoplasms (MPN), and in particular th

152 ch as TNFalpha are elevated in patients with myeloproliferative neoplasms (MPN), but their contributi

153 observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap synd

154 s in chronic myeloid malignancies, including myeloproliferative neoplasms (MPN), myelodysplastic synd

155 K2(V617F) are central to the pathogenesis of myeloproliferative neoplasms (MPN), suggesting that smal

156 or FGFR1, or with PCM1-JAK2" In addition to myeloproliferative neoplasms (MPN), these patients can p

157 ut in most cases of myelodysplasia (MDS) and myeloproliferative neoplasms (MPN), underlying pathogeni

158 tion of the malignant cells in patients with myeloproliferative neoplasms (MPN).

159 ancer-initiating cells in JAK2V617F-positive myeloproliferative neoplasms (MPN): (i) the JAK2V617F mu

160 yeloid malignancies including MDS (n = 386), myeloproliferative neoplasms (MPNs) (n = 55), MDS/MPNs (

161 onal karyotypic defects, who tend to develop myeloproliferative neoplasms (MPNs) and acute myeloid le

162 on of Vav or Rac or Pak delayed the onset of myeloproliferative neoplasms (MPNs) and corrected the as

163 ations in the pseudokinase domain of JAK2 in myeloproliferative neoplasms (MPNs) and in other hematol

164 ciated with Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) and JAK2 V617F clona

165 se (LOX), the level of which is increased in myeloproliferative neoplasms (MPNs) and other conditions

166 Myeloproliferative neoplasms (MPNs) are a group of clona

167 Myeloproliferative neoplasms (MPNs) are a group of relat

168 Myeloproliferative neoplasms (MPNs) are a group of relat

169 Chronic myeloproliferative neoplasms (MPNs) are a group of relat

170 Myeloproliferative neoplasms (MPNs) are a set of chronic

171 Myeloproliferative neoplasms (MPNs) are associated with

172 Myeloproliferative neoplasms (MPNs) are associated with

173 Patients with myeloproliferative neoplasms (MPNs) are at significant,

174 Myeloproliferative neoplasms (MPNs) are characterized by

175 mia, acute myeloid leukemia (AML), and other myeloproliferative neoplasms (MPNs) are genetically hete

176 Myeloproliferative neoplasms (MPNs) are the most common

177 Human myeloproliferative neoplasms (MPNs) are thought to refle

178 Myeloproliferative neoplasms (MPNs) arise in the hematop

179 The majority of patients with myeloproliferative neoplasms (MPNs) carry a somatic JAK2

180 m many patients with leukemia, including the myeloproliferative neoplasms (MPNs) chronic myeloid leuk

181 Health Organization (WHO) classification of myeloproliferative neoplasms (MPNs) comprises several en

182 of the JAK2 V617F mutation in the classical myeloproliferative neoplasms (MPNs) essential thrombocyt

183 fatal complication of Philadelphia-negative myeloproliferative neoplasms (MPNs) for which optimal tr

184 JAK2V617F(+) myeloproliferative neoplasms (MPNs) frequently progress

185 ) inhibitor ruxolitinib for the treatment of myeloproliferative neoplasms (MPNs) has led to studies o

186 Philadelphia-negative classical myeloproliferative neoplasms (MPNs) include polycythemia

187 been identified in most cases of Ph-negative myeloproliferative neoplasms (MPNs) including polycythem

188 Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) including polycythem

189 Leukemic transformation (LT) of myeloproliferative neoplasms (MPNs) is associated with a

190 ssociation between somatic JAK2 mutation and myeloproliferative neoplasms (MPNs) is now well establis

191 g factor in Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) is the acquisition o

192 The role of somatic JAK2 mutations in clonal myeloproliferative neoplasms (MPNs) is well established.

193 Myeloproliferative neoplasms (MPNs) often carry JAK2(V61

194 he Philadelphia chromosomal-negative chronic myeloproliferative neoplasms (MPNs) originate at the lev

195 y of JAK2 and MPL mutations in patients with myeloproliferative neoplasms (MPNs) provided important i

196 617F mutation in these 3 clinically distinct myeloproliferative neoplasms (MPNs) remained unclear.

