ライフサイエンスコーパス: polycythemia vera

1 coid receptor has been reported increased in polycythemia vera.

2 e in primary cells from patients with CML or polycythemia vera.

3 esembled human essential thrombocythemia and polycythemia vera.

4 ls, but not T cells, in patients with CML or polycythemia vera.

5 r impact on current diagnostic approaches in polycythemia vera.

6 r of myeloproliferative diseases, especially polycythemia vera.

7 lume, and improving symptoms associated with polycythemia vera.

8 of multiple genetic events in the genesis of polycythemia vera.

9 uch as anemia, myelodysplastic syndrome, and polycythemia vera.

10 patients with essential thrombocythemia and polycythemia vera.

11 mutation status and in relation to those of polycythemia vera.

12 a is an immunomodulatory agent used to treat polycythemia vera.

13 ms showed that CALR mutations were absent in polycythemia vera.

14 sis obtained at time of initial diagnosis of polycythemia vera.

15 hematopoietic progenitors from patients with polycythemia vera.

16 l thrombocythemia, 1.4 (95% CI, 1.2-1.7) for polycythemia vera, 1.7 (95% CI, 0.8-4.0) for myelofibros

17 % of patients with MMM, 33% of patients with polycythemia vera, 12% of patients with essential thromb

18 Twenty-one (39%) had polycythemia vera, 3 (5.6%) used estrogens, 11 (20%) had

19 7F mutational status: 290 with MMM, 242 with polycythemia vera, 318 with essential thrombocythemia (E

20 28 with essential thrombocythemia, 3063 with polycythemia vera, 547 with myelofibrosis, and 1720 with

21 lecular method for classifying patients with polycythemia vera according to disease behavior, indepen

22 h essential thrombocythemia (ET) rather than polycythemia vera (allelic chi(2) P=7.3 x 10(-7)).

23 yelofibrosis, essential thrombocythemia, and polycythemia vera among prospective cohorts in the Unite

24 impaired in platelets from 20 patients with polycythemia vera and 3 with idiopathic myelofibrosis, b

25 ns in myeloproliferative disorders (> 95% in polycythemia vera and about half of patients with essent

26 Present in greater than 90% of patients with polycythemia vera and approximately 50% of patients with

27 We used mouse models of induced anemia, polycythemia vera and beta-thalassemia in which macropha

28 , as well as the pathological progression of polycythemia vera and beta-thalassemia, by modulating er

29 Frequently linked to polycythemia vera and chronic myeloid leukemia, myelofib

30 on the pathogenesis and disease phenotype of polycythemia vera and essential thrombocythemia are high

31 t understanding of the molecular genetics of polycythemia vera and essential thrombocythemia, with an

32 We determined that polycythemia vera and essential thrombocytosis are chara

33 The differentially methylated genes in polycythemia vera and essential thrombocytosis were invo

34 We have studied 48 patients with polycythemia vera and four patients with idiopathic myel

35 mbopoietin receptor MpI is characteristic of polycythemia vera and idiopathic myelofibrosis.

36 reduced or absent in 34 of 34 patients with polycythemia vera and in 13 of 14 patients with idiopath

37 ine kinase (JAK2V617F) in most patients with polycythemia vera and in approximately half of those wit

38 s the complexity of the molecular biology of polycythemia vera and indicates likely interaction of mu

39 n myeloproliferative disorders, particularly polycythemia vera and myelodysplastic syndromes.

40 rombocythemia from related disorders such as polycythemia vera and myelofibrosis.

41 is present in the majority of patients with polycythemia vera and one-half of those with essential t

42 In 2005, JAK2V617F was described in polycythemia vera and other BCR-ABL myeloproliferative d

43 as reported in granulocytes of patients with polycythemia vera and other myeloproliferative neoplasms

44 Distinguishing between polycythemia vera and other polycythemic disorders can b

45 sizing the importance of distinction between polycythemia vera and PFCP.

46 (MPNs), including essential thrombocythemia, polycythemia vera and primary myelofibrosis (PMF), are a

47 Data on the use of interferon for polycythemia vera and the potential leukemogenesis of hy

48 ithout bone marrow disease, 15 patients with polycythemia vera, and 17 patients with essential thromb

49 essential thrombocythemia, 145 patients with polycythemia vera, and 96 patients with myelofibrosis.

50 ions are present in almost all patients with polycythemia vera, and in approximately half of those wi

51 for patients with essential thrombocythemia, polycythemia vera, and myelofibrosis, respectively.

