ライフサイエンスコーパス: MPN

1 MPNs are also associated with aberrant expression and ac

2 ed a hematopoietic neoplasm (4 MDS, 1 AML, 1 MPN, and 2 MDS/MPN) and 3 patients (1.1%) developed BM f

3 most probable number (MPN)/2 hands and 1000 MPN/225 cm(2) floor.

4 detect somatic mutations in a cohort of 197 MPN patients and followed clonal evolution and the impac

5 hibition on human NK cells in a cohort of 28 MPN patients with or without ruxolitinib treatment and 2

6 splicing, and signaling cooperate with the 3 MPN drivers and play a key role in the PMF pathogenesis.

7 stage genome-wide association study of 3,437 MPN cases and 10,083 controls, we identify two SNPs with

8 mimic dual pathway activation and develop a MPN-phenotype with leukocytosis (neutrophils and monocyt

9 ic myeloid leukemia from classic BCR-ABL1(-) MPNs, which are largely defined by mutations in JAK2, CA

10 to restore normal hematopoiesis and abrogate MPN-like disease in animals lacking the inositol phospha

11 In addition, MPNs show unexpected layers of genetic complexity, with

12 haploinsufficiency results in an aggressive MPN with death at a murine prepubertal age of 20 to 35 d

13 ogression, and improved quality of life (all MPN).

14 Such features should allow MPN multivariable sensors to be an attractive high value

15 PO) receptor (MPL) significantly ameliorates MPN development in JAK2V617F(+) transgenic mice, whereas

16 number of hematopoietic neoplasms (MDS, AML, MPN, and MDS/MPN) was calculated and adjusted for sex, a

17 , mutations that drive the development of an MPN phenotype occur in a mutually exclusive manner in 1

18 l3 (Nucleolar protein 3) in mice leads to an MPN resembling primary myelofibrosis (PMF).

19 rtent puncture of myocardium between LBN and MPN (7.6% versus 6.8%, P=0.76).

20 Of the 404 patients, LBN and MPN were used in 46% and 54% of patients, respectively.

21 e clinicopathologic features of both MDS and MPN diseases.

22 opting treatment strategies used for MDS and MPN.

23 tor persistent cells, murine MPN models, and MPN patient samples.

24 /-) mice showed increased reconstitution and MPN disease initiation potential compared with JAK2-V617

25 Myb-Like, SWIRM, and MPN domains 1 (MYSM1) is a metalloprotease that deubiqui

26 Myb-like, SWIRM, and MPN domains 1 (MYSM1) is a transcriptional regulator med

27 uction and colony formation by primary CD34+ MPN stem/progenitor cells from patients.

28 causing transformation of nonlethal chronic MPNs into aggressive lethal leukemias with >30% blasts i

29 Both heterogeneity of classical MPNs and prognosis are determined by a specific genomic

30 molecule production from two gene clusters (MPN and SYR) found to be essential for in vivo virulence

31 a (Peg-IFNalpha 2a), significantly decreased MPN colony-forming unit-granulocyte macrophage and burst

32 ugs can each alone or in combination deplete MPN HSCs.

33 to exacerbated MPN and to donor-cell-derived MPN following stem cell transplantation.

34 of JAK-STAT pathway activation in different MPNs, and in patients without JAK2 mutations, has not be

35 cent evidence has demonstrated that to drive MPN transformation, JAK2V617F needs to directly associat

36 is and might influence the JAK2-V617F-driven MPN phenotype.

37 in protein BRCC36 associates with pseudo DUB MPN(-) proteins KIAA0157 or Abraxas, which are essential

38 roduced by monocytes, leading to exacerbated MPN and to donor-cell-derived MPN following stem cell tr

39 Despite common biological features, MPNs display diverse disease phenotypes as a result of b

40 sion and Tet2 loss resulted in a more florid MPN phenotype than that seen with either allele alone.

41 ibition is a viable therapeutic approach for MPN patients.

42 However, the therapeutic armamentarium for MPN is still largely inadequate for coping with patients

43 additional cellular components necessary for MPN development.

44 PINT, and GFI1B All SNP ORs were similar for MPN patients and controls who were V617F carriers.

45 and NF-E2 overexpression is not specific for MPN; these transcripts were also significantly elevated

46 Current treatment options for MPNs include cytoreduction by hydroxyurea and JAK1/2 inh

47 Although developed as targeted therapies for MPNs, current JAK2 inhibitors do not preferentially targ

48 ressing cells, specifically in biopsies from MPN patients.

