ライフサイエンスコーパス: polycythemia

1 iple paragangliomas or somatostatinomas, and polycythemia.

2 le PGLs and somatostatinomas associated with polycythemia.

3 ell indices often increased due to secondary polycythemia.

4 glioma and somatostatinoma, both of whom had polycythemia.

5 nt functions of VHL are perturbed in Chuvash polycythemia.

6 s associated with a disease known as Chuvash polycythemia.

7 tor of HIF, have increased EPO synthesis and polycythemia.

8 uppressed hepatic Epo and the development of polycythemia.

9 he adverse effects of preoperative anemia or polycythemia.

10 (Epo)-independent erythroid hyperplasia and polycythemia.

11 ted with increased erythropoietin levels and polycythemia.

12 STAT5 are required for Friend virus-induced polycythemia.

13 use model of cavernous liver hemangiomas and polycythemia.

14 by augmentation of hypoxic sensing, Chuvash polycythemia.

15 eflected a transient erythropoietin-mediated polycythemia.

16 olecular basis for hypoxia-induced excessive polycythemia.

17 al domain-encoding VHL mutations would cause polycythemia.

18 h tumor development, but rather with Chuvash polycythemia, a heritable disease characterized by eleva

19 However, the extreme polycythemia and accompanying increased mortality due to

20 oped pulmonary hypertension independently of polycythemia and enhanced normoxic respiration similar t

21 esulted in extreme HIF signaling, leading to polycythemia and excessive bone accumulation by overstim

22 vidence of cobalt's effects on the body (eg, polycythemia and goiter).

23 Autopsies of these animals revealed intense polycythemia and hemorrhagic patches in the lung parench

24 ontributing factors appear to be exaggerated polycythemia and hypoxemia, and lower and sluggish CBF c

25 been detected in up to 90% of patients with polycythemia and in a sizeable proportion of patients wi

26 t not Hif1a, genetically suppressed both the polycythemia and pulmonary hypertension in the VhlR/R mi

27 Similarly to what was reported in Chuvash polycythemia and some other instances of HIFs upregulati

28 te the prevalence of preoperative anemia and polycythemia and their effects on 30-day postoperative o

29 utive HIF-2 activity in the adult results in polycythemia and vascular tumorigenesis.

30 right ventricular systolic pressure) but not polycythemia and was associated with abnormal musculariz

31 me and represents a useful tool for studying polycythemias and investigating potential therapeutics.

32 y suppressed the development of hemangiomas, polycythemia, and Hif-induced gene expression.

33 ted syndrome of hepatic cirrhosis, dystonia, polycythemia, and hypermanganesemia in cases without env

34 dominantly exhibit expansion of neutrophils, polycythemia, and increased lifespan.

35 Such patients also presented with PPGL and polycythemia, and later on, some presented with duodenal

36 of circulating Epo lead to reticulocytosis, polycythemia, and suppression of hepatic hepcidin mRNA.

37 for the observed protection of Tibetans from polycythemia at high altitude.

38 imination of tubular Vegfa caused pronounced polycythemia because of increased renal erythropoietin (

39 d in the affected homozygote with congenital polycythemia but not in her, or her-heterozygous relativ

40 tion of CML-like leukemia by BCR-ABL1 and of polycythemia by JAK2(V617F), and validate STAT5a/b and t

41 the elucidation of the molecular basis of a polycythemia caused by augmentation of hypoxic sensing,

42 verexpression of epo mRNA resulted in severe polycythemia, characterized by a striking increase in th

43 In addition to polycythemia, Chuvash patients have pulmonary hypertensi

44 and if preoperative management of anemia or polycythemia decreases the risk of postoperative mortali

45 The increase in red blood cell mass (polycythemia) due to the reduced oxygen availability (hy

46 However, recessively inherited congenital polycythemia, exemplified by Chuvash polycythemia, has b

47 genital polycythemia, exemplified by Chuvash polycythemia, has been associated with 2 separate 3' VHL

48 Studies in patients with polycythemia have demonstrated that ACEIs are effective

49 raganglioma (PPGL) syndromes associated with polycythemia have previously been described in associati

50 39.0%), normal hematocrit (39.0%-53.9%), and polycythemia (hematocrit > or =54%).

51 Vhl(R/R) mice developed polycythemia highly similar to the human disease.

52 dic polycythemia (SP), and 3 with hereditary polycythemia (HP).

53 n, especially in high-risk groups, including polycythemia-hyperviscosity syndrome, hypertension, and

54 s to high altitude include hyperventilation, polycythemia, hypoxic pulmonary vasoconstriction-increas

55 retrovirus that causes erythroblastosis and polycythemia in mice.

56 JAK2(V617F) failed to induce polycythemia in recipients after deletion of Stat5a/b, a

57 tiplano are not protected from high-altitude polycythemia in the same way, yet they exhibit other ada

58 thropoiesis, resulting in the development of polycythemia in Vhl(R/R) mice.

59 ults in increased hepatic Epo production and polycythemia independent of Hif-1alpha.

60 Chuvash polycythemia is a disorder with elevated HIF.

61 Chuvash polycythemia is a hypoxia-sensing disorder characterized

62 In this study, because excessive polycythemia is a predominant trait in some high-altitud

63 Polycythemia is often associated with erythropoietin (EP

64 Polycythemia is prevented by the loss of either HIF2alph

65 s effects of polycythemia rather than reduce polycythemia itself.