197 The molecular etiology of myeloproliferative neoplasms (MPNs) remains incompletely

198 The molecular pathophysiology of myeloproliferative neoplasms (MPNs) remains poorly under

199 Reported survival in patients with myeloproliferative neoplasms (MPNs) shows great variatio

200 Myeloproliferative neoplasms (MPNs) such as chronic myel

201 presence of known mutations in patients with myeloproliferative neoplasms (MPNs) with clinical outcom

202 smal nocturnal hemoglobinuria (PNH) and some myeloproliferative neoplasms (MPNs), and recently in hem

203 an early somatic event in most patients with myeloproliferative neoplasms (MPNs), and the study of th

204 in clinical development for the treatment of myeloproliferative neoplasms (MPNs), B cell acute lympho

205 e main mutation involved in BCR/ABL-negative myeloproliferative neoplasms (MPNs), but its effect on h

206 mutational status of TET1, TET2, and TET3 in myeloproliferative neoplasms (MPNs), chronic myelomonocy

207 ients with the chronic Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocy

208 hibitors were developed for the treatment of myeloproliferative neoplasms (MPNs), following the disco

209 The myeloproliferative neoplasms (MPNs), including essential

210 studies have reported familial clustering of myeloproliferative neoplasms (MPNs), including polycythe

211 tients with Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs), is unknown.

212 leukemias, myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPNs), non-Hodgkin lymphom

213 mmune modulation is present in patients with myeloproliferative neoplasms (MPNs), the risk of AMD in

214 for testing drugs with potential effects on myeloproliferative neoplasms (MPNs), we first performed

215 n shown to contribute to the pathogenesis of myeloproliferative neoplasms (MPNs).

216 tients with Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs).

217 for the treatment of patients suffering from myeloproliferative neoplasms (MPNs).

218 of patients with polycythemia vera and other myeloproliferative neoplasms (MPNs).

219 ) is an effective treatment of patients with myeloproliferative neoplasms (MPNs).

220 re the central role of JAK/STAT signaling in myeloproliferative neoplasms (MPNs).

221 m involved in diseases such as leukemias and myeloproliferative neoplasms (MPNs).

222 Jak2V617F, a critical pathogenic mutation in myeloproliferative neoplasms (MPNs).

223 bone marrow (BM) samples from patients with myeloproliferative neoplasms (MPNs).

224 mportant signaling molecule in patients with myeloproliferative neoplasms (MPNs).

225 s been detected in most cases of Ph-negative myeloproliferative neoplasms (MPNs).

226 17F mutant is the major determinant of human myeloproliferative neoplasms (MPNs).

227 ling, in 2 patients with JAK2 V617F-negative myeloproliferative neoplasms (MPNs).

228 e majority of patients with BCR-ABL-negative myeloproliferative neoplasms (MPNs).

229 re associated with a significant fraction of myeloproliferative neoplasms (MPNs).

230 ng the molecular pathogenesis of CALR-mutant myeloproliferative neoplasms (MPNs).

231 th thrombosis, such as arterial stenosis and myeloproliferative neoplasms (MPNs).

232 mutation is present in >80% of patients with myeloproliferative neoplasms (MPNs).

233 t common cooccurring classes of mutations in myeloproliferative neoplasms (MPNs).

234 eosinophilic myeloid neoplasms [eosinophilic myeloproliferative neoplasms (MPNs)].

235 atients with myeloid malignancies, including myeloproliferative neoplasms, myelodysplastic syndrome,

236 stem cells in myeloid malignancies, such as myeloproliferative neoplasms, myelodysplastic syndromes,

237 Among these myeloproliferative neoplasms, myelofibrosis has the most

238 nse of completeness, with most patients with myeloproliferative neoplasm now having a biological basi

239 lomonocytic leukemia (JMML) is an aggressive myeloproliferative neoplasm of childhood associated with

240 lomonocytic leukemia (JMML) is an aggressive myeloproliferative neoplasm of young children initiated

241 Records of 1445 patients with CML/myeloproliferative neoplasm or other hematologic maligna

242 is of a further 146 myelodysplastic syndrome/myeloproliferative neoplasm patients revealed an additio

243 is or disease progression of BCR-ABL-induced myeloproliferative neoplasm (PN).

