ライフサイエンスコーパス: thrombocythemia

1 yelofibrosis and polycythemia vera/essential thrombocythemia.

2 olism (VTE) in pregnant women with essential thrombocythemia.

3 choice for high-risk patients with essential thrombocythemia.

4 s with idiopathic myelofibrosis or essential thrombocythemia.

5 3 has therapeutic potential for treatment of thrombocythemia.

6 muscle-invasive bladder cancer and essential thrombocythemia.

7 cells obtained from patients with essential thrombocythemia.

8 ormation between the 2 subtypes of essential thrombocythemia.

9 JAK2-mutated than in CALR-mutated essential thrombocythemia.

10 5 years in those with JAK2-mutated essential thrombocythemia.

11 to distinguish early-stage PV from essential thrombocythemia.

12 primary myelofibrosis (PMF) with presenting thrombocythemia.

13 types of 1.2 (95% CI, 1.0-1.6) for essential thrombocythemia, 1.4 (95% CI, 1.2-1.7) for polycythemia

14 wedish [28%]) in 161 patients with essential thrombocythemia, 145 patients with polycythemia vera, an

15 subjects developed overt MPD (8/11 essential thrombocythemia, 3/11 PV) after the diagnosis of BCS (me

16 for patients with MPNs (2628 with essential thrombocythemia, 3063 with polycythemia vera, 547 with m

17 NDs (9%; n = 22) or patients with essential thrombocythemia (6%; n = 15).

18 Essential thrombocythemia, a clonal myeloproliferative neoplasm wi

19 Essential thrombocythemia, a myeloproliferative neoplasm, is assoc

20 biologic and clinical features of essential thrombocythemia according to JAK2 or CALR mutation statu

21 Molecular lesions in essential thrombocythemia affect two distinct pathways: cytokine s

22 degree of clonal heterogeneity in essential thrombocythemia, although the clinical significance of t

23 g with polycythemia vera than with essential thrombocythemia, an increased risk of thrombosis, and an

24 were detected in 67% of those with essential thrombocythemia and 88% of those with primary myelofibro

25 Adult TGFbeta1-deficient mice exhibit thrombocythemia and a mild bleeding disorder that is sho

26 Among 281 patients with essential thrombocythemia and calreticulin (CALR) mutation, we fou

27 The main molecular basis of essential thrombocythemia and hereditary thrombocytosis is acquire

28 large proportions of patients with essential thrombocythemia and idiopathic myelofibrosis, and less f

29 eloproliferative disorders such as essential thrombocythemia and idiopathic myelofibrosis.

30 logy of platelet diseases, such as essential thrombocythemia and immune thrombocytopenia, and contrib

31 approximately 50% of patients with essential thrombocythemia and its presence has been associated wit

32 ALR) gene are seen in about 30% of essential thrombocythemia and myelofibrosis patients.

33 g the clonal expansion observed in essential thrombocythemia and polycythemia vera patients.

34 with the notion that JAK2-mutated essential thrombocythemia and polycythemia vera represent differen

35 Similarly, in essential thrombocythemia and polycythemia vera, treatments are pr

36 types that closely resembled human essential thrombocythemia and polycythemia vera.

37 at higher levels in patients with essential thrombocythemia and polycythemia vera.

38 cythemia vera, and roughly half of essential thrombocythemia and primary myelofibrosis acquire a uniq

39 ossibility that polycythemia vera, essential thrombocythemia and primary myelofibrosis are also cause

40 Polycythemia vera, essential thrombocythemia and primary myelofibrosis are myeloproli

41 f patients with polycythemia vera, essential thrombocythemia and primary myelofibrosis has diagnostic

42 ximately 6% and 14% of JAK2 V617F- essential thrombocythemia and primary myelofibrosis patients, resp

43 ra and about half of patients with essential thrombocythemia and primary myelofibrosis) has led the W

44 In essential thrombocythemia and primary myelofibrosis, CALR mutation

45 approximately 50% of patients with essential thrombocythemia and primary myelofibrosis, it has been h

46 ndividuals with polycythemia vera, essential thrombocythemia and primary myelofibrosis, there likely

47 ia vera and one-half of those with essential thrombocythemia and primary myelofibrosis.

