ライフサイエンスコーパス: thrombocythemia

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

2 choice for high-risk patients with essential thrombocythemia.

3 s with idiopathic myelofibrosis or essential thrombocythemia.

4 muscle-invasive bladder cancer and essential thrombocythemia.

5 cells obtained from patients with essential thrombocythemia.

6 ormation between the 2 subtypes of essential thrombocythemia.

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

8 5 years in those with JAK2-mutated essential thrombocythemia.

9 to distinguish early-stage PV from essential thrombocythemia.

10 primary myelofibrosis (PMF) with presenting thrombocythemia.

11 yelofibrosis and polycythemia vera/essential thrombocythemia.

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

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

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

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

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

17 Essential thrombocythemia, a myeloproliferative neoplasm, is assoc

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

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

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

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

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

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

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

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

26 eloproliferative disorders such as essential thrombocythemia and idiopathic myelofibrosis.

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

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

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

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

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

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

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

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

35 Polycythemia vera, essential thrombocythemia and primary myelofibrosis are myeloproli

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

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

38 In essential thrombocythemia and primary myelofibrosis, CALR mutation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 phenotype of polycythemia vera and essential thrombocythemia are highlighted.

64 The pathogenesis of essential thrombocythemia as a clonal myeloproliferative disorder

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 Essential thrombocythemia (ET) is an indolent myeloproliferative n

93 Essential thrombocythemia (ET) is characterized by enhanced platel

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

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

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

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

98 Essential thrombocythemia (ET) manifests substantial interpatient

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 2 with polycythemia vera, 318 with essential thrombocythemia (ET), 88 with myelodysplastic syndrome,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 Among patients with essential thrombocythemia or primary myelofibrosis with nonmutated

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

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

155 pective, multicenter cohort of 776 essential thrombocythemia patients.

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

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

158 25.3 (SD, 17.2) for patients with essential thrombocythemia, polycythemia vera, and myelofibrosis, r

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

160 1, 1994, and December 31, 2013, of essential thrombocythemia, polycythemia vera, myelofibrosis, or un

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

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

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

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

165 The genetic lexicon of essential thrombocythemia remains incomplete.

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

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

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

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

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

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

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

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

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

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