52 neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primary myelofibrosis are mainly

53 e neoplasms (MPNs) essential thrombocytosis, polycythemia vera, and primary myelofibrosis has ushered

54 erative neoplasms--essential thrombocytosis, polycythemia vera, and primary myelofibrosis--are acquir

55 More than 95% of cases of polycythemia vera, and roughly half of essential thrombo

56 s was intact in platelets from patients with polycythemia vera, and the tyrosine kinases and substrat

57 ccurrence of the myeloproliferative disorder polycythemia vera are also discussed, emphasizing the im

58 Diagnosis and therapy of polycythemia vera are controversial since the molecular

59 tions were detected in the germ line of rare polycythemia vera, as well as certain leukemia patients,

60 The most common primary polycythemia, polycythemia vera, as well as the only likely endemic co

61 q-) myeloproliferative neoplasms, especially polycythemia vera, by promoting erythroid differentiatio

62 treatment recommendations for patients with polycythemia vera call for maintaining a hematocrit of l

63 JAK2(V617F) and FLT3(ITD)-positive polycythemia vera cells and acute myeloid leukemia cells

64 The detection rate of JAK2 V617F mutants for polycythemia vera, chronic idiopathic myelofibrosis, and

65 e show that allele loss on chromosome 20q in polycythemia vera does not commonly involve mitotic reco

66 stinguish the in vitro growth abnormality of polycythemia vera erythroid progenitors from that seen i

67 is explains why JAK2V617F is associated with polycythemia vera, essential thrombocythemia (ET), and p

68 Polycythemia vera, essential thrombocythemia and primary

69 V617F)) is observed in most individuals with polycythemia vera, essential thrombocythemia and primary

70 ine kinases in the majority of patients with polycythemia vera, essential thrombocythemia and primary

71 has therapeutic efficacy in the treatment of polycythemia vera, essential thrombocythemia and primary

72 ive disorders suggested the possibility that polycythemia vera, essential thrombocythemia and primary

73 play a critical role in the pathogenesis of polycythemia vera, essential thrombocythemia, and idiopa

74 d a web-based cohort of 726 individuals with polycythemia vera, essential thrombocythemia, and myelof

75 2) tyrosine kinase was recently described in polycythemia vera, essential thrombocythemia, and myelof

76 and 13.0 mutations per patient in samples of polycythemia vera, essential thrombocythemia, and myelof

77 e in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloi

78 yeloproliferative neoplasms (MPNs) including polycythemia vera, essential thrombocythemia, and primar

79 plays a central role in the pathogenesis of polycythemia vera, essential thrombocythemia, and primar

80 eloproliferative disorders (MPDs), including polycythemia vera, essential thrombocythemia, and primar

81 the JAK2 (V617F) mutation was identified in polycythemia vera, essential thrombocythemia, and primar

82 tients with the myeloproliferative disorders polycythemia vera, essential thrombocythemia, myelofibro

83 rearrangements in AML, and JAK2 mutations in polycythemia vera, essential thrombocytosis, and chronic

84 tive myeloproliferative neoplasms, including polycythemia vera, essential thrombocytosis, and myelofi

85 R) assay to study genome-wide methylation in polycythemia vera, essential thrombocytosis, and PMF sam

86 The myeloproliferative disorders polycythemia vera, essential thrombocytosis, and primary

87 fits in myelofibrosis therapy, their role in polycythemia vera/essential thrombocythemia treatment is

88 used for the treatment of myelofibrosis and polycythemia vera/essential thrombocythemia.

89 show epigenetic differences between PMF and polycythemia vera/essential thrombocytosis and reveal me

90 ransgenic mouse model of Jak2-V617F-mediated polycythemia vera/essential thrombocytosis.

91 ients with World Health Organization-defined polycythemia vera evaluated at the time of initial diagn

92 The abnormality appears to distinguish polycythemia vera from other-forms of erythrocytosis.

93 ted essential thrombocythemia and those with polycythemia vera had a similar risk of thrombosis, whic

94 6 of 20 (30%) with PMF, whereas 52 cases of polycythemia vera had nonmutated CALR.

95 Men with polycythemia vera had twice as many up-regulated or down

96 ress in understanding the molecular basis of polycythemia vera has been elusive.

97 marrow mononuclear cells from patients with polycythemia vera; however, these effects were attenuate

98 to have a clinical benefit in patients with polycythemia vera in a phase 2 study.

