ライフサイエンスコーパス: essential thrombocythemia

1 tment of myelofibrosis and polycythemia vera/essential thrombocythemia.

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

3 e drug of choice for high-risk patients with essential thrombocythemia.

4 of patients with idiopathic myelofibrosis or essential thrombocythemia.

5 tudies of muscle-invasive bladder cancer and essential thrombocythemia.

6 n vitro in cells obtained from patients with essential thrombocythemia.

7 tic transformation between the 2 subtypes of essential thrombocythemia.

8 s lower in JAK2-mutated than in CALR-mutated essential thrombocythemia.

9 s 29% at 15 years in those with JAK2-mutated essential thrombocythemia.

10 specially to distinguish early-stage PV from essential thrombocythemia.

11 or the subtypes of 1.2 (95% CI, 1.0-1.6) for essential thrombocythemia, 1.4 (95% CI, 1.2-1.7) for pol

12 6%], and Swedish [28%]) in 161 patients with essential thrombocythemia, 145 patients with polycythemi

13 ven of 41 subjects developed overt MPD (8/11 essential thrombocythemia, 3/11 PV) after the diagnosis

14 , 4.6-5.9) for patients with MPNs (2628 with essential thrombocythemia, 3063 with polycythemia vera,

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

16 Essential thrombocythemia, a clonal myeloproliferative n

17 Essential thrombocythemia, a myeloproliferative neoplasm

18 We studied biologic and clinical features of essential thrombocythemia according to JAK2 or CALR muta

19 Molecular lesions in essential thrombocythemia affect two distinct pathways:

20 surprising degree of clonal heterogeneity in essential thrombocythemia, although the clinical signifi

21 presenting with polycythemia vera than with essential thrombocythemia, an increased risk of thrombos

22 mutations were detected in 67% of those with essential thrombocythemia and 88% of those with primary

23 Among 281 patients with essential thrombocythemia and calreticulin (CALR) mutati

24 The main molecular basis of essential thrombocythemia and hereditary thrombocytosis

25 era (PV), large proportions of patients with essential thrombocythemia and idiopathic myelofibrosis,

26 h other myeloproliferative disorders such as essential thrombocythemia and idiopathic myelofibrosis.

27 athophysiology of platelet diseases, such as essential thrombocythemia and immune thrombocytopenia, a

28 V617F) in approximately 50% of patients with essential thrombocythemia and its presence has been asso

29 ticulin (CALR) gene are seen in about 30% of essential thrombocythemia and myelofibrosis patients.

30 n mimicking the clonal expansion observed in essential thrombocythemia and polycythemia vera patients

31 consistent with the notion that JAK2-mutated essential thrombocythemia and polycythemia vera represen

32 Similarly, in essential thrombocythemia and polycythemia vera, treatme

33 oped phenotypes that closely resembled human essential thrombocythemia and polycythemia vera.

34 re present at higher levels in patients with essential thrombocythemia and polycythemia vera.

35 es of polycythemia vera, and roughly half of essential thrombocythemia and primary myelofibrosis acqu

36 Polycythemia vera, essential thrombocythemia and primary myelofibrosis are

37 sted the possibility that polycythemia vera, essential thrombocythemia and primary myelofibrosis are

38 majority of patients with polycythemia vera, essential thrombocythemia and primary myelofibrosis has

39 Approximately 6% and 14% of JAK2 V617F- essential thrombocythemia and primary myelofibrosis pati

40 ythemia vera and about half of patients with essential thrombocythemia and primary myelofibrosis) has

41 In essential thrombocythemia and primary myelofibrosis, CAL

42 vera and approximately 50% of patients with essential thrombocythemia and primary myelofibrosis, it

43 in most individuals with polycythemia vera, essential thrombocythemia and primary myelofibrosis, the

44 vera and in approximately half of those with essential thrombocythemia and primary myelofibrosis.

45 icacy in the treatment of polycythemia vera, essential thrombocythemia and primary myelofibrosis.

46 d myeloproliferative leukemia (MPL)-negative essential thrombocythemia and primary myelofibrosis.

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

48 derstanding of the molecular pathogenesis of essential thrombocythemia and related disorders, and off

49 ding the thrombogenic role of neutrophils in essential thrombocythemia and this might partly explain

50 Patients with JAK2-mutated essential thrombocythemia and those with polycythemia ve

51 erative neoplasms (MF > polycythemia vera or essential thrombocythemia) and that LCN2 was elaborated

52 with polycythemia vera, 12% of patients with essential thrombocythemia, and 0% of normal controls.