244 f BM failure characterizing the prototypical myeloproliferative neoplasm primary myelofibrosis.

245 -STAT pathway appears to be activated in all myeloproliferative neoplasms, regardless of founding dri

246 revision of the International Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG

247 ia for myelodysplastic syndromes nor the IWG Myeloproliferative Neoplasms Research and Treatment (IWG

248 rding to the International Working Group for Myeloproliferative Neoplasms Research and Treatment crit

249 ished by ELN and International Working Group-Myeloproliferative Neoplasms Research and Treatment.

250 creatic cancer (risk = 1.5%; SIR = 256), and myeloproliferative neoplasms (risk = 0.7%; SIR = 764).

251 equencing in 1107 samples from patients with myeloproliferative neoplasms showed that CALR mutations

252 lop a Stat5-dependent, fatal myelodysplastic/myeloproliferative neoplasm, similar to human chronic my

253 %) had associated myeloid neoplasm: 55 (45%) myeloproliferative neoplasm (SM-MPN), 36 (29%) chronic m

254 man diseases of myelodysplastic syndrome and myeloproliferative neoplasms such as erythroid dysplasia

255 a, T-cell acute lymphoblastic leukemia, or a myeloproliferative neoplasm, suggesting an important rol

256 ate a broadly applicable 18-item instrument (Myeloproliferative Neoplasm Symptom Assessment Form [MPN

257 cy and independency and consideration of the Myeloproliferative Neoplasm Symptom Assessment Form as a

258 erexpression in murine bone marrow induces a myeloproliferative neoplasm that advances AML over time.

259 yelomonocytic leukemia (JMML) is a pediatric myeloproliferative neoplasm that bears distinct characte

260 Primary myelofibrosis is a myeloproliferative neoplasm that is a precursor to myelo

261 Polycythemia vera (PV) is a chronic myeloproliferative neoplasm that is associated with a su

262 ssential thrombocythemia (ET) is an indolent myeloproliferative neoplasm that may be complicated by v

263 at methotrexate is a promising treatment for myeloproliferative neoplasms that could be translated in

264 hepatomegaly, hypercellular bone marrow, and myeloproliferative neoplasms that progresses to acute my

265 sine kinase pathways is a shared theme among myeloproliferative neoplasms, the pathogenetic basis of

266 in epigenetic regulators frequently occur in myeloproliferative neoplasms, their effects on the epige

267 of Ikaros was associated with progression of myeloproliferative neoplasms to acute myeloid leukemia a

268 ding chronic myelomonocytic leukemia and MDS-myeloproliferative neoplasms) to explore the role of acq

269 constitutively active and has been linked to myeloproliferative neoplasms, was recently shown to comp

270 n of the CALR mutants to the pathogenesis of myeloproliferative neoplasms, we engrafted lethally irra

271 XL1, and IDH1/2 mutations in myelodysplastic/myeloproliferative neoplasms, we hypothesized that they

272 nsights into a possible role of microRNAs in myeloproliferative neoplasms, we performed short RNA mas

273 y cause of eosinophilia or a PDGFR -positive myeloproliferative neoplasm were excluded.

274 The risks of myeloproliferative neoplasms were modestly increased wit

275 a represent different phenotypes of a single myeloproliferative neoplasm, whereas CALR-mutated essent

276 ukemia (CMML) is a myelodysplastic syndrome/ myeloproliferative neoplasm whose diagnosis is currently

277 ic neutrophilic leukemia (CNL) is a distinct myeloproliferative neoplasm with a high prevalence (>80%

278 nocytic leukemia (CMML) is a myelodysplastic/myeloproliferative neoplasm with variable clinical cours

279 of 2 patients with myelodysplastic syndrome/myeloproliferative neoplasms with 17q acquired uniparent

280 The majority of these mice develop myeloproliferative neoplasms with a less-aggressive phen

281 neoplasms, but the molecular pathogenesis of myeloproliferative neoplasms with nonmutated JAK2 is obs

282 ations were found in 70 to 84% of samples of myeloproliferative neoplasms with nonmutated JAK2, in 8%

283 LR were found in a majority of patients with myeloproliferative neoplasms with nonmutated JAK2.