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

1 nous leukemia, myelodysplastic syndrome, and myeloproliferative disorders).

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

3 lomonocytic leukemia (JMML) is a rare clonal myeloproliferative disorder.

4 s noted in more than half of patients with a myeloproliferative disorder.

5 smic tyrosine kinase JAK2 in patients with a myeloproliferative disorder.

6 atory features that were characteristic of a myeloproliferative disorder.

7 osinophilic syndrome (HES) and an underlying myeloproliferative disorder.

8 a retroviral transduction assay results in a myeloproliferative disorder.

9 nsion of repopulating cells accompanied by a myeloproliferative disorder.

10 ype 1 in patients with an atypical stem cell myeloproliferative disorder.

11 Chronic myelogenous leukemia is a myeloproliferative disorder.

12 ematopoiesis that can best be described as a myeloproliferative disorder.

13 n in Jak2 is associated with a proportion of myeloproliferative disorders.

14 w discusses how this process is unfolding in myeloproliferative disorders.

15 ne investigated as a potential treatment for myeloproliferative disorders.

16 ling in the Philadelphia chromosome negative myeloproliferative disorders.

17 derstanding of the molecular pathogenesis of myeloproliferative disorders.

18 2 have been identified in JAK2V617F negative myeloproliferative disorders.

19 veloping a specifically targeted therapy for myeloproliferative disorders.

20 se 2, found in the majority of patients with myeloproliferative disorders.

21 use for diseases such as leukemias and other myeloproliferative disorders.

22 eatment of JAK2(V617F)-positive PV and other myeloproliferative disorders.

23 on in Jak2 has recently been associated with myeloproliferative disorders.

24 derstanding of the molecular pathogenesis of myeloproliferative disorders.

25 V617F, and the pathogenesis of JAK2-negative myeloproliferative disorders.

26 patients with myelodysplastic syndromes and myeloproliferative disorders.

27 diagnosis, classification, and treatment of myeloproliferative disorders.

28 has recently been shown for the JAK2 gene in myeloproliferative disorders.

29 onocytic hyperplasia and progressed to fatal myeloproliferative disorders.

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

31 myelopoiesis under normal conditions and in myeloproliferative disorders.

32 RAPL expression is widely abrogated in human myeloproliferative disorders.

33 odysplastic characteristics with features of myeloproliferative disorders.

34 ell as methylation of these genes in several myeloproliferative disorders.

35 gulated protein tyrosine kinases involved in myeloproliferative disorders.

36 signaling pathway may contribute to various myeloproliferative disorders.

37 ntial use in the treatment of thrombotic and myeloproliferative disorders.

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

39 sions observed in patients with leukemia and myeloproliferative disorders.

40 ausal role of an activating JAK2 mutation in myeloproliferative disorders.

41 cilitates progression to the blast phases of myeloproliferative disorders.

42 cell disease, myelodysplastic syndromes, and myeloproliferative disorders.

43 potentially vascular events) associated with myeloproliferative disorders.

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

45 Primary polycythaemia is a myeloproliferative disorder, a non-malignant stem-cell d

46 mia (CML), the phenotype closely resembles a myeloproliferative disorder affecting the megakaryocytic

47 22 of 26 patients with clinical evidence of myeloproliferative disorder and 1 patient with clinicall

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

49 iscovered that nearly all cases of transient myeloproliferative disorder and acute megakaryocytic leu

50 eness of the role of trisomy 21 in transient myeloproliferative disorder and acute megakaryocytic leu

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

52 rmed stem cells that give rise to a distinct myeloproliferative disorder and T-lymphoblastic leukemia

53 itors, including the Down syndrome-transient myeloproliferative disorder and the thrombocytopenia abs

54 findings suggest new avenues for therapy of myeloproliferative disorders and atherosclerosis.

55 ents with polycythemia vera or other chronic myeloproliferative disorders and control subjects.