66 al retardation, hypotonia and sometimes with polycythemia, leukopenia, and neutropenia.

67 Patients were found to have polycythemia, multiple PGLs, and duodenal somatostatinom

68 additional patients presenting with PPGL and polycythemia, no further mutations have been discovered.

69 ffect the development of vascular tumors and polycythemia, nor did it suppress the increased expressi

70 d thrombocythemia, but without leukocytosis, polycythemia, or marrow fibrosis, displaying features re

71 id onset of cardiomyopathy, who also exhibit polycythemia, pericardial effusion, or goiter should be

72 d EpoRs from primary familial and congenital polycythemia (PFCP) patients lacking the 3 important tyr

73 throcytes in primary familial and congenital polycythemia (PFCP).

74 increased renal Epo production and resulting polycythemia, presumably to counterbalance microvascular

75 ts (10 women, 4 men) with confirmed PPGL and polycythemia prospectively underwent (68)Ga-DOTATATE (13

76 logical responses to chronic hypoxia include polycythemia, pulmonary arterial remodeling, and vasocon

77 serve to mitigate the deleterious effects of polycythemia rather than reduce polycythemia itself.

78 ents with essential thrombocythemia (ET) and polycythemia rubra vera (PV) stems from thrombotic event

79 emonstrated neutrophil overexpression of the polycythemia rubra vera-1 (PRV-1) gene in polycythemia v

80 ferentiation events in a log-log malignancy, polycythemia rubra vera.

81 ditary thrombocytosis (HT), 11 with sporadic polycythemia (SP), and 3 with hereditary polycythemia (H

82 a vera (PV) but not in secondary or spurious polycythemia (SP).

83 responses with data from studies of Chuvash polycythemia suggested that other aspects of the Chuvash

84 onal imaging signature of patients with PPGL-polycythemia syndromes is still unknown, and because the

85 sm-specific; its presence excludes secondary polycythemia, thrombocytosis, or bone marrow fibrosis fr

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

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

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

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

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

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

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

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

94 Polycythemia vera (PV) and essential thrombocythemia (ET

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

96 7F mutation is present in most patients with polycythemia vera (PV) and in some patients with essenti

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

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

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

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

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

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

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

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

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

106 Polycythemia vera (PV) is a chronic myeloproliferative n

107 Polycythemia vera (PV) is a chronic myeloproliferative n

108 Polycythemia vera (PV) is a clonal disorder characterize

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

110 Polycythemia vera (PV) is characterized by an increased

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

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

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

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

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

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

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

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

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

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

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

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

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

124 Polycythemia vera (PV) treatment with interferon alpha (

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 617F is an acquired mutation associated with polycythemia vera (PV), essential thrombocythemia (ET),

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

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

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

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

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

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

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

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

149 17F) in hematopoietic cells, which develop a polycythemia vera (PV)-like disorder evolving into myelo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 We determined that polycythemia vera and essential thrombocytosis are chara

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

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

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

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

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

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

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

174 Distinguishing between polycythemia vera and other polycythemic disorders can b

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

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

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

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

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

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

181 6 of 20 (30%) with PMF, whereas 52 cases of polycythemia vera had nonmutated CALR.

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

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

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

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

186 Polycythemia vera is mainly related to JAK2 mutations, w

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

188 Polycythemia vera is the ultimate phenotypic consequence

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

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

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

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

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

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

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

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

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

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

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

200 Although most polycythemia vera patients carry the JAK2V617F mutation,

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

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

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

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

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

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

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

208 We present data from 51 polycythemia vera patients.

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

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

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

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

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

214 7% of SP patients diagnosed according to the Polycythemia Vera Study Group or World Health Organizati

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

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

217 Polycythemia vera was more prevalent in BCS than in PVT

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

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

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

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

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

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

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

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

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

227 7F mutational status: 290 with MMM, 242 with polycythemia vera, 318 with essential thrombocythemia (E

228 28 with essential thrombocythemia, 3063 with polycythemia vera, 547 with myelofibrosis, and 1720 with

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

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

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

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

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

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

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

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

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

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

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

240 Polycythemia vera, essential thrombocythemia and primary

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 hematopoietic progenitors from patients with polycythemia vera.

276 coid receptor has been reported increased in polycythemia vera.

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

278 esembled human essential thrombocythemia and polycythemia vera.

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

280 r impact on current diagnostic approaches in polycythemia vera.

281 r of myeloproliferative diseases, especially polycythemia vera.

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

283 lume, and improving symptoms associated with polycythemia vera.

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

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

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

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

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

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

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

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

292 bin SS genotype and 15 subjects with Chuvash polycythemia (VHL(R200W) homozygotes with constitutive u

293 echanisms underlying the development of this polycythemia, we generated mice homozygous for the R200W

294 Even mild degrees of preoperative anemia or polycythemia were associated with an increased risk of 3

295 R200W germline mutation in VHL have Chuvash polycythemia, whereas heterozygous carriers are free of

296 The loss of all PHD isoforms results in both polycythemia, which is caused by Epo overproduction, and

297 Patients with Chuvash polycythemia, who are homozygous for a missense mutation

298 nscripts were also significantly elevated in polycythemias with augmented hypoxia-inducible factor ac

299 mechanisms by which erythroid progenitors in polycythemias with defects of hypoxia sensing and EPOR m

300 those mutated in primary familial congenital polycythemia, with preservation of the proximal tyrosine

301 any combination of two PHD isoforms induces polycythemia without steatosis complications, whereas th