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 ted for a suspicion of Philadelphia-negative myeloproliferative disease (MPD), were retrospectively e

5 nile myelomonocytic leukemia (JMML), a fatal myeloproliferative disease (MPD).

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

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

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

9 ITD significantly shortened the latency of a myeloproliferative disease compared with FLT3-ITD alone

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

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

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

13 between stem cell quiescence/homeostasis and myeloproliferative disease while also giving novel insig

14 overexpress CREB in myeloid cells develop a myeloproliferative disease with splenomegaly and aberran

15 ten in mice lacking G-CSF, the splenomegaly, myeloproliferative disease, and splenic HSC accumulation

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

17 er, mutant IDH1 greatly accelerated onset of myeloproliferative disease-like myeloid leukemia in mice

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

19 the older mice developed a nontransplantable myeloproliferative disease.

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

21 in mice leads to increased susceptibility to myeloproliferative disease.

22 an paradigm with therapeutic implications in myeloproliferative disease.

23 sulted in increased mortality accompanied by myeloproliferative disease.

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

25 We examined these issues in the case of myeloproliferative diseases and neoplasms (MPN), a colle

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

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

28 are diagnosed with self-regressing transient myeloproliferative disorder (TMD), and 20% to 30% of tho

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

30 karyocytic proliferation disorder (transient myeloproliferative disorder [TMD]).

31 n syndrome (trisomy 21)-associated transient myeloproliferative disorder and acute megakaryoblastic l

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

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

34 etic defects, aged Runx3 KO mice developed a myeloproliferative disorder characterized by myeloid-dom

35 I-expressing hematopoietic cells developed a myeloproliferative disorder characterized by overproduct

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

37 CSF3R T618I, is sufficient to drive a lethal myeloproliferative disorder in a murine bone marrow tran

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

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

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

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

42 CML is a myeloproliferative disorder that results from dysregulat

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

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

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

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

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

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

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

50 Because the therapies for myeloproliferative disorders differ, our data have major

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

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

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

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

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

56 ne investigated as a potential treatment for myeloproliferative disorders.

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

58 es to treat the energy imbalance observed in myeloproliferative disorders.

59 RAPL expression is widely abrogated in human myeloproliferative disorders.

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

61 increases p4EBP and pAKT levels and induces myeloproliferative expansion of plasmatocytes and crysta

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

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

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

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

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

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

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

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

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

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

72 Platelet LNK deficiency increases myeloproliferative leukemia virus oncogene signaling and

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

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

75 ascade are reviewed, including JAK2 exon 12, myeloproliferative leukemia virus oncogene, LNK (also kn

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

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

78 ed with defects in hematopoiesis, leading to myeloproliferative-like disease (leukemoid reaction), an

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

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

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

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

83 he reconstituted mice had developed a clonal myeloproliferative/myelodysplastic disorder originating

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

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

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

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

88 Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasia arising from the oncogenic

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

90 2(-/-)bone marrow failed to develop CML-like myeloproliferative neoplasia.

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

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

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

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

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

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

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

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

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

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

101 Myeloproliferative neoplasm (MPN) patients frequently sh

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

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

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

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

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

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

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

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

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

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

112 7F mutation is found in most patients with a myeloproliferative neoplasm (MPN).

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

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

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

116 Myelofibrosis is a chronic myeloproliferative neoplasm characterised by splenomegal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Current drugs for myeloproliferative neoplasm-associated myelofibrosis, in

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

146 a phenotype resembling the nonacute phase of myeloproliferative neoplasm.

147 myelodysplastic syndrome or myelodysplastic/myeloproliferative neoplasm.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 Myeloproliferative neoplasms (MPNs) are a group of clona

172 Myeloproliferative neoplasms (MPNs) are a group of relat

173 Myeloproliferative neoplasms (MPNs) are a group of relat

174 Myeloproliferative neoplasms (MPNs) are a set of chronic

175 Myeloproliferative neoplasms (MPNs) are associated with

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

177 Myeloproliferative neoplasms (MPNs) are characterized by

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

179 Human myeloproliferative neoplasms (MPNs) are thought to refle

180 Myeloproliferative neoplasms (MPNs) arise in the hematop

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

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

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

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

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

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

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

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

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

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

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

192 Myeloproliferative neoplasms (MPNs) often carry JAK2(V61

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

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

195 Myeloproliferative neoplasms (MPNs) such as chronic myel

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

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

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

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

200 The myeloproliferative neoplasms (MPNs), including essential

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 The myeloproliferative neoplasms are a group of haematologic

232 Myeloproliferative neoplasms are clonal disorders charac

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

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

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

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

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

238 Patients with myeloproliferative neoplasms carrying CALR mutations pre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 Myeloproliferative neoplasms, including polycythemia ver

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

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

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

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

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

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

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 atures of both myelodysplastic syndromes and myeloproliferative neoplasms.

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

273 of PDGFRB are uncommon Philadelphia-negative myeloproliferative neoplasms.

274 nant erythroid precursors from patients with myeloproliferative neoplasms.

275 om patients with chronic myeloid leukemia or myeloproliferative neoplasms.

276 contributes to impaired megakaryopoiesis in myeloproliferative neoplasms.

277 re phenotypic drivers in the pathogenesis of myeloproliferative neoplasms.

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

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

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

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

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

283 te megakaryoblastic leukemia and a subset of myeloproliferative neoplasms.

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

285 r understanding of the pathogenetic basis of myeloproliferative neoplasms.

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

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

288 he pathogenic mutant CALR-MPL interaction in 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 acrophage progenitors (GMPs), resulting in a myeloproliferative phenotype with accumulation of GMPs i

292 matory cytokine production, which promotes a myeloproliferative phenotype.

293 omotes myeloid differentiation to engender a myeloproliferative phenotype.

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

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

296 acute leukemia, myelodysplastic syndrome, or myeloproliferative syndrome were included.

297 ir deficiency results in a fatal lympho- and myeloproliferative syndrome.

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