53 h MPNs (4 with primary myelofibrosis, 6 with essential thrombocythemia, and 2 with polycythemia vera)

54 AK2 V617F as a risk factor for thrombosis in essential thrombocythemia, and have also shown a tight a

55 le in the pathogenesis of polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis.

56 neoplasms, including polycythemia vera (PV), essential thrombocythemia, and myelofibrosis (MF) (both

57 t of 726 individuals with polycythemia vera, essential thrombocythemia, and myelofibrosis and 252 637

58 was recently described in polycythemia vera, essential thrombocythemia, and myelofibrosis with myeloi

59 per patient in samples of polycythemia vera, essential thrombocythemia, and myelofibrosis, respective

60 ferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with m

61 entory) to assess symptoms of myelofibrosis, essential thrombocythemia, and polycythemia vera among p

62 eoplasms (MPNs) including polycythemia vera, essential thrombocythemia, and primary myelofibrosis sho

63 erative neoplasms (MPNs), polycythemia vera, essential thrombocythemia, and primary myelofibrosis, ar

64 ity of patients with polycythemia vera (PV), essential thrombocythemia, and primary myelofibrosis.

65 le in the pathogenesis of polycythemia vera, essential thrombocythemia, and primary myelofibrosis.

66 sorders (MPDs), including polycythemia vera, essential thrombocythemia, and primary myelofibrosis.

67 utation was identified in polycythemia vera, essential thrombocythemia, and primary myelofibrosis.

68 Patients with essential thrombocythemia are at increased risk of arter

69 d disease phenotype of polycythemia vera and essential thrombocythemia are highlighted.

70 The pathogenesis of essential thrombocythemia as a clonal myeloproliferative

71 Although it is in vogue to consider essential thrombocythemia as more than one disease in te

72 A recent study of patients with essential thrombocythemia at high risk of thrombosis bec

73 iagnosis, approximately 10% of patients with essential thrombocythemia develop myelofibrosis and abou

74 Treatments for high-risk essential thrombocythemia (ET) address thrombocytosis, d

75 s well as approximately 50% of patients with essential thrombocythemia (ET) and idiopathic myelofibro

76 cythemia vera (PV) and in some patients with essential thrombocythemia (ET) and myeloid metaplasia/my

77 pal morbidity and mortality in patients with essential thrombocythemia (ET) and polycythemia rubra ve

78 -alpha (rIFN-alpha) therapy in patients with essential thrombocythemia (ET) and polycythemia vera (PV

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

80 Essential thrombocythemia (ET) and polycythemia vera (PV

81 The goal of therapy for patients with essential thrombocythemia (ET) and polycythemia vera (PV

82 pean LeukemiaNet (ELN) response criteria for essential thrombocythemia (ET) and polycythemia vera (PV

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

84 main Ph(-) MPDs are polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis

85 tected in approximately 40% of patients with essential thrombocythemia (ET) and primary myelofibrosis

86 Essential thrombocythemia (ET) and primary myelofibrosis

87 ecently discovered in patients with sporadic essential thrombocythemia (ET) and primary myelofibrosis

88 PL) mutations are specific to JAK2-unmutated essential thrombocythemia (ET) and primary myelofibrosis

89 t that has recently been approved for use in essential thrombocythemia (ET) and related disorders.

90 characterized in polycythemia vera (PV) and essential thrombocythemia (ET) and shown to contribute t

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

92 lar mechanisms of polycythemia vera (PV) and essential thrombocythemia (ET) are challenging the tradi

93 High platelet counts in essential thrombocythemia (ET) can be effectively lowere

94 mical resistance to aspirin in patients with essential thrombocythemia (ET) can be reversed by twice

95 with World Health Organization (WHO)-defined essential thrombocythemia (ET) compared with early/prefi

96 in patients with polycythemia vera (PV) and essential thrombocythemia (ET) has been associated with

97 Diagnosis of essential thrombocythemia (ET) has been updated in the l

98 myeloproliferative disorders (MPDs), such as essential thrombocythemia (ET) have increased risk of th

99 eas patients with polycythemia vera (PV) and essential thrombocythemia (ET) have moderately reduced s

100 Essential thrombocythemia (ET) is an indolent myeloproli

101 Essential thrombocythemia (ET) is characterized by abnor

102 Essential thrombocythemia (ET) is characterized by enhan

103 e role of histopathology in the diagnosis of essential thrombocythemia (ET) is controversial, and the