48 n approximately half of those with essential thrombocythemia and primary myelofibrosis.

49 he treatment of polycythemia vera, essential thrombocythemia and primary myelofibrosis.

50 liferative leukemia (MPL)-negative essential thrombocythemia and primary myelofibrosis.

51 g of the molecular pathogenesis of essential thrombocythemia and related disorders, and offers opport

52 hrombogenic role of neutrophils in essential thrombocythemia and this might partly explain the superi

53 Patients with JAK2-mutated essential thrombocythemia and those with polycythemia vera had a s

54 oplasms (MF > polycythemia vera or essential thrombocythemia) and that LCN2 was elaborated by MF myel

55 ythemia vera, 12% of patients with essential thrombocythemia, and 0% of normal controls.

56 with primary myelofibrosis, 6 with essential thrombocythemia, and 2 with polycythemia vera) and 5 con

57 as a risk factor for thrombosis in essential thrombocythemia, and have also shown a tight association

58 pathogenesis of polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis.

59 including polycythemia vera (PV), essential thrombocythemia, and myelofibrosis (MF) (both primary an

60 ndividuals with polycythemia vera, essential thrombocythemia, and myelofibrosis and 252 637 populatio

61 ly described in polycythemia vera, essential thrombocythemia, and myelofibrosis with myeloid metaplas

62 t in samples of polycythemia vera, essential thrombocythemia, and myelofibrosis, respectively.

63 isorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibros

64 assess symptoms of myelofibrosis, essential thrombocythemia, and polycythemia vera among prospective

65 MPNs) including polycythemia vera, essential thrombocythemia, and primary myelofibrosis show an inher

66 oplasms (MPNs), polycythemia vera, essential thrombocythemia, and primary myelofibrosis, are hematopo

67 ients with polycythemia vera (PV), essential thrombocythemia, and primary myelofibrosis.

68 pathogenesis of polycythemia vera, essential thrombocythemia, and primary myelofibrosis.

69 PDs), including polycythemia vera, essential thrombocythemia, and primary myelofibrosis.

70 s identified in polycythemia vera, essential thrombocythemia, and primary myelofibrosis.

71 Patients with essential thrombocythemia are at increased risk of arterial thromb

72 phenotype of polycythemia vera and essential thrombocythemia are highlighted.

73 The pathogenesis of essential thrombocythemia as a clonal myeloproliferative disorder

74 lthough it is in vogue to consider essential thrombocythemia as more than one disease in terms of bot

75 A recent study of patients with essential thrombocythemia at high risk of thrombosis because of ad

76 galy, megakaryocytic hyperplasia, and marked thrombocythemia, but without leukocytosis, polycythemia,

77 approximately 10% of patients with essential thrombocythemia develop myelofibrosis and about 3% devel

78 Treatments for high-risk essential thrombocythemia (ET) address thrombocytosis, disease-rel

79 approximately 50% of patients with essential thrombocythemia (ET) and idiopathic myelofibrosis (IMF)

80 era (PV) and in some patients with essential thrombocythemia (ET) and myeloid metaplasia/myelofibrosi

81 ity and mortality in patients with essential thrombocythemia (ET) and polycythemia rubra vera (PV) st

82 Essential thrombocythemia (ET) and polycythemia vera (PV) are clon

83 Patients with essential thrombocythemia (ET) and polycythemia vera (PV) have an

84 goal of therapy for patients with essential thrombocythemia (ET) and polycythemia vera (PV) is to re

85 miaNet (ELN) response criteria for essential thrombocythemia (ET) and polycythemia vera (PV) issued i

86 FN-alpha) therapy in patients with essential thrombocythemia (ET) and polycythemia vera (PV).

87 PEG-IFN-alpha-2a) in patients with essential thrombocythemia (ET) and polycythemia vera (PV).

88 Essential thrombocythemia (ET) and primary myelofibrosis (PMF) are

89 scovered in patients with sporadic essential thrombocythemia (ET) and primary myelofibrosis (PMF) lac

90 ) MPDs are polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF).