49 ation fork progression in primary cells from MPN patients, reveal unexpected disease-restricted diffe

50 erived JAK2V617F-positive erythroblasts from MPN patients also demonstrated impaired replication fork

51 erived JAK2V617F-positive erythroblasts from MPN patients displayed increased ROS levels and reduced

52 ate somatic mutations in serial samples from MPN patients.

53 Using benzylguanine (BG)-functionalized MPNs and model cell lines expressing either SNAP-tagged

54 endogenous functional defect of NK cells in MPN was further aggravated by ruxolitinib treatment.

55 ated in malignant and non-malignant cells in MPN.

56 hypothesized that acquired MPO deficiency in MPN could be associated with the presence of CALR mutati

57 st description of acquired MPO deficiency in MPN, we provide the molecular correlate associated with

58 inhibition would show increased efficacy in MPN models and primary samples.

59 that ruxolitinib impairs NK cell function in MPN patients, offering an explanation for increased infe

60 on when considering using Ezh2 inhibitors in MPN.

61 JAK2(V617F), the main mutation involved in MPN, is considered as a risk factor for thrombosis, alth

62 anscriptional signature of TET2 mutations in MPN patent samples.

63 peared, suggesting that the mutation rate in MPN is rather low.

64 ceptor, MPL, is the key cytokine receptor in MPN development, and these mutations all activate MPL-JA

65 esult, rarely induce molecular remissions in MPN patients.

66 tions all activate MPL-JAK-STAT signaling in MPN stem cells.

67 tes that JAK2 remains an essential target in MPN cells that survive in the setting of chronic JAK inh

68 consequences of JAK2V617F-TET2 comutation in MPNs, particularly as it pertains to HSCs.

69 nderstanding of thrombohemorrhagic events in MPNs and highlight the critical role of ECs in the patho

70 normalities are present in megakaryocytes in MPNs and that these appear to be associated with progres

71 olecular or clinicopathological responses in MPNs suggests a need for development of better therapies

72 he mechanisms that mediate transformation in MPNs are not fully delineated, and clinically utilized J

73 tivating the p53 pathway, thereby increasing MPN CD34(+) cell apoptosis.

74 The mechanisms by which CALR mutants induce MPN are unknown.

75 tutional and acquired factors that influence MPN stem cells, and likely also as a result of heterogen

76 tioned whether JAK2-V617F alone can initiate MPN.

77 ecificity of many members of the OTU and JAB/MPN/Mov34 metalloenzyme DUB families and highlight that

78 atalytic site within the deubiquitinase JAB1/MPN/Mov34 (JAMM)/MPN domain.

79 ored by a Brr2 cofactor, the C-terminal Jab1/MPN domain of the Prp8 protein.

80 ndamental in the development of JAK2V617F(+) MPNs, highlighting an entirely novel target for therapeu

81 of the cellular effects of a non-JAK2V617F, MPN-associated JAK2 mutation; provides insights into new

82 y eliminated the total number of JAKV617F(+) MPN hematopoietic progenitor cells.

83 hin the deubiquitinase JAB1/MPN/Mov34 (JAMM)/MPN domain.

84 that mutations in Ptpn11 induce a JMML-like MPN through cell-autonomous mechanisms that are dependen

85 nificantly by measured levels of E. coli(log MPN/100 mL) (chi(2) > 8.7; p < 0.003).

86 tic neoplasm (4 MDS, 1 AML, 1 MPN, and 2 MDS/MPN) and 3 patients (1.1%) developed BM failure characte

87 blished involving 3 independent academic MDS/MPN workshops (March 2013, December 2013, and June 2014)

88 atopoietic neoplasms (MDS, AML, MPN, and MDS/MPN) was calculated and adjusted for sex, age, and follo

89 tive in patients with lower-risk MDS and MDS/MPN.

90 ed as aCML and the remaining 69 (51%) as MDS/MPN-U.

91 ve neoplasms (MPN) overlapping diseases (MDS/MPN).

92 , which could be of prognostic value for MDS/MPN patients.