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

57 Myeloproliferative disorders and myelodysplastic syndrom

58 antineoplastic agent commonly used to treat myeloproliferative disorders and other nonneoplastic con

59 resent in patients with myelofibrosis due to myeloproliferative disorders and that these features are

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

61 ce, displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of

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

63 pulation, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atheroscler

64 ents with AML, DS infants with the transient myeloproliferative disorder, and Epstein-Barr Virus (EBV

65 er, a preleukemic condition termed transient myeloproliferative disorder, and increased incidence of

66 matory demyelinating polyradiculoneuropathy, myeloproliferative disorder, and monoclonal gammopathy o

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

68 tribute to the pathogenesis of JAK2-negative myeloproliferative disorders, and led to the discovery o

69 617F)) in essential thrombocythemia, related myeloproliferative disorders, and the impact on clinical

70 n to alter the diagnostic criteria for these myeloproliferative disorders, and these changes are revi

71 The classic BCR-ABL negative myeloproliferative disorders are at a crossroads of rapi

72 Patients with myeloproliferative disorders are at a high risk of devel

73 The myeloproliferative disorders are clonal disorders with f

74 Myelodysplasia and the myeloproliferative disorders are clonal hematopoietic st

75 this study, we have used the murine CML-like myeloproliferative disorder as a platform to characteriz

76 myeloid leukemia (CML) or polycythemia vera, myeloproliferative disorders associated with the BCR-ABL

77 leiotropic phenotype of JAK2V617F-associated myeloproliferative disorders been delineated.

78 Thus, oncogenic K-ras induces a myeloproliferative disorder but not AML, indicating that

79 Cre, LSL-Nras(G12D) mice develop an indolent myeloproliferative disorder but ultimately die of a dive

80 ated by thrombopoietin (THPO), is mutated in myeloproliferative disorders but rarely in AML.

81 D mutant proteins are sufficient to induce a myeloproliferative disorder, but are insufficient to rec

82 LSL-Kras(G12D) mice, which die of aggressive myeloproliferative disorder by 4 months of age.

83 oduct will contribute to progression of this myeloproliferative disorder by constitutive activation o

84 nt progress in the molecular pathogenesis of myeloproliferative disorders calls for a paradigm shift

85 In patients with myeloproliferative disorders CD177 mRNA overexpression i

86 romyelomonocyte leukemic cell line) and MPD (myeloproliferative disorder cell line), following differ

87 ogene causes chronic myelogenous leukemia, a myeloproliferative disorder characterized by clonal expa

88 causes chronic myelogenous leukemia (CML), a myeloproliferative disorder characterized by clonal expa

89 ICSBP-deficient mice develop a myeloproliferative disorder characterized by cytokine hy

90 anded MDR1-transduced stem cells developed a myeloproliferative disorder characterized by high periph

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

92 ile myelomonocytic leukemia is an aggressive myeloproliferative disorder characterized by malignant t

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

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

95 pathic hypereosinophilic syndrome (HES) is a myeloproliferative disorder characterized by persistent

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

97 myelodysplastic syndromes (MDSs) and chronic myeloproliferative disorders (CMDs) to population-based

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

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

100 The majority of the BCR-ABL-negative myeloproliferative disorders express the mutant JAK2, JA

101 n mouse haematopoietic stem cells leads to a myeloproliferative disorder, followed by acute T-lymphob

102 Human myeloproliferative disorders form a range of clonal haem

103 n blood counts relative to mutation-negative myeloproliferative disorders; future preclinical researc

104 f Janus kinase 2 and associated mutations in myeloproliferative disorders (> 95% in polycythemia vera

105 sis of essential thrombocythemia as a clonal myeloproliferative disorder has been clearly established

106 the classic Philadelphia-chromosome negative myeloproliferative disorders has made it a much anticipa

107 ysiology of Philadelphia-chromosome negative myeloproliferative disorders has significantly advanced

108 ing acute megakaryocytic leukemia, transient myeloproliferative disorder, Hirschsprung disease, duode

109 I571-treated mice were cured of the CML-like myeloproliferative disorder, however, and STI571-treated

110 ripheral blood and bone marrow, suggesting a myeloproliferative disorder; however, granulocyte precur

111 ated kinase 2 (JAK2) mutations are common in myeloproliferative disorders; however, although they are

112 was first described in 1879, classified as a myeloproliferative disorder in 1951, and characterized a

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

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

115 Bone marrow chimeras confirmed that the myeloproliferative disorder in lal(-/-) mice was primari

116 etroviral transduction efficiently induces a myeloproliferative disorder in mice resembling human CML

117 FLT3-ITDs induced an oligoclonal myeloproliferative disorder in mice, characterized by sp

118 le to generate specifically kRASG12D-induced myeloproliferative disorder in recipient fish.