91 approximately 40% of patients with essential thrombocythemia (ET) and primary myelofibrosis (PMF).

92 ons are specific to JAK2-unmutated essential thrombocythemia (ET) and primary myelofibrosis (PMF).

93 recently been approved for use in essential thrombocythemia (ET) and related disorders.

94 ized in polycythemia vera (PV) and essential thrombocythemia (ET) and shown to contribute to a higher

95 Patients with essential thrombocythemia (ET) are at high risk for both thrombosi

96 isms of polycythemia vera (PV) and essential thrombocythemia (ET) are challenging the traditional dia

97 High platelet counts in essential thrombocythemia (ET) can be effectively lowered by treat

98 stance to aspirin in patients with essential thrombocythemia (ET) can be reversed by twice daily dosi

99 Health Organization (WHO)-defined essential thrombocythemia (ET) compared with early/prefibrotic pri

100 ts with polycythemia vera (PV) and essential thrombocythemia (ET) has been associated with an increas

101 Diagnosis of essential thrombocythemia (ET) has been updated in the last World

102 ferative disorders (MPDs), such as essential thrombocythemia (ET) have increased risk of thrombosis a

103 ts with polycythemia vera (PV) and essential thrombocythemia (ET) have moderately reduced survival in

104 Essential thrombocythemia (ET) is an indolent myeloproliferative n

105 Essential thrombocythemia (ET) is characterized by abnormal megaka

106 Essential thrombocythemia (ET) is characterized by enhanced platel

107 histopathology in the diagnosis of essential thrombocythemia (ET) is controversial, and there has bee

108 Essential thrombocythemia (ET) is heterogeneous with respect to na

109 ficant proportion of patients with essential thrombocythemia (ET) lacking JAK2(V617F) or MPL mutation

110 cently discovered in patients with essential thrombocythemia (ET) lacking the JAK2V617F and MPLW515 m

111 Essential thrombocythemia (ET) manifests substantial interpatient

112 ns of MPL exon 10 in patients with essential thrombocythemia (ET) or primary myelofibrosis (PMF), fir

113 pproximately half of patients with essential thrombocythemia (ET) or primary myelofibrosis (PMF).

114 Essential Thrombocythemia (ET) patients at high-risk of thrombosis

115 IFNalpha therapy in a cohort of 31 essential thrombocythemia (ET) patients with CALR mutations (mean

116 and Rotunno et al demonstrate that essential thrombocythemia (ET) patients with calreticulin mutation

117 are found in approximately 50% of essential thrombocythemia (ET) patients, suggesting that convergin

118 ating activation of platelets from essential thrombocythemia (ET) patients.

119 V) patients, but not in those from essential thrombocythemia (ET) patients.

120 curate prediction of thrombosis in essential thrombocythemia (ET) provides the platform for prospecti

121 ve cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia vera (alle

122 s higher activity in patients with essential thrombocythemia (ET) than in polycythemia vera (PV) and

123 cked oncogenic colony formation in essential thrombocythemia (ET) through inverse agonism.

124 Essential thrombocythemia (ET) was first described in 1934, and su

125 mutational spectrum is detected in essential thrombocythemia (ET) with mutations in JAK2, the thrombo

126 tients with myelofibrosis (MF) and essential thrombocythemia (ET) with nonmutated Janus kinase 2 (JAK

127 s: 30 with PV, 22 with SP, 14 with essential thrombocythemia (ET), 12 with myelofibrosis with myeloid

128 ients with thrombocytosis-164 with essential thrombocythemia (ET), 19 with reactive thrombocytosis (R

129 Polycythemia vera (PV) and essential thrombocythemia (ET), 2 subtypes of myeloproliferative n

130 2 with polycythemia vera, 318 with essential thrombocythemia (ET), 88 with myelodysplastic syndrome,

131 including polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF).

