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 he relevance of screen hits for treatment of myeloproliferative neoplasms.

7 atures of both myelodysplastic syndromes and myeloproliferative neoplasms.

8 lerosis and myefibrosis are complications of myeloproliferative neoplasms.

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

10 of PDGFRB are uncommon Philadelphia-negative myeloproliferative neoplasms.

11 nant erythroid precursors from patients with myeloproliferative neoplasms.

12 om patients with chronic myeloid leukemia or myeloproliferative neoplasms.

13 most common molecular event associated with myeloproliferative neoplasms.

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

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

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

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

18 te megakaryoblastic leukemia and a subset of myeloproliferative neoplasms.

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

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

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

22 meshift mutations in exon 9 are prevalent in myeloproliferative neoplasms.

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

24 nhibitors are now successfully used to treat myeloproliferative neoplasms.

25 contributes to impaired megakaryopoiesis in myeloproliferative neoplasms.

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

27 re phenotypic drivers in the pathogenesis of myeloproliferative neoplasms.

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

29 r understanding of the pathogenetic basis of myeloproliferative neoplasms.

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

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

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

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

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

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

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

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

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

39 ly described NFE2 mutations in patients with myeloproliferative neoplasms and demonstrated that expre

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

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

42 JAK2 clinical mutations cause myeloproliferative neoplasms and leukemia, and the mutat

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

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

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

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

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

48 Ten percent of ECD cases are associated with myeloproliferative neoplasms and/or myelodysplastic synd

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

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

51 way and epigenetic regulators play a role in myeloproliferative neoplasms, and JAK inhibitors are now

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

53 of arthritis, inflammatory bowel disease and myeloproliferative neoplasms, and numerous ongoing clini

54 The myeloproliferative neoplasms are a group of haematologic

55 Myeloproliferative neoplasms are clonal disorders charac

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

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

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

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

60 Current drugs for myeloproliferative neoplasm-associated myelofibrosis, in

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

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

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

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

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

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

67 Patients with myeloproliferative neoplasms carrying CALR mutations pre

68 Polycythaemia vera is a myeloproliferative neoplasm characterised by excessive p

69 Myelofibrosis is a chronic myeloproliferative neoplasm characterised by splenomegal

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

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

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

73 Myelofibrosis is a severe myeloproliferative neoplasm characterized by increased n

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

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

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

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

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

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

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

81 107 months (range, 13-362 months) after CML/myeloproliferative neoplasm diagnosis, 66 patients (4.6%

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

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

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

85 The classic myeloproliferative neoplasms--essential thrombocytosis,

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

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

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

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

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

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

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

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

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

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

96 Myeloproliferative neoplasms, including polycythemia ver

97 Philadelphia chromosome-negative myeloproliferative neoplasms, including polycythemia ver

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

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

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

101 anscriptional output of somatic mutations in myeloproliferative neoplasms is dependent on the native

102 Symptomatic burden in myeloproliferative neoplasms is present in most patients

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

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

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

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

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

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

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

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

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

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

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

114 mally described, such as the myelodysplastic/myeloproliferative neoplasms (MDS/MPNs).

115 re than 90% of patients with myelodysplastic/myeloproliferative neoplasms (MDSs/MPNs) harbor somatic

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

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

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

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

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

121 leukemias (AMLs) evolving from an antecedent myeloproliferative neoplasm (MPN) are characterized by a

122 Patients with Philadelphia-negative myeloproliferative neoplasm (MPN) are prone to the devel

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

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

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

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

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

128 Constitutive JAK2 signaling is central to myeloproliferative neoplasm (MPN) pathogenesis and resul

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

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

131 Myeloproliferative neoplasm (MPN) patients frequently sh

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

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

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

135 Myeloproliferative neoplasm (MPN) symptoms are troubleso

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

137 Primary myelofibrosis (PMF) is a myeloproliferative neoplasm (MPN) that leads to progress

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

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

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

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

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

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

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

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

146 mounts in myelodysplastic syndrome (MDS) and myeloproliferative neoplasm (MPN).