93 ising laboratory and clinical experts in MDS/MPN was established involving 3 independent academic MDS

94 emia, atypical chronic myeloid leukemia, MDS/MPN-Unclassifiable, ring sideroblasts associated with ma

95 vance, we studied 308 patients with MDS, MDS/MPN, or acute myeloid leukemia evolving from MDS.

96 ures of a pediatric unclassifiable mixed MDS/MPN and mimics many clinical manifestations of JMML in t

97 myelodysplastic syndrome (MDS), or mixed MDS/MPN overlap syndrome (including chronic myelomonocytic l

98 separation from unclassifiable MDS/MPN (MDS/MPN-U).

99 AML), myeloproliferative neoplasm (MPN), MDS/MPN, or otherwise unexplained cytopenia (for >6 mo).

100 ic syndrome/myeloproliferative neoplasm (MDS/MPN) by the World Health Organization and also shares so

101 odysplastic/myeloproliferative neoplasm (MDS/MPN) largely defined morphologically.

102 odysplastic/myeloproliferative neoplasm (MDS/MPN).

103 dysplastic/myeloproliferative neoplasms (MDS/MPN) has considerably improved.

104 dysplastic/myeloproliferative neoplasms (MDS/MPN), respectively.

105 th the prognosis of patients with MDS or MDS/MPN, the role of ASXL1 in erythropoiesis remains unclear

106 ions were not detected either in aCML or MDS/MPN-U.

107 and cytogenetics could further stratify MDS/MPN-U but not aCML patient risks.

108 The MDS/MPN-U category is heterogeneous, and patient risk can be

109 allow its separation from unclassifiable MDS/MPN (MDS/MPN-U).

110 mmendations for most adult patients with MDS/MPN.

111 MDS/MPNs have clinicopathologic features of both MDS and MPN

112 proliferative neoplasms (MPNs) (n = 55), MDS/MPNs (n = 169), and AML (n = 450) were analyzed for cohe

113 dysplastic/myeloproliferative neoplasms (MDS/MPNs), including chronic myelomonocytic leukemia, atypic

114 dysplastic/myeloproliferative neoplasms (MDS/MPNs).

115 icle summarizes the molecular aspects of MDS/MPNs and provides an overview of classic and emerging th

116 new insights into the genetic nature of MDS/MPNs.

117 Soil had >120000 mean MPN E. coli per gram.

118 tions cooperate with JAK2(V617F) to modulate MPN phenotype.

119 tion with DNA and purification of monovalent MPNs, (iii) modular targeting of MPNs to cell-surface re

120 This new model represents a murine MPN model with features of a pediatric unclassifiable mi

121 ty in JAK inhibitor persistent cells, murine MPN models, and MPN patient samples.

122 CHZ868 showed significant activity in murine MPN models and induced reductions in mutant allele burde

123 ective in vivo against JAK2(V617F)(+) murine MPN-like disease and also against JAK2(V617F)(+), CALR(d

124 re was significantly enriched in JAK2-mutant MPN patients consistent with a shared mechanism of trans

125 n-dependent kinase 6 (Cdk6) and MycNol3(-/-) MPN Thy1(+)LSK cells share significant molecular similar

126 is tool are a magnetoplasmonic nanoparticle (MPN) actuator that delivers defined spatial and mechanic

127 known as monolayer-protected nanoparticles (MPNs).

128 Use of micropuncture needle (MPN) may decrease the risk of complications.

129 patients and CALR mutations in JAK2-negative MPN patients.

130 me-wide significance in JAK2(V617F)-negative MPN: rs12339666 (JAK2; meta-analysis P=1.27 x 10(-10)) a

131 tral phenotypic driver of BCR -ABL1-negative MPNs and a unifying therapeutic target.

132 ereditary thrombocytosis and triple-negative MPNs.

133 aematopoiesis, myeloproliferative neoplasia (MPN) and leukaemia.

134 syndrome (MDS)/myeloproliferative neoplasm (MPN) for which no current standard of care exists.

135 pe of classical myeloproliferative neoplasm (MPN) is in large part elucidated.

136 syndrome (MDS)/myeloproliferative neoplasm (MPN) overlap disorders characterized by monocytosis, mye

137 central role in myeloproliferative neoplasm (MPN) pathogenesis.

138 Myeloproliferative neoplasm (MPN) patients frequently show co-occurrence of JAK2-V617

139 in platelets of myeloproliferative neoplasm (MPN) patients, but not in platelets from healthy control

140 bserved in most myeloproliferative neoplasm (MPN) patients.