119 ur results can explain the absence of clonal myeloproliferative disorders in mice (lifetime, 2 years)

120 has recently been described in a spectrum of myeloproliferative disorders including myelofibrosis wit

121 oid progenitors is a major characteristic of myeloproliferative disorders, including chronic myeloid

122 may contribute to phenotypic diversity among myeloproliferative disorders, including in the presence

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

124 tyrosine kinase (V617F) and bcr/abl-negative myeloproliferative disorders, including MMM.

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

126 Mll5 did not alter the phenotype of a fatal myeloproliferative disorder induced by oncogenic Kras in

127 brafish embryos, including rhabdomyosarcoma, myeloproliferative disorder, intestinal hyperplasia, and

128 Investigational approaches to myeloproliferative disorders involve targeting the bone

129 A recently described atypical myeloproliferative disorder is invariably associated wit

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

131 A major cause of morbidity in myeloproliferative disorders is thrombosis, although the

132 f pathologists and clinical investigators in myeloproliferative disorders; it was subsequently presen

133 matologic malignancies, including leukemias, myeloproliferative disorders, lymphomas, and multiple my

134 Cdc42-deficient mice developed a fatal myeloproliferative disorder manifested by significant le

135 gulated mast cell growth associated with the myeloproliferative disorder, mastocytosis.

136 obstruction to hepatic venous outflow, with myeloproliferative disorder (MPD) accounting for up to 4

137 nsformed with BCR-ABL(P210) initiated both a myeloproliferative disorder (MPD) and B-lymphoid leukemi

138 ature T-cell lymphomas (CD4(+), CD8(+)) or a myeloproliferative disorder (MPD) at increased rates and

139 etroviral transduction efficiently induces a myeloproliferative disorder (MPD) in mice resembling hum

140 etroviral transduction efficiently induces a myeloproliferative disorder (MPD) in mice resembling hum

141 BCR-ABL efficiently induces a myeloproliferative disorder (MPD) in mice, but progressi

142 mpared the effects of inhibitors of MEK in a myeloproliferative disorder (MPD) initiated by inactivat

143 PL) mutations, MPLW515L/K, were described in myeloproliferative disorder (MPD) patients.

144 ation of JunB in postnatal mice results in a myeloproliferative disorder (MPD) resembling early human

145 emia/lymphoma syndrome usually presents as a myeloproliferative disorder (MPD) that evolves to acute

146 mphoma syndrome usually presents itself as a myeloproliferative disorder (MPD) that evolves to acute

147 /-) hematopoietic stem cells develop a fatal myeloproliferative disorder (MPD) that models JMML.

148 zyme 12/15-lipoxygenase (12/15-LO) develop a myeloproliferative disorder (MPD) that progresses to tra

149 Chronic myelogenous leukemia is a myeloproliferative disorder (MPD) that, over time, progr

150 murine models ICSBP deficiency results in a myeloproliferative disorder (MPD) with increased mature

151 terozygous Nf1 mutant mice develop a similar myeloproliferative disorder (MPD), and adoptive transfer

152 BCS patients are found to have an underlying myeloproliferative disorder (MPD), antiplatelet therapy

153 myeloid and T-lymphoid lineages and develop myeloproliferative disorder (MPD).

154 tic leukemia, and Nf1 mutant mice model this myeloproliferative disorder (MPD).

155 e myelomonocytic leukemia (JMML), which is a myeloproliferative disorder (MPD).

156 The chronic myeloproliferative disorders (MPD) are clonal hematopoie

157 Myeloproliferative disorders (MPD) are stem cell-derived

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

159 myelodysplastic syndromes (MDS), overlap MDS/myeloproliferative disorders (MPD), MPD, and acute myelo

160 elofibrosis, and less frequently in atypical myeloproliferative disorders (MPD).