104 Essential thrombocythemia (ET) is heterogeneous with res

105 in a significant proportion of patients with essential thrombocythemia (ET) lacking JAK2(V617F) or MP

106 ne were recently discovered in patients with essential thrombocythemia (ET) lacking the JAK2V617F and

107 Essential thrombocythemia (ET) manifests substantial int

108 ccurs in approximately half of patients with essential thrombocythemia (ET) or primary myelofibrosis

109 ed mutations of MPL exon 10 in patients with essential thrombocythemia (ET) or primary myelofibrosis

110 Essential Thrombocythemia (ET) patients at high-risk of

111 sponse to IFNalpha therapy in a cohort of 31 essential thrombocythemia (ET) patients with CALR mutati

112 umi et al and Rotunno et al demonstrate that essential thrombocythemia (ET) patients with calreticuli

113 ents, they are found in approximately 50% of essential thrombocythemia (ET) patients, suggesting that

114 ates indicating activation of platelets from essential thrombocythemia (ET) patients.

115 ia vera (PV) patients, but not in those from essential thrombocythemia (ET) patients.

116 Accurate prediction of thrombosis in essential thrombocythemia (ET) provides the platform for

117 7F)-positive cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia

118 thway shows higher activity in patients with essential thrombocythemia (ET) than in polycythemia vera

119 t also blocked oncogenic colony formation in essential thrombocythemia (ET) through inverse agonism.

120 Essential thrombocythemia (ET) was first described in 19

121 s a wider mutational spectrum is detected in essential thrombocythemia (ET) with mutations in JAK2, t

122 ound in patients with myelofibrosis (MF) and essential thrombocythemia (ET) with nonmutated Janus kin

123 88 subjects: 30 with PV, 22 with SP, 14 with essential thrombocythemia (ET), 12 with myelofibrosis wi

124 of 183 patients with thrombocytosis-164 with essential thrombocythemia (ET), 19 with reactive thrombo

125 Polycythemia vera (PV) and essential thrombocythemia (ET), 2 subtypes of myeloproli

126 th MMM, 242 with polycythemia vera, 318 with essential thrombocythemia (ET), 88 with myelodysplastic

127 ms (MPNs), including polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF).

128 neoplasms, including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

129 2V617F is associated with polycythemia vera, essential thrombocythemia (ET), and primary myelofibrosi

130 tion associated with polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

131 henotypes, including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

132 stem cells, of which polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

133 ms (MPNs), including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

134 lasms (MPNs) include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

135 3 subtypes, that is, polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

136 Polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

137 sms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosi

138 e more common in polycythemia vera (PV) than essential thrombocythemia (ET), but their prevalence and

139 that can manifest as polycythemia vera (PV), essential thrombocythemia (ET), or primary myelofibrosis

140 lycythemia vera (PV) is not a continuum from essential thrombocythemia (ET), that survival in ET is l

141 s in patients with polycythemia vera (PV) or essential thrombocythemia (ET).

142 chronic idiopathic myelofibrosis (CIMF), and essential thrombocythemia (ET).

143 ng features reminiscent of the human disease essential thrombocythemia (ET).

144 e other two being polycythemia vera (PV) and essential thrombocythemia (ET).

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

146 s in patients with polycythemia vera (PV) or essential thrombocythemia (ET).

147 eat patients with polycythemia vera (PV) and essential thrombocythemia (ET).

148 demonstrated that a 3-member subset defines essential thrombocythemia (ET).

149 ained applicable to primary (0.718) and post-essential thrombocythemia (ET)/polycythemia vera (PV) my

150 (MPNs) comprises several entities including essential thrombocythemia (ET); primary myelofibrosis (P

151 mited in their capacity to delineate clonal (essential thrombocythemia [ET]) from nonclonal (reactive

152 fic to each subtype (polycythemia vera [PV], essential thrombocythemia [ET], prefibrotic myelofibrosi

153 MPN subtypes (essential thrombocythemia [ET]; polycythemia vera [PV])

154 receptor (TpoR) drive sporadic and familial essential thrombocythemias (ETs).

