ライフサイエンスコーパス: polycythemia vera

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

2 hematopoietic progenitors from patients with polycythemia vera.

3 coid receptor has been reported increased in polycythemia vera.

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

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

6 esembled human essential thrombocythemia and polycythemia vera.

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

8 r impact on current diagnostic approaches in polycythemia vera.

9 r of myeloproliferative diseases, especially polycythemia vera.

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

11 patients with essential thrombocythemia and polycythemia vera.

12 lume, and improving symptoms associated with polycythemia vera.

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

14 eoplasms (MPNs), including myelofibrosis and polycythemia vera.

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

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

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

18 % of patients with MMM, 33% of patients with polycythemia vera, 12% of patients with essential thromb

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

20 7F mutational status: 290 with MMM, 242 with polycythemia vera, 318 with essential thrombocythemia (E

21 28 with essential thrombocythemia, 3063 with polycythemia vera, 547 with myelofibrosis, and 1720 with

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

23 2V617F mutation in a patient presenting with polycythemia vera (aged 34 years).

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

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

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

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

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

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

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

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

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

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

34 We determined that polycythemia vera and essential thrombocytosis are chara

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

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

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

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

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

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

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

42 ated Jak2V617F- and MPLW515L-driven onset of polycythemia vera and myelofibrosis disease hallmarks, r

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

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

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

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

47 Distinguishing between polycythemia vera and other polycythemic disorders can b

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

49 The clinical phenotype of primary and post-polycythemia vera and postessential thrombocythemia myel

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

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

52 6 with essential thrombocythemia, and 2 with polycythemia vera) and 5 controls underwent (68)Ga-penti

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

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

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

56 a of chronic inflammation, beta-thalassemia, polycythemia vera, and myelodysplastic syndromes.

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

58 in patients with essential thrombocythemia, polycythemia vera, and myelofibrosis.

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

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

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

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

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

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

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

66 ertide in patients with phlebotomy-dependent polycythemia vera are unknown.

67 rder to raise awareness among clinicians for polycythemia vera, as it can in fact be used as a differ

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

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

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

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

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

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

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

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

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

77 Polycythemia vera, essential thrombocythemia and primary

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 6 of 20 (30%) with PMF, whereas 52 cases of polycythemia vera had nonmutated CALR.

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

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

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

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

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

110 pective observational study of patients with polycythemia vera in US clinical practices (REVEAL) stud

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

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

113 Polycythemia vera is a chronic myeloproliferative neopla

114 Polycythemia vera is mainly related to JAK2 mutations, w

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

116 Polycythemia vera is the ultimate phenotypic consequence

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

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

119 BMT recipients developed a polycythemia vera-like phenotype (elevated hematocrit an

120 However, these mice then developed a polycythemia vera-like phenotype at 10 weeks of age.

121 th primary and postessential thrombocythemia/polycythemia vera MF subgroups.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 Although most polycythemia vera patients carry the JAK2V617F mutation,

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

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

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

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

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

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

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

149 We present data from 51 polycythemia vera patients.

150 on observed in essential thrombocythemia and polycythemia vera patients.

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

152 nosis includes myeloproliferative neoplasms (polycythemia vera, primary myelofibrosis, chronic myeloi

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

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

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

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

157 ns across three key areas: cancer treatment, polycythemia vera (PV) and anemia, and infectious diseas

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

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

160 lecularly inter-related, the other two being polycythemia vera (PV) and essential thrombocythemia (ET

161 Polycythemia vera (PV) and essential thrombocythemia (ET

162 f drugs are available to treat patients with polycythemia vera (PV) and essential thrombocythemia (ET

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

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

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

166 7F mutation is present in most patients with polycythemia vera (PV) and in some patients with essenti

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

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

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

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

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

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

173 Polycythemia vera (PV) belongs to the BCR-ABL1-negative

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

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

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

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

178 Since its discovery, polycythemia vera (PV) has challenged clinicians respons

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

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

181 Polycythemia vera (PV) is a chronic myeloproliferative n

182 Polycythemia vera (PV) is a chronic myeloproliferative n

183 Polycythemia vera (PV) is a clonal disorder characterize

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

185 Polycythemia vera (PV) is a clonal myeloproliferative di

186 Polycythemia vera (PV) is a hematopoietic stem cell neop

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

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

189 Polycythemia vera (PV) is a myeloproliferative neoplasm

190 Polycythemia vera (PV) is a myeloproliferative neoplasm

191 Polycythemia vera (PV) is a myeloproliferative neoplasm

192 Polycythemia vera (PV) is a Philadelphia chromosome-nega

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

194 Polycythemia vera (PV) is characterized by an increased

195 Polycythemia vera (PV) is characterized by JAK/STAT acti

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

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

198 ents with essential thrombocythemia (ET) and polycythemia vera (PV) is to reduce thrombotic events by

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

200 718) and post-essential thrombocythemia (ET)/polycythemia vera (PV) myelofibrosis (0.701) improving p

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

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

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

204 controlling the degree of erythrocytosis in polycythemia vera (PV) patients as well as correcting an

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

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

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

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

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

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

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

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

213 Polycythemia vera (PV) treatment with interferon alpha (

214 Polycythemia vera (PV) was first described by Louis Henr

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

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

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

218 Red cell overproduction is seen in polycythemia vera (PV), a bone marrow myeloproliferative

219 Polycythemia vera (PV), a myeloproliferative neoplasm ch

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

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

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

223 risk of thrombosis and disease evolution in polycythemia vera (PV), as much of the published literat

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

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

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

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

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

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

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

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

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

233 617F is an acquired mutation associated with polycythemia vera (PV), essential thrombocythemia (ET),

234 rative neoplasms (MPNs) that can manifest as polycythemia vera (PV), essential thrombocythemia (ET),

235 HSCs), display diverse phenotypes, including polycythemia vera (PV), essential thrombocythemia (ET),

236 abnormal hematopoietic stem cells, of which polycythemia vera (PV), essential thrombocythemia (ET),

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

238 The 3 subtypes, that is, polycythemia vera (PV), essential thrombocythemia (ET),

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

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

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

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

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

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

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

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

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

248 17F) in hematopoietic cells, which develop a polycythemia vera (PV)-like disorder evolving into myelo

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

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

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

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

253 ssential thrombocythemia, myelofibrosis, and polycythemia vera (PV).

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

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

256 in disease, using a JAK2-dependent model of polycythemia vera (PV).

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

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

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

260 lar responses (HRs and MRs, respectively) in polycythemia vera (PV); however, patients do not respond

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

262 PN subtypes (essential thrombocythemia [ET]; polycythemia vera [PV]) were compared with each other to

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

264 across all MPNs or specific to each subtype (polycythemia vera [PV], essential thrombocythemia [ET],

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

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

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

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

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

270 In patients with polycythemia vera, rusfertide treatment was associated w

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

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

273 7% of SP patients diagnosed according to the Polycythemia Vera Study Group or World Health Organizati

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

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

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

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

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

279 Similarly, in essential thrombocythemia and polycythemia vera, treatments are primarily aimed at red

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

281 Polycythemia vera was more prevalent in BCS than in PVT

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

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

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

285 DNMT3A mutations in patients with polycythemia vera were heterogeneous and not enriched in

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

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

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

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

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

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

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