161 on mutation in the majority of patients with myeloproliferative disorders (MPD).

162 lofibrosis (PMF) as pathogenetically related myeloproliferative disorders (MPD).

163 an associated myelodysplastic syndrome (MDS)/myeloproliferative disorder [MPD]) based on in vitro stu

164 chromosomal abnormality associated with the myeloproliferative disorders (MPDs) and is also found in

165 is present in the majority of patients with myeloproliferative disorders (MPDs) and is implicated in

166 Because myeloproliferative disorders (MPDs) are a frequent cause

167 Myeloproliferative disorders (MPDs) are characterized by

168 Myeloproliferative disorders (MPDs) are characterized by

169 Myeloproliferative disorders (MPDs) are clonal malignanc

170 Myeloproliferative disorders (MPDs) are thought to be cl

171 ffective therapeutic agent for patients with myeloproliferative disorders (MPDs) or sickle cell disea

172 alence of this mutation in either "atypical" myeloproliferative disorders (MPDs) or the myelodysplast

173 Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, e

174 heral blood CD34(+) cells of 2 patients with myeloproliferative disorders (MPDs) who acquired the JAK

175 Eosinophilia is common in myeloproliferative disorders (MPDs) with abnormalities o

176 Myeloproliferative disorders (MPDs), either transient or

177 7F) mutation was found in most patients with myeloproliferative disorders (MPDs), including polycythe

178 ation (JAK2 V617F) is present in the chronic myeloproliferative disorders (MPDs), polycythemia vera (

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

180 2-V617F, a critical JAK2 mutation in various myeloproliferative disorders (MPDs).

181 aditional diagnostic classification of these myeloproliferative disorders (MPDs).

182 ine kinase was recently described in chronic myeloproliferative disorders (MPDs).

183 ly decreased on platelets from patients with myeloproliferative disorders (MPDs).

184 tients with Philadelphia chromosome-negative myeloproliferative disorders (MPDs).

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

186 The chronic myelogenous leukemia (CML)-like myeloproliferative disorder observed in the BCR/ABL muri

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

188 enile myelomonocytic leukemia, an aggressive myeloproliferative disorder of childhood.

189 kemia is an aggressive and frequently lethal myeloproliferative disorder of childhood.

190 lastic disorder reminiscent of the transient myeloproliferative disorder of Down syndrome.

191 me present with lymphoblastic lymphoma and a myeloproliferative disorder, often accompanied by pronou

192 We present here seven patients with myeloproliferative disorders or myelodysplastic syndrome

193 on and differentiation can lead to leukemia, myeloproliferative disorders, or marrow failure; however

194 ocus on the pathophysiology of thrombosis in myeloproliferative disorders, particularly in terms of t

195 chromosome 20 is a recurrent abnormality in myeloproliferative disorders, particularly polycythemia

196 athogenesis, including a contribution to the myeloproliferative disorder phenotype by a gain-of-funct

197 Familial or childhood occurrence of the myeloproliferative disorder polycythemia vera are also d

198 occurs in the majority of patients with the myeloproliferative disorders polycythemia vera, essentia

199 The myeloproliferative disorders polycythemia vera, essentia

200 molecular lesion in eosinophilia-associated myeloproliferative disorders, predicting a favorable res

201 Current therapy for myeloproliferative disorders remains largely based on pr

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

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

204 chromosomal aberrations and develop a fatal myeloproliferative disorder resembling chronic myelomono

205 mice known to develop, after long latency, a myeloproliferative disorder resembling human CML.