141 omotes an acute myeloproliferative neoplasm (MPN) that recapitulates many features of JMML and MP-CMM

142 ibrosis, a rare myeloproliferative neoplasm (MPN), but clinical trials are also being conducted in in

143 risk MDS or MDS/myeloproliferative neoplasm (MPN), including chronic myelomonocytic leukemia, accordi

144 leukemia (AML), myeloproliferative neoplasm (MPN), MDS/MPN, or otherwise unexplained cytopenia (for >

145 occurring as a myeloproliferative neoplasm (MPN), myelodysplastic syndrome (MDS), or mixed MDS/MPN o

146 suffering from myeloproliferative neoplasm (MPN), whereas bleeding is less frequent.

147 L), a childhood myeloproliferative neoplasm (MPN).

148 patients with a myeloproliferative neoplasm (MPN).

149 omes (MDS) and myeloproliferative neoplasms (MPN) are hematologically diverse stem cell malignancies

150 oliferation in myeloproliferative neoplasms (MPN) is driven by somatic mutations in JAK2, CALR or MPL

151 patients with myeloproliferative neoplasms (MPN) led to clinical development of Janus kinase (JAK) i

152 DS) or MDS and myeloproliferative neoplasms (MPN) overlapping diseases (MDS/MPN).

153 he majority of myeloproliferative neoplasms (MPN) patients, including JAK2 mutations in the majority

154 lar biology of myeloproliferative neoplasms (MPN) remains incompletely understood.

155 patients with myeloproliferative neoplasms (MPN), and in particular those with myelofibrosis and ext

156 In addition to myeloproliferative neoplasms (MPN), these patients can present with myelodysplastic sy

157 ling myeloproliferative disorders/neoplasms (MPNs), including varying degrees of extramedullary hemat

158 MDS (n = 386), myeloproliferative neoplasms (MPNs) (n = 55), MDS/MPNs (n = 169), and AML (n = 450) we

159 ain of JAK2 in myeloproliferative neoplasms (MPNs) and in other hematologic malignancies highlighted

160 osome-negative myeloproliferative neoplasms (MPNs) and JAK2 V617F clonal hematopoiesis in the general

161 s increased in myeloproliferative neoplasms (MPNs) and other conditions associated with pathological

162 Myeloproliferative neoplasms (MPNs) are a group of clonal disorders characterized by a

163 Myeloproliferative neoplasms (MPNs) are a group of related clonal hematologic disorder

164 Myeloproliferative neoplasms (MPNs) are a group of related clonal hemopoietic stem cel

165 Myeloproliferative neoplasms (MPNs) are a set of chronic hematopoietic neoplasms with

166 Myeloproliferative neoplasms (MPNs) are associated with a shortened life expectancy.

167 Myeloproliferative neoplasms (MPNs) are characterized by the clonal expansion of one o

168 ML), and other myeloproliferative neoplasms (MPNs) are genetically heterogeneous but frequently displ

169 Myeloproliferative neoplasms (MPNs) arise in the hematopoietic stem cell (HSC) compart

170 patients with myeloproliferative neoplasms (MPNs) carry a somatic JAK2-V617F mutation.

171 JAK2V617F(+) myeloproliferative neoplasms (MPNs) frequently progress into leukemias, but the factor

172 e treatment of myeloproliferative neoplasms (MPNs) has led to studies of ruxolitinib in other clinica

173 tive classical myeloproliferative neoplasms (MPNs) include polycythemia vera (PV), essential thromboc

174 osome-negative myeloproliferative neoplasms (MPNs) is the acquisition of a V617F mutation in Janus ki

175 ions in clonal myeloproliferative neoplasms (MPNs) is well established.

176 Myeloproliferative neoplasms (MPNs) often carry JAK2(V617F), MPL(W515L), or CALR(del52

177 gative chronic myeloproliferative neoplasms (MPNs) originate at the level of the hematopoietic stem c

178 patients with myeloproliferative neoplasms (MPNs) with clinical outcome, thereby proposing a molecul

179 patients with myeloproliferative neoplasms (MPNs), and the study of these chronic myeloid malignanci

180 osome-negative myeloproliferative neoplasms (MPNs), is unknown.

