ライフサイエンスコーパス: myeloproliferative

1 variants, we identified ZMYM3 (zinc finger, myeloproliferative, and mental retardation-type 3) as a

2 myelodysplastic syndromes, with or without a myeloproliferative component.

3 -ITD in vivo model, SYK is indispensable for myeloproliferative disease (MPD) development, and SYK ov

4 GATA1s-producing mutations promote transient myeloproliferative disease and acute megakaryoblastic le

5 eas somatic PTPN11 mutations cause childhood myeloproliferative disease and contribute to some solid

6 anus kinase 2 (JAK2) abrogates initiation of myeloproliferative disease and substantial disease regre

7 and Dok2 gene inactivation, which induces a myeloproliferative disease in aging mice.

8 on with NPM1c rapidly leads to an aggressive myeloproliferative disease in mice with a latency of 31.

9 o the development of gamma radiation-induced myeloproliferative disease in NQO2(-/-) mice.

10 na (+/-) mice spontaneously develop a lethal myeloproliferative disease resembling human atypical chr

11 including the associations between JAK2 and myeloproliferative disease, HOXB13 and cancer of prostat

12 g (HH) ligand secretion and loss of PTCH2 in myeloproliferative disease, which drives canonical and n

13 ere represent likely drivers or modifiers of myeloproliferative disease.

14 sulted in increased mortality accompanied by myeloproliferative disease.

15 the older mice developed a nontransplantable myeloproliferative disease.

16 fluences the development of FLT3-ITD-induced myeloproliferative disease.

17 erates, and differentiates to give rise to a myeloproliferative disease.

18 lts, including associations with infections, myeloproliferative diseases and associated conditions, s

19 ene in mice leads to gamma radiation-induced myeloproliferative diseases.

20 drome (DS) infants are born with a transient myeloproliferative disorder (DS-TMD) that spontaneously

21 Myeloproliferative disorder (MPD) was observed in murine

22 in whom it is often preceded by a transient myeloproliferative disorder (TMD).

23 ts supports redefinition of the disease as a myeloproliferative disorder and provides opportunities t

24 12D), trap Ras in the active state and cause myeloproliferative disorder and T cell leukemia (T-ALL)

25 Langerhans cell histiocytosis (LCH) is a myeloproliferative disorder characterized by lesions com

26 Chronic myeloid leukaemia (CML) is a myeloproliferative disorder characterized by the genetic

27 novel useful tool for establishing a clonal myeloproliferative disorder in JAK2 and MPL wt patients

28 Juvenile myelomonocytic leukemia (JMML) is a myeloproliferative disorder of childhood caused by mutat

29 topoietic stem cell transplantation (AHSCT), Myeloproliferative Disorder Research Consortium 101 tria

30 mutations in CSF3R are sufficient to drive a myeloproliferative disorder resembling aCML and CNL that

31 CML is a myeloproliferative disorder that results from dysregulat

32 , acute megakaryoblastic leukemia, transient myeloproliferative disorder, and a group of related cong

33 aling can translate into the occurrence of a myeloproliferative disorder.

34 venous shunts (23%), lung disease (16%), and myeloproliferative disorders (8%).

35 lso is associated with a risk for developing myeloproliferative disorders (MPD), including juvenile m

36 Patients with myeloproliferative disorders (MPDs), such as essential t

37 roven beneficial effects in the treatment of myeloproliferative disorders and inflammatory conditions

38 mice: it increases both the severity of the myeloproliferative disorders and the self-renewal proper

39 A high metabolic rate in myeloproliferative disorders is a common complication of

40 The Myeloproliferative Disorders Research Consortium (MPD-RC

41 of disorders including inherited cytopenias, myeloproliferative disorders, and erythromegakaryocytic

42 Using three different mouse models of myeloproliferative disorders, including mice with defect

43 ities in these processes are associated with myeloproliferative disorders, including thrombocytopenia

44 Four out of 25 primary mice succumbed to myeloproliferative disorders, some of which progressed t

45 RAPL expression is widely abrogated in human myeloproliferative disorders.

46 mimics for the treatment of inflammatory and myeloproliferative disorders.

47 ne investigated as a potential treatment for myeloproliferative disorders.

48 the BM niche and affects the development of myeloproliferative disorders.

49 sis of hematological malignancies or chronic myeloproliferative disorders.

50 he adjacent kinase domain (JH1) resulting in myeloproliferative disorders.

51 eloped a clinical picture closely resembling myeloproliferative disorders/neoplasms (MPNs), including

52 n thrombopoietin (TPO) and its receptor, the myeloproliferative leukemia (MPL) virus oncogene, have b

53 been reported in Janus kinase 2 (JAK2)- and myeloproliferative leukemia (MPL)-negative essential thr

54 in (TPO), on binding to its cognate receptor myeloproliferative leukemia (MPL).

55 ) of the human thrombopoietin receptor (TpoR/myeloproliferative leukemia [MPL] protein), encoded by e

56 What role does myeloproliferative leukemia virus (MPL), a key regulator

57 ding those in JAK2, calreticulin (CALR), and myeloproliferative leukemia virus (MPL), abnormally acti

58 ell variability, and thrombopoietin/cellular myeloproliferative leukemia virus liganding is dispensab

59 us kinase 2 (JAK2), calreticulin (CALR), and myeloproliferative leukemia virus oncogene (MPL) mutatio

60 Calreticulin (CALR) and myeloproliferative leukemia virus oncogene (MPL) mutatio

61 s increased signaling via the thrombopoietin/myeloproliferative leukemia virus oncogene (MPL) pathway

62 Thrombopoietin (Thpo)/myeloproliferative leukemia virus oncogene (Mpl) signali

63 its receptor, the cellular homologue of the myeloproliferative leukemia virus oncogene (Mpl), is the

64 Platelet LNK deficiency increases myeloproliferative leukemia virus oncogene signaling and

65 unction variant that promotes thrombopoietin/myeloproliferative leukemia virus oncogene signaling and

66 nstrating reduced LNK function and increased myeloproliferative leukemia virus oncogene signaling.