99 K2V617F is sufficient for the development of polycythemia vera in recipient mice.

100 ulated or down-regulated genes as women with polycythemia vera, in a comparison of gene expression in

101 hematopoietic progenitors from patients with polycythemia vera, induction of Mnk kinase activity is r

102 Polycythemia vera is mainly related to JAK2 mutations, w

103 receptors are all constitutively activated, polycythemia vera is the potential ultimate clinical phe

104 Polycythemia vera is the ultimate phenotypic consequence

105 reas expression of Jak2V617F alone induced a polycythemia vera-like disease, concomitant loss of Ezh2

106 it(V558;T669I/+) mice developed a pronounced polycythemia vera-like erythrocytosis in conjunction wit

107 intermediate-2 or high-risk primary MF, post-polycythemia vera MF, or post-essential thrombocythemia

108 ied in patients with 20q deletion-associated polycythemia vera, myelodysplastic syndrome, and acute m

109 ars; P = .03) and more prone to develop post-polycythemia vera myelofibrosis (2.2 vs 0.8 per 100 pati

110 e-2 or high-risk primary myelofibrosis, post-polycythemia vera myelofibrosis, or post-essential throm

111 ntial thrombocythemia myelofibrosis, or post-polycythemia vera myelofibrosis.

112 out a defined molecular drug target, such as polycythemia vera, myelofibrosis with myeloid metaplasia

113 mber 31, 2013, of essential thrombocythemia, polycythemia vera, myelofibrosis, or unclassifiable MPNs

114 ients with chronic myeloid leukemia (CML) or polycythemia vera, myeloproliferative disorders associat

115 sease entities compared to healthy controls (polycythemia vera, n = 192, P = 2.9 x 10(-16); essential

116 s from healthy individuals and patients with polycythemia vera or beta-thalassemia.

117 idiopathic myelofibrosis (IMF) or end-stage polycythemia vera or essential thrombocythemia received

118 ents with myeloproliferative neoplasms (MF > polycythemia vera or essential thrombocythemia) and that

119 r those whose MF has evolved from antecedent polycythemia vera or essential thrombocythemia, presents

120 gative myeloproliferative disorder, that is, polycythemia vera or essential thrombocytosis.

121 ere isolated from the blood of patients with polycythemia vera or other chronic myeloproliferative di

122 reviously unrecognized molecular pathways in polycythemia vera outside the canonical JAK2 pathway tha

123 myelofibrosis, and their potential value in polycythemia vera, outside of special circumstances (eg,

124 rogenitor colony formation from JAK2V617F(+) polycythemia vera patients (IC(50) = 67nM) versus health

125 t JAK2 on phenotype is discussed, as not all polycythemia vera patients appear to be homozygous for t

126 Although most polycythemia vera patients carry the JAK2V617F mutation,

127 tor assays, and analysis of donor cells from polycythemia vera patients harboring a Janus kinase 2 V6

128 om CD34(+) cells isolated from JAK2 V617F(+) polycythemia vera patients more efficiently than either

129 r) vs best available therapy (BAT) in ET and polycythemia vera patients resistant or intolerant to HC

130 man testis cDNA library with sera from three polycythemia vera patients who responded to IFN-alpha an

131 MPD6 elicits IgG Ab responses in a subset of polycythemia vera patients, as well as patients with chr

132 In low-risk polycythemia vera patients, only phlebotomy and primary

133 although they are detected in virtually all polycythemia vera patients, they are found in approximat

134 We present data from 51 polycythemia vera patients.

135 increased erythropoiesis and accentuated the polycythemia vera phenotype, but did not alter platelet

136 the addition of EPO mimicked the behavior of polycythemia vera progenitors; however, we show that ant

137 The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but

138 JAK2V617F in subjects with BCS (n = 41) and polycythemia vera (PV) (n = 20) and in hematologically n

139 kinase JAK2, is found in most patients with polycythemia vera (PV) and a substantial proportion of p

140 nt insights into the molecular mechanisms of polycythemia vera (PV) and essential thrombocythemia (ET

141 duce the risk of thrombosis in patients with polycythemia vera (PV) and essential thrombocythemia (ET

142 Polycythemia vera (PV) and essential thrombocythemia (ET

143 latelet activation has been characterized in polycythemia vera (PV) and essential thrombocythemia (ET

144 duced life expectancy, whereas patients with polycythemia vera (PV) and essential thrombocythemia (ET

145 acy in cell line and mouse models of the MPN polycythemia vera (PV) and essential thrombocytosis (ET)

146 7F mutation is present in most patients with polycythemia vera (PV) and in some patients with essenti