155 Median survival in essential thrombocythemia exceeds 20 years and clinical

156 stratification, and molecular distinction of essential thrombocythemia from related disorders such as

157 Patients with essential thrombocythemia have a persistent platelet cou

158 Approximately 90% of individuals with essential thrombocythemia have genetic variants that upr

159 ies involving increased platelet production (Essential Thrombocythemia, Idiopathic Thrombocytopenic P

160 The annual incidence rate of essential thrombocythemia in the US is 1.5/100 000 perso

161 do occur in young patients; for example, for essential thrombocythemia, in particular, there is a sec

162 olitinib is in late-phase clinical trials in essential thrombocythemia, in which it could fill an imp

163 entified in a family with autosomal dominant essential thrombocythemia, increased cell growth resulti

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

165 proliferative neoplasm, whereas CALR-mutated essential thrombocythemia is a distinct disease entity.

166 Essential thrombocythemia is a rare clonal myeloprolifer

167 hemic, or fibrotic disease transformation in essential thrombocythemia is an infrequent occurrence wi

168 al risk factors for thrombosis, persons with essential thrombocythemia may be treated with low-dose a

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

170 imary MF, post-polycythemia vera MF, or post-essential thrombocythemia MF were randomly assigned betw

171 ost-polycythemia vera myelofibrosis, or post-essential thrombocythemia myelofibrosis to receive oral

172 2 V617F-negative primary myelofibrosis, post-essential thrombocythemia myelofibrosis, or post-polycyt

173 loproliferative disorders polycythemia vera, essential thrombocythemia, myelofibrosis with myeloid me

174 eloproliferative neoplasms (MPNs), including essential thrombocythemia, myelofibrosis, and polycythem

175 vera, chronic idiopathic myelofibrosis, and essential thrombocythemia (n = 103) was similar to the p

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

177 lofibrosis or myelofibrosis (MF) preceded by essential thrombocythemia or polycythemia vera were enro

178 gic parameters of patients with JAK2-mutated essential thrombocythemia or polycythemia vera were rela

179 Approximately one-fourth of patients with essential thrombocythemia or primary myelofibrosis carry

180 Approximately 50 to 60% of patients with essential thrombocythemia or primary myelofibrosis carry

181 y the JAK2V617F mutation, half of those with essential thrombocythemia or primary myelofibrosis do no

182 Most patients with essential thrombocythemia or primary myelofibrosis that

183 culin, have been found in most patients with essential thrombocythemia or primary myelofibrosis with

184 Among patients with essential thrombocythemia or primary myelofibrosis with

185 sequencing technology, further insights into essential thrombocythemia pathogenesis are likely close

186 in a prospective, multicenter cohort of 776 essential thrombocythemia patients.

187 eloproliferative neoplasms (MPNs), including essential thrombocythemia, polycythemia vera and primary

188 complications are prevalent in patients with essential thrombocythemia, polycythemia vera, and myelof

189 16.3), and 25.3 (SD, 17.2) for patients with essential thrombocythemia, polycythemia vera, and myelof

190 egative myeloproliferative neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primar

191 n January 1, 1994, and December 31, 2013, of essential thrombocythemia, polycythemia vera, myelofibro

192 evolved from antecedent polycythemia vera or essential thrombocythemia, presents many challenges to t

193 cardiovascular complications (mainly PV and essential thrombocythemia), prevention of hematological

194 osis (IMF) or end-stage polycythemia vera or essential thrombocythemia received allogeneic hematopoie

195 2 tyrosine kinase mutation (JAK2 (V617F)) in essential thrombocythemia, related myeloproliferative di

196 The genetic lexicon of essential thrombocythemia remains incomplete.

197 data imply that the aim of cytoreduction in essential thrombocythemia should be to keep the platelet

198 them two to three times less likely to have essential thrombocythemia than carriers with high PGSs.

199 00 mg/d) is suggested for most patients with essential thrombocythemia to lower thrombosis risk.

200 sis therapy, their role in polycythemia vera/essential thrombocythemia treatment is still being defin

201 with polycythemia vera, and 17 patients with essential thrombocythemia was also studied.

202 Using a mouse model of JAK2 V617F essential thrombocythemia, we show that a lack of CRLF3

203 g the myeloproliferation which characterizes essential thrombocythemia, whereas the phenotypic conseq

204 lso a biomarker of a subset of patients with essential thrombocythemia who are at increased risk of t

205 gic and molecular responses in patients with essential thrombocythemia who had not had a response to

206 lar responses were observed in patients with essential thrombocythemia who received imetelstat.

207 molecular genetics of polycythemia vera and essential thrombocythemia, with an emphasis on JAK2V617F