67 es thrombopoietin signaling via its receptor myeloproliferative leukemia virus oncogene.

68 hematopoietic growth factor receptor c-MPL (myeloproliferative leukemia), the receptor for thrombopo

69 RBPJ(-/-) mice prevented the development of myeloproliferative-like disease and cytokine induction.

70 ematopoietic homeostasis and leads to lethal myeloproliferative-like disease.

71 ur in other myeloproliferative neoplasms and myeloproliferative-myelodysplastic overlap neoplasms.

72 venile myelomonocytic leukaemia, a childhood myeloproliferative/myelodysplastic disease caused by upr

73 It is classified as an overlap myeloproliferative/myelodysplastic neoplasm by the World

74 ells (HSCs) causes perturbed haematopoiesis, myeloproliferative neoplasia (MPN) and leukaemia.

75 ttenuates BCR-ABL1 oncogene-induced CML-like myeloproliferative neoplasia (MPN) but enhances MLL-AF9

76 Here, we show that myeloproliferative neoplasia (MPN) progressively remodel

77 Analysis of BM from patients carrying myeloproliferative neoplasia also revealed elevated expr

78 model of chronic myeloid leukemia (CML)-like myeloproliferative neoplasia by repressing an inhibitory

79 uced chronic myelogenous leukemia (CML)-like myeloproliferative neoplasia in a mouse retroviral trans

80 2(-/-)bone marrow failed to develop CML-like myeloproliferative neoplasia.

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

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

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

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

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

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

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

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

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

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

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

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

93 Myeloproliferative neoplasm (MPN) patients frequently sh

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

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

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

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

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

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

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

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

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

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

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

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

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

107 7F mutation is found in most patients with a myeloproliferative neoplasm (MPN).

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

109 Polycythaemia vera is a myeloproliferative neoplasm characterised by excessive p

110 Myelofibrosis is a chronic myeloproliferative neoplasm characterised by splenomegal

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

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

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

114 Myelofibrosis is a severe myeloproliferative neoplasm characterized by increased n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 Current drugs for myeloproliferative neoplasm-associated myelofibrosis, in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Myeloproliferative neoplasms (MPNs) are a set of chronic

170 Myeloproliferative neoplasms (MPNs) are associated with

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

172 Myeloproliferative neoplasms (MPNs) are blood cancers th

173 Myeloproliferative neoplasms (MPNs) are characterized by

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

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

176 Myeloproliferative neoplasms (MPNs) arise in the hematop

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

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

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

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

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

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

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

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

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

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

187 Myeloproliferative neoplasms (MPNs) often carry JAK2(V61

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

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

190 Myeloproliferative neoplasms (MPNs) such as chronic myel

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

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

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

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

195 The myeloproliferative neoplasms (MPNs), including essential

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 The myeloproliferative neoplasms are a group of haematologic

231 Myeloproliferative neoplasms are clonal disorders charac

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

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

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

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

236 Patients with myeloproliferative neoplasms carrying CALR mutations pre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 Myeloproliferative neoplasms, including polycythemia ver

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

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

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

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

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

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

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

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

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

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

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

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

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

272 atures of both myelodysplastic syndromes and myeloproliferative neoplasms.

273 lerosis and myefibrosis are complications of myeloproliferative neoplasms.

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

275 of PDGFRB are uncommon Philadelphia-negative myeloproliferative neoplasms.

276 nant erythroid precursors from patients with myeloproliferative neoplasms.

277 om patients with chronic myeloid leukemia or myeloproliferative neoplasms.

278 most common molecular event associated with myeloproliferative neoplasms.

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

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

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

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

283 nhibitors are now successfully used to treat myeloproliferative neoplasms.

284 contributes to impaired megakaryopoiesis in myeloproliferative neoplasms.

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

286 re phenotypic drivers in the pathogenesis of myeloproliferative neoplasms.

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

288 r understanding of the pathogenetic basis of myeloproliferative neoplasms.

289 APL-deficient mice develop a fully-penetrant myeloproliferative neoplastic process.

290 able model, brain, lung, and ovarian cancer; myeloproliferative or myelodysplastic disorders; stage I

291 anism(s) by which a CALR mutation leads to a myeloproliferative phenotype has been clarified only in

292 acrophage progenitors (GMPs), resulting in a myeloproliferative phenotype with accumulation of GMPs i

293 matory cytokine production, which promotes a myeloproliferative phenotype.

294 t expression of mutant NFE2 in mice causes a myeloproliferative phenotype.

295 omotes myeloid differentiation to engender a myeloproliferative phenotype.

296 ed FLT3 signaling in vivo and suppressed the myeloproliferative phenotypes in FLT3-ITD knock-in mice,

297 features of a Philadelphia-negative chronic myeloproliferative syndrome or chronic myelomonocytic le

298 bosis, and atherogenesis, as occurs in human myeloproliferative syndromes.

299 naling is a major driver in juvenile and the myeloproliferative variant of chronic myelomonocytic leu

300 enile myelomonocytic leukemia (JMML) and the myeloproliferative variant of chronic myelomonocytic leu