132 including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (MF).

133 Polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) co

134 , of which polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) ha

135 associated with polycythemia vera, essential thrombocythemia (ET), and primary myelofibrosis (PMF) wh

136 , that is, polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), a

137 including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).

138 iated with polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).

139 including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).

140 s) include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).

141 including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).

142 mon in polycythemia vera (PV) than essential thrombocythemia (ET), but their prevalence and significa

143 anifest as polycythemia vera (PV), essential thrombocythemia (ET), or primary myelofibrosis.

144 vera (PV) is not a continuum from essential thrombocythemia (ET), that survival in ET is less than m

145 ted that a 3-member subset defines essential thrombocythemia (ET).

146 nts with polycythemia vera (PV) or essential thrombocythemia (ET).

147 iopathic myelofibrosis (CIMF), and essential thrombocythemia (ET).

148 s reminiscent of the human disease essential thrombocythemia (ET).

149 o being polycythemia vera (PV) and essential thrombocythemia (ET).

150 (MF), polycythemia vera (PV), and essential thrombocythemia (ET).

151 nts with polycythemia vera (PV) or essential thrombocythemia (ET).

152 ts with polycythemia vera (PV) and essential thrombocythemia (ET).

153 icable to primary (0.718) and post-essential thrombocythemia (ET)/polycythemia vera (PV) myelofibrosi

154 mprises several entities including essential thrombocythemia (ET); primary myelofibrosis (PMF); and M

155 heir capacity to delineate clonal (essential thrombocythemia [ET]) from nonclonal (reactive thrombocy

156 h subtype (polycythemia vera [PV], essential thrombocythemia [ET], prefibrotic myelofibrosis [MF], an

157 MPN subtypes (essential thrombocythemia [ET]; polycythemia vera [PV]) were compa

158 (TpoR) drive sporadic and familial essential thrombocythemias (ETs).

159 Median survival in essential thrombocythemia exceeds 20 years and clinical course is

160 tion, and molecular distinction of essential thrombocythemia from related disorders such as polycythe

161 Patients with essential thrombocythemia have a persistent platelet count of 450

162 roximately 90% of individuals with essential thrombocythemia have genetic variants that upregulate th

163 thrombocytopenia or in gain-of-function and thrombocythemia (HT), and are important models to analyz

164 ing increased platelet production (Essential Thrombocythemia, Idiopathic Thrombocytopenic Purpura) an

165 The annual incidence rate of essential thrombocythemia in the US is 1.5/100 000 persons.

166 n young patients; for example, for essential thrombocythemia, in particular, there is a second peak i

167 s in late-phase clinical trials in essential thrombocythemia, in which it could fill an important voi

168 n a family with autosomal dominant essential thrombocythemia, increased cell growth resulting from su

169 The median age at diagnosis of essential thrombocythemia is 59 years.

170 ive neoplasm, whereas CALR-mutated essential thrombocythemia is a distinct disease entity.

171 Essential thrombocythemia is a rare clonal myeloproliferative neop

172 fibrotic disease transformation in essential thrombocythemia is an infrequent occurrence with a 15-ye

173 ctors for thrombosis, persons with essential thrombocythemia may be treated with low-dose aspirin, ei

174 Patients with essential thrombocythemia may carry JAK2 (V617F), an MPL substitut

175 post-polycythemia vera MF, or post-essential thrombocythemia MF were randomly assigned between Decemb

176 and post-polycythemia vera and postessential thrombocythemia myelofibrosis (MF) is dominated by splen

177 themia vera myelofibrosis, or post-essential thrombocythemia myelofibrosis to receive oral ruxolitini

178 gative primary myelofibrosis, post-essential thrombocythemia myelofibrosis, or post-polycythemia vera

179 ative disorders polycythemia vera, essential thrombocythemia, myelofibrosis with myeloid metaplasia,