206 ronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplasti

207 onic myelomonocytic leukemia/myelodysplastic/myeloproliferative disorder similar to that seen in huma

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

209 a sizeable proportion of patients with other myeloproliferative disorders such as essential thrombocy

210 ations in chronic myeloid leukemia and other myeloproliferative disorders suggested the possibility t

211 poietic cells into irradiated mice induces a myeloproliferative disorder that did not respond to L-74

212 ytogenetic abnormality seen in a nonspecific myeloproliferative disorder that is associated with T-ce

213 ous miRNA, miR-125b, caused a dose-dependent myeloproliferative disorder that progressed to a lethal

214 id differentiation, and the development of a myeloproliferative disorder that progresses to acute mye

215 on of HoxA10 in murine bone marrow induces a myeloproliferative disorder that progresses to AML over

216 nd that expression of Bcr-Abl/p210 induced a myeloproliferative disorder that resembled the chronic p

217 CML is a myeloproliferative disorder that results from dysregulat

218 activity in eosinophilia-associated chronic myeloproliferative disorders that are characterized by a

219 a (ET) and polycythemia vera (PV) are clonal myeloproliferative disorders that are often difficult to

220 The molecular mechanisms in myeloproliferative disorders that prevent apoptosis indu

221 the diagnosis of an underlying Ph1-negative myeloproliferative disorder, that is, polycythemia vera

222 ribed in polycythemia vera and other BCR-ABL myeloproliferative disorders; the particular discovery h

223 derstanding of the molecular pathogenesis of myeloproliferative disorders, though many questions rema

224 2 related hematopoietic diseases: transient myeloproliferative disorder (TMD) and acute megakaryobla

225 al erythropoietic porphyria (CEP), transient myeloproliferative disorder (TMD) and acute megarakaryob

226 the pathogenesis of Down syndrome-transient myeloproliferative disorder (TMD) and Down syndrome-acut

227 th Down syndrome (DS) present with transient myeloproliferative disorder (TMD) at or shortly after bi

228 Both DS-AMKL and the related transient myeloproliferative disorder (TMD) have GATA1 mutations a

229 ) and in nearly every patient with transient myeloproliferative disorder (TMD), a "preleukemia" that

230 ividuals with DS who are born with transient myeloproliferative disorder (TMD), a clonal preleukemia,

231 a (AMKL); DS newborns present with transient myeloproliferative disorder (TMD), a preleukemic form of

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

233 en reported in Down syndrome (DS), transient myeloproliferative disorder (TMD), and acute megakaryobl

234 Transient myeloproliferative disorder (TMD), restricted to newborn

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

236 4%-5% of newborns with DS develop transient myeloproliferative disorder (TMD).

237 ndividuals with Down syndrome with transient myeloproliferative disorder (TMD, also called transient

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

239 scriptional regulatory genes, whereas in the myeloproliferative disorders tyrosine kinases are freque

240 617F in the Philadelphia-chromosome negative myeloproliferative disorders, unlike bcr/abl tyrosine ki

241 atients were further subdivided into primary myeloproliferative disorders versus secondary thrombocyt

242 It is of note, however, that no case of myeloproliferative disorder was observed.

243 se levels are elevated in some patients with myeloproliferative disorders, we examined their utility

244 ral blood mononuclear cells of patients with myeloproliferative disorders, we isolated numerous genes

245 To study clonal evolution in myeloproliferative disorders, we used stochastic models

246 h regulation of ROS levels and the resulting myeloproliferative disorder when dysregulated.

247 sent a novel in vivo model for a Myc-induced myeloproliferative disorder which can be controlled.

248 t mice, as they age, spontaneously develop a myeloproliferative disorder, which progresses from myelo

249 Patients with myeloproliferative disorders who were treated with hydro

250 ogenous murine locus rapidly induces a fatal myeloproliferative disorder with 100% penetrance charact

251 Somatic inactivation of Nf1 induces a myeloproliferative disorder with 100% penetrance that is

252 Sca(+/AE) mice develop a spontaneous myeloproliferative disorder with a latency of 6 months a

253 ion studies, HoxA10 overexpression induces a myeloproliferative disorder with accumulation of mature

254 hrocytosis (familial polycythemia) is a rare myeloproliferative disorder with an autosomal dominant m

255 First, a myeloproliferative disorder with features characteristic

256 was efficacious in treatment of progressive myeloproliferative disorder with organomegaly.

257 -formatted siRNA against SHIP1 resulted in a myeloproliferative disorder, with striking similarities

258 studies are needed to elucidate the cause of myeloproliferative disorders without known disease allel