181 ndromes (MDS), myeloproliferative neoplasms (MPNs), non-Hodgkin lymphomas, and classical Hodgkin lymp

182 patients with myeloproliferative neoplasms (MPNs), the risk of AMD in these patients may be increase

183 nt fraction of myeloproliferative neoplasms (MPNs).

184 of CALR-mutant myeloproliferative neoplasms (MPNs).

185 l stenosis and myeloproliferative neoplasms (MPNs).

186 patients with myeloproliferative neoplasms (MPNs).

187 f mutations in myeloproliferative neoplasms (MPNs).

188 athogenesis of myeloproliferative neoplasms (MPNs).

189 osome-negative myeloproliferative neoplasms (MPNs).

190 suffering from myeloproliferative neoplasms (MPNs).

191 T signaling in myeloproliferative neoplasms (MPNs).

192 o distance between the medial plantar nerve (MPN) and Henry's knot.

193 Nol3(-/-) MPN mice harbor an expanded Thy1(+)LSK stem cell populat

194 ing that certain triple-negative ETs are not MPNs.

195 no HIV-1 were used for most probable number (MPN) assays supplemented with CF and Rpf-deficient CF, t

196 EXX Quantitray for the most probable number (MPN) of E. coli.

197 entrations were of 100 most probable number (MPN)/2 hands and 1000 MPN/225 cm(2) floor.

198 can recruit normal p53, like in the case of MPN cells, but also p53 mutants, such as p53 M133K in hu

199 o investigate a well-characterized cohort of MPN patients.

200 04 and MPLY591 mutants in a bigger cohort of MPN.

201 -V617F mice did not ameliorate the course of MPN, but rather enhanced thrombocytosis and shortened th

202 ignancies have paralleled the development of MPN-targeted therapies that have had a significant impac

203 ribute synergistically to the development of MPN.

204 echanisms underlying the clonal dominance of MPN stem cells advances, this will help facilitate the d

205 ic DSBs resulting in enhanced elimination of MPN primary cells, including the disease-initiating cell

206 that can favor the survival and expansion of MPN stem cells over normal HSC, further sustaining and d

207 including JAK2 mutations in the majority of MPN patients and CALR mutations in JAK2-negative MPN pat

208 covery of mutations in CALR, the majority of MPN patients now bear an identifiable marker of clonal d

209 We used a model of MPN, which is induced by co-expression of the oncoprotei

210 sregulated myelopoiesis in a murine model of MPN.

211 F-E2 transgene was reported to be a model of MPN.

212 the transgenic JAK2V617F model, the onset of MPN was delayed in animals lacking IL-33 in radio-resist

213 lar pathways involved in the pathogenesis of MPN is facilitating the development of clinical trials w

214 etter understand the precise pathogenesis of MPN.

215 t promote the development and progression of MPN through profound detrimental effects on haematopoiet

216 nus kinase (JAK) inhibitors for treatment of MPN.

217 specific genomic landscape, that is, type of MPN driver mutations, association with other mutations,

218 The use of MPN is associated with decreased incidence of major comp

219 dings have revolutionized the diagnostics of MPNs and led to development of novel JAK2 therapeutics.

220 The genomic landscape of MPNs is more complex than initially thought and involves

221 he megakaryocytic lineage of mouse models of MPNs and in patients with MPNs.

222 e for IL-33 signaling in the pathogenesis of MPNs.

223 ions are enriched in more advanced phases of MPNs such as myelofibrosis and leukemic transformation,

224 In perspective, molecular profiling of MPNs might also allow for accurate evaluation and monito

225 ssibility of neoplastic tissue, the study of MPNs has provided a window into the earliest stages of t

226 four major stages: (i) chemical synthesis of MPNs, (ii) conjugation with DNA and purification of mono

227 monovalent MPNs, (iii) modular targeting of MPNs to cell-surface receptors, and (iv) control of spat

228 s and the niche to prevent transformation of MPNs into leukemias.

229 The effects of RG7112 and Peg-IFNalpha 2a on MPN progenitor cells were dependent on blocking p53-MDM2

230 PCI (proteasome, COP9 signalosome, eIF3) or MPN (Mpr1, Pad1, amino-terminal) domains constitute the

231 blation or Lariat procedure using the LBN or MPN.

232 ete polyalanine-level models of the eIF3 PCI/MPN core and of two peripheral subunits.

233 the DHX29-bound 43S complex, showing the PCI/MPN core at approximately 6 A resolution.