180 rative neoplasms (MPNs), including essential thrombocythemia, myelofibrosis, and polycythemia vera (P

181 onic idiopathic myelofibrosis, and essential thrombocythemia (n = 103) was similar to the previously

182 vera, n = 192, P = 2.9 x 10(-16); essential thrombocythemia, n = 78, P = 8.2 x 10(-9) and myelofibro

183 JAK2V617F(+)Mpl(-/-) mice exhibited reduced thrombocythemia, neutrophilia, splenomegaly, and neoplas

184 or myelofibrosis (MF) preceded by essential thrombocythemia or polycythemia vera were enrolled into

185 ters of patients with JAK2-mutated essential thrombocythemia or polycythemia vera were related to the

186 imately 50 to 60% of patients with essential thrombocythemia or primary myelofibrosis carry a mutatio

187 mately one-fourth of patients with essential thrombocythemia or primary myelofibrosis carry a somatic

188 V617F mutation, half of those with essential thrombocythemia or primary myelofibrosis do not, suggest

189 Most patients with essential thrombocythemia or primary myelofibrosis that was not as

190 e been found in most patients with essential thrombocythemia or primary myelofibrosis with nonmutated

191 Among patients with essential thrombocythemia or primary myelofibrosis with nonmutated

192 will yield strategies to treat patients with thrombocythemia or thrombocytopenia.

193 technology, further insights into essential thrombocythemia pathogenesis are likely close at hand.

194 pective, multicenter cohort of 776 essential thrombocythemia patients.

195 mation and increased risk of bleeding, while thrombocythemia (platelet counts greater than 600,000/mi

196 rative neoplasms (MPNs), including essential thrombocythemia, polycythemia vera and primary myelofibr

197 25.3 (SD, 17.2) for patients with essential thrombocythemia, polycythemia vera, and myelofibrosis, r

198 ons are prevalent in patients with essential thrombocythemia, polycythemia vera, and myelofibrosis.

199 eloproliferative neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primary myelofib

200 1, 1994, and December 31, 2013, of essential thrombocythemia, polycythemia vera, myelofibrosis, or un

201 ndices across both primary and postessential thrombocythemia/polycythemia vera MF subgroups.

202 om antecedent polycythemia vera or essential thrombocythemia, presents many challenges to the hematol

203 cular complications (mainly PV and essential thrombocythemia), prevention of hematological progressio

204 or end-stage polycythemia vera or essential thrombocythemia received allogeneic hematopoietic cell t

205 kinase mutation (JAK2 (V617F)) in essential thrombocythemia, related myeloproliferative disorders, a

206 The genetic lexicon of essential thrombocythemia remains incomplete.

207 y that the aim of cytoreduction in essential thrombocythemia should be to keep the platelet count, an

208 MPD, we identified 34 patients with sporadic thrombocythemia (ST), 16 with hereditary thrombocytosis

209 to three times less likely to have essential thrombocythemia than carriers with high PGSs.

210 s suggested for most patients with essential thrombocythemia to lower thrombosis risk.

211 ite problem occurs in the case of hereditary thrombocythemia: translational efficiency is increased b

212 y, their role in polycythemia vera/essential thrombocythemia treatment is still being defined.

213 ythemia vera, and 17 patients with essential thrombocythemia was also studied.

214 Using a mouse model of JAK2 V617F essential thrombocythemia, we show that a lack of CRLF3 leads to l

215 ate STAT1, promoting platelet production and thrombocythemia, whereas homozygous progenitors activate

216 oproliferation which characterizes essential thrombocythemia, whereas the phenotypic consequences of

217 arker of a subset of patients with essential thrombocythemia who are at increased risk of thromboembo

218 lecular responses in patients with essential thrombocythemia who had not had a response to or who had

219 ses were observed in patients with essential thrombocythemia who received imetelstat.

220 genetics of polycythemia vera and essential thrombocythemia, with an emphasis on JAK2V617F pathophys