147 7F mutation is found in most patients with a myeloproliferative neoplasm (MPN).

148 ate downstream signalling and are drivers of myeloproliferative neoplasm (MPN).

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

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

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

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

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

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

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

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

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

158 riptional and genetic tumor heterogeneity in myeloproliferative neoplasms (MPN) stem and progenitor c

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

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

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

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

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

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

165 cells (HSC), such as in human "early-stage" myeloproliferative neoplasms (MPN).

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

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

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

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

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

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

172 Myeloproliferative neoplasms (MPNs) are a group of clona

173 Myeloproliferative neoplasms (MPNs) are a group of relat

174 Myeloproliferative neoplasms (MPNs) are a group of relat

175 Myeloproliferative neoplasms (MPNs) are a set of chronic

176 Myeloproliferative neoplasms (MPNs) are associated with

177 Myeloproliferative neoplasms (MPNs) are associated with

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

179 Myeloproliferative neoplasms (MPNs) are blood cancers th

180 Myeloproliferative neoplasms (MPNs) are characterized by

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

182 Ph-negative myeloproliferative neoplasms (MPNs) are hematological ca

183 Myeloproliferative neoplasms (MPNs) are the most common

184 Human myeloproliferative neoplasms (MPNs) are thought to refle

185 Myeloproliferative neoplasms (MPNs) arise in the hematop

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

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

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

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

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

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

192 Over 80% of patients with myeloproliferative neoplasms (MPNs) harbor the acquired

193 n of JAK2 mutations as disease-initiating in myeloproliferative neoplasms (MPNs) has led to new and e

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

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

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

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

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

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

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

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

202 Myeloproliferative neoplasms (MPNs) often carry JAK2(V61

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

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

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

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

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

208 Myeloproliferative neoplasms (MPNs) such as chronic myel

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

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

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

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

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

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

215 e 2 (JAK2) is an oncogenic driver in several myeloproliferative neoplasms (MPNs), including essential

216 The myeloproliferative neoplasms (MPNs), including essential

217 anus kinase (JAK)1/2 inhibitor used to treat myeloproliferative neoplasms (MPNs), including myelofibr

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

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

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

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

222 ng cause of death in patients with JAK2V617F myeloproliferative neoplasms (MPNs).

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

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

225 otspot for somatic mutations associated with myeloproliferative neoplasms (MPNs).

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

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

228 ticulin mutations (CALR) are frequent within myeloproliferative neoplasms (MPNs).

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

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

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

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

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

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

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

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

237 17F mutant is the major determinant of human myeloproliferative neoplasms (MPNs).

238 ticulin are present in ~20% of patients with myeloproliferative neoplasms (MPNs).

239 al to the pathogenesis of mutant JAK2-driven myeloproliferative neoplasms (MPNs).

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

241 ividuals and from patients with CALR-mutated myeloproliferative neoplasms (MPNs).

242 it pertains to altered calcium signaling in myeloproliferative neoplasms (MPNs).

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

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

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

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

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

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

249 Among these myeloproliferative neoplasms, myelofibrosis has the most

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

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

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

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

254 KIT and PDGFRA kinases found in cancers and myeloproliferative neoplasms, particularly in gastrointe

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

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

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

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

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

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

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

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

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

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

265 nd use of antiplatelet therapy, depending on myeloproliferative neoplasm subtype and mutational statu

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

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

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

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

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

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

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

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

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

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

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

277 ng from previous myelodysplastic syndrome or myeloproliferative neoplasm, the presence of therapy-rel

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

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

280 e, risk factors and treatment strategies for myeloproliferative neoplasm thrombosis and bleeding, inc

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

282 D34(+) cells from patients with CALR-mutated myeloproliferative neoplasms to study how somatic mutati

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

284 myeloid leukemia (aCML), and myelodysplastic/myeloproliferative neoplasms, unclassifiable (MDS/MPN-U)

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

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

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

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

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

290 The risks of myeloproliferative neoplasms were modestly increased wit

291 ss were seen in platelets from patients with myeloproliferative neoplasms, where TNF-alpha levels are

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

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

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

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

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

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

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

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

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