147 We show here that PP2A is inactive in polycythemia vera (PV) and other myeloproliferative neop

148 Treatment of polycythemia vera (PV) and primary myelofibrosis (PMF) C

149 with essential thrombocythemia (ET) than in polycythemia vera (PV) and was proposed to be promoting

150 Primary myelofibrosis (PMF) and polycythemia vera (PV) are chronic myeloproliferative ne

151 Essential thrombocythemia (ET) and polycythemia vera (PV) are clonal myeloproliferative dis

152 n of the JAK2V617F mutation in most cases of polycythemia vera (PV) as well as approximately 50% of p

153 he polycythemia rubra vera-1 (PRV-1) gene in polycythemia vera (PV) but not in secondary or spurious

154 mbopoietin receptor (c-mpl) in patients with polycythemia vera (PV) but not in those with reactive er

155 ype is quite different from that observed in polycythemia vera (PV) caused by JAK2 V617F, whereas bot

156 Although a large proportion of patients with polycythemia vera (PV) harbor a valine-to-phenylalanine

157 ents with essential thrombocythemia (ET) and polycythemia vera (PV) have an increased incidence of ac

158 y-forming units-erythroid from patients with polycythemia vera (PV) have enhanced sensitivity to EP a

159 Polycythemia vera (PV) is a chronic myeloproliferative n

160 Polycythemia vera (PV) is a chronic myeloproliferative n

161 Polycythemia vera (PV) is a clonal disorder characterize

162 Polycythemia vera (PV) is a clonal hematologic disease c

163 Polycythemia vera (PV) is a clonal myeloproliferative di

164 Polycythemia vera (PV) is a human clonal hematologic dis

165 Polycythemia vera (PV) is a human clonal hematological d

166 Polycythemia vera (PV) is an acquired clonal disorder ch

167 Polycythemia vera (PV) is characterized by an increased

168 i et al make the important observations that polycythemia vera (PV) is not a continuum from essential

169 nts with hydroxyurea resistant or intolerant polycythemia vera (PV) is steadily increasing.

170 teria for essential thrombocythemia (ET) and polycythemia vera (PV) issued in 2009 have been widely a

171 V617F JAK2 mutation occurs in patients with polycythemia vera (PV) or essential thrombocythemia (ET)

172 gic and molecular responses in patients with polycythemia vera (PV) or essential thrombocythemia (ET)

173 ively, but are not observed in patients with polycythemia vera (PV) or other myeloid disorders.

174 K2V617F was present in ECs in the vessels of polycythemia vera (PV) patients with BCS using laser cap

175 on alpha (rIFNalpha) can induce remission in polycythemia vera (PV) patients, but gauging the depth o

176 erferon (IFN-alpha) is effective therapy for polycythemia vera (PV) patients, but it is frequently in

177 response was impaired in erythroblasts from polycythemia vera (PV) patients, but not in those from e

178 HEL92.1.7 cells (HEL) and primary cells from polycythemia vera (PV) patients.

179 sion of the thrombopoietin receptor, Mpl, in polycythemia vera (PV) platelets and megakaryocytes usin

180 homozygous for JAK2V617F are more common in polycythemia vera (PV) than essential thrombocythemia (E

181 xon 12 are frequently found in patients with polycythemia vera (PV) that do not carry a JAK2-V617F mu

182 Polycythemia vera (PV) treatment with interferon alpha (

183 tance and intolerance to hydroxyurea (HU) in polycythemia vera (PV) were proposed by the European Leu

184 ndiseased) donors (NDs) and 16 patients with polycythemia vera (PV) were studied.

185 Two prospectively studied patients with polycythemia vera (PV) whose platelet counts showed mark

186 gulated JAK signaling in myelofibrosis (MF), polycythemia vera (PV), and essential thrombocythemia (E

187 CD34+ cells isolated from patients with IMF, polycythemia vera (PV), and G-CSF-mobilized healthy volu

188 Pruritus occurs frequently in patients with polycythemia vera (PV), and the pathophysiology of PV-as

189 ms (MPNs) chronic myeloid leukemia (CML) and polycythemia vera (PV), but whether STAT5 is essential f

190 as recently discovered in most patients with polycythemia vera (PV), chronic idiopathic myelofibrosis

191 In beta-thalassemia and polycythemia vera (PV), disordered erythropoiesis trigge

192 h Organization (WHO) criteria for diagnosing polycythemia vera (PV), especially in "early-stage" pati

193 In 1951 William Dameshek classified polycythemia vera (PV), essential thombocytosis (ET), an

194 The three main Ph(-) MPDs are polycythemia vera (PV), essential thrombocythemia (ET) a

195 tive myeloproliferative neoplasms, including polycythemia vera (PV), essential thrombocythemia (ET),

196 eloproliferative neoplasms (MPNs), including polycythemia vera (PV), essential thrombocythemia (ET),

197 617F is an acquired mutation associated with polycythemia vera (PV), essential thrombocythemia (ET),

198 Polycythemia vera (PV), essential thrombocythemia (ET),

199 myeloproliferative neoplasms (MPNs) include polycythemia vera (PV), essential thrombocythemia (ET),

200 yeloproliferative neoplasms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET),

201 Myeloproliferative neoplasms, including polycythemia vera (PV), essential thrombocythemia, and m

202 ase was found in a majority of patients with polycythemia vera (PV), essential thrombocythemia, and p

203 chronic myeloproliferative disorders (MPDs), polycythemia vera (PV), idiopathic myelofibrosis (IMF),

204 ation is present in almost all patients with polycythemia vera (PV), large proportions of patients wi

205 In the current model of the pathogenesis of polycythemia vera (PV), the JAK2V617F mutation arises in

206 on is present in virtually all patients with polycythemia vera (PV), whereas JAK2617V>F also occurs i

207 Jak2V617F evoked all major features of human polycythemia vera (PV), which included marked increase i

208 17F) in hematopoietic cells, which develop a polycythemia vera (PV)-like disorder evolving into myelo

209 ents with essential thrombocythemia (ET) and polycythemia vera (PV).

210 n the overwhelming majority of patients with polycythemia vera (PV).

211 has been approved as second-line therapy for polycythemia vera (PV).

212 l approach to the diagnosis and treatment of polycythemia vera (PV).

213 ous leukemia (AML and CML, respectively) and polycythemia vera (PV).

214 Janus kinase 2 (JAK2) mutations define polycythemia vera (PV).

215 ns have ever been reported in the context of polycythemia vera (PV).

216 pressing JAK2V617F and in an animal model of polycythemia vera (PV).

217 chronic lymphocytic leukemia (CLL; n = 18), polycythemia vera (PV; n = 16), or myelodysplastic syndr

218 A cohort of 317 patients with MPN (142 polycythemia vera [PV], 94 ET, and 81 MF) was screened f

219 In patients with polycythemia vera, reduced expression of MpI by platelet

220 emia vera, suggesting that erythropoiesis in polycythemia vera remains under the control of macrophag

221 e controversial since the molecular basis of polycythemia vera remains unknown.

222 t JAK2-mutated essential thrombocythemia and polycythemia vera represent different phenotypes of a si

223 pathway in cells from patients with CML and polycythemia vera, respectively, but not in cells from a

224 iopsy specimens from 370 patients with ET by Polycythemia Vera Study Group (PVSG) criteria were asses

225 The Polycythemia Vera Study Group (PVSG) was organized in 19

226 7% of SP patients diagnosed according to the Polycythemia Vera Study Group or World Health Organizati

227 cohorts including 132 WHO-defined ET and 234 Polycythemia Vera Study Group-defined ET patients.

228 tment in a JAK2(V617F)-driven mouse model of polycythemia vera, suggesting that erythropoiesis in pol

229 had a greater likelihood of presenting with polycythemia vera than with essential thrombocythemia, a

230 e prognosis than essential thrombocytosis or polycythemia vera, the molecular distinctions between th

231 In patients with polycythemia vera, those with a hematocrit target of les

232 peripheral-blood cells from 19 patients with polycythemia vera, using oligonucleotide microarray tech

233 Polycythemia vera was more prevalent in BCS than in PVT

234 ion might be involved in the pathogenesis of polycythemia vera, we examined thrombopoietin-induced ty

235 hat are specifically upregulated in acquired polycythemia vera were also upregulated in VHL(P138L) gr

236 MF) preceded by essential thrombocythemia or polycythemia vera were enrolled into a prospective phase

237 th JAK2-mutated essential thrombocythemia or polycythemia vera were related to the mutant allele burd

238 The cause of polycythemia vera, which originates from a multipotent h

239 present the case of a 63-year-old woman with polycythemia vera who developed a progressive focal neur

240 nib versus standard therapy in patients with polycythemia vera who had an inadequate response to or h

241 domly assigned 365 adults with JAK2-positive polycythemia vera who were being treated with phlebotomy

242 These mice develop a MPN mimicking polycythemia vera with large amplification of myeloid ma

243 laboratory test to establish a diagnosis of polycythemia vera would be highly desirable; however, no