234 ), previously associated with V617F-positive MPN.

235 ationale for testing these therapies in post-MPN AML.

236 In vitro studies revealed that post-MPN AML cells were sensitive to decitabine, the JAK1/2 i

237 e Mx1-Cre system, p110beta ablation prevents MPN, improves HSC function and suppresses leukaemia init

238 At the same time, primary MPN cell samples from individual patients displayed a hi

239 ), CALR(del52)(+), and MPL(W515L)(+) primary MPN xenografts.

240 imulating factor or arsenic trioxide reduced MPN-initiating cell frequencies and the combination of i

241 ioxide and imatinib can eliminate refractory MPN-initiating cells and reduce disease relapse.

242 L3 receptor antagonists effectively reverses MPN development induced by the Ptpn11-mutated bone marro

243 ficiencies in DSB repair pathways sensitized MPN cells to synthetic lethality triggered by PARP inhib

244 ells (ECs), the mice developed a significant MPN, characterized by thrombocytosis, neutrophilia, and

245 s the magnitude of force exerted on a single MPN.

246 without HIV-1 yielded higher CF-supplemented MPN counts compared with counterparts with HIV-1.

247 cells/mm(3) displayed higher CF-supplemented MPN counts compared with participants with HIV-1 with CD

248 ly mutated HSC, which initiates and sustains MPNs, is termed MPN stem cells.

249 ts can present with myelodysplastic syndrome/MPN, as well as de novo or secondary mixed-phenotype leu

250 ment of therapies that preferentially target MPN stem cells over normal HSC.

251 JAK2 inhibitors do not preferentially target MPN stem cells, and as a result, rarely induce molecular

252 which initiates and sustains MPNs, is termed MPN stem cells.

253 Our studies demonstrate that MPN can be initiated from a single HSC and illustrate th

254 We previously demonstrated that MPN cells become persistent to type I JAK inhibitors tha

255 Here we show that MPN progenitor cells are characterized by marked alterat

256 The MPN phenotype induced by JAK2-V617F was accentuated in J

257 The MPN(+) domain protein BRCC36 associates with pseudo DUB

258 The MPN-restricted driver mutations, including those in JAK2

259 between the stability of mutant Envs and the MPN of V2 bnAb, PG9, as well as an inverse correlation b

260 As the MPN clone expands, it exerts cell-extrinsic effects on c

261 ngs are likely to be of relevance beyond the MPN field.

262 We performed a combined GWAS of the MPN cases plus V617F carriers in the control population

263 to its complementary oligonucleotide on the MPN.

264 The protracted clinical course of the MPNs has limited the use of potentially toxic treatment

265 These MPN sensing materials distinctively stand out from other

266 For these MPN cases plus V617F carriers, we replicated the germ li

267 Although these MPNs are sensitive to tyrosine kinase inhibitors such as

268 ndividuals with a predisposition not only to MPN, but also to JAK2 V617F clonal hematopoiesis, a more

269 hat multiple germline variants predispose to MPN and link constitutional differences in MYB expressio

270 ptors in live cells by adjusting the muMT-to-MPN distance.

271 and 1.5 (95% CI, 1.1-2.1) for unclassifiable MPNs.

272 hemia vera, myelofibrosis, or unclassifiable MPNs.

273 myelofibrosis, and 1720 with unclassifiable MPNs) and 4.3 (95% CI, 4.1-4.4) for the 77445 controls,

274 result of heterogeneity in the HSC in which MPN-initiating mutations arise.

275 pericardial effusions with LBN compared with MPN (8.1% versus 0.9%; P<0.001).

276 ncrease in other complications compared with MPN (open heart surgery to repair cardiac laceration [6

277 intended to compare the outcomes of LBN with MPN for EA.

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

279 suppressor function of EZH2 in patients with MPN and call for caution when considering using Ezh2 inh

280 We assessed causes of death in patients with MPN and matched controls using both relative risks and a

281 Patients with MPN had an overall higher mortality rate than that of ma

282 Survival in patients with MPN increased over time, mainly because of decreased pro

283 that are under evaluation for patients with MPN on the basis of current guidelines, patient risk str

284 from cardiovascular disease in patients with MPN versus controls (16.8% v 15.2%) or cerebrovascular d

285 fied (CEL, NOS) is assigned to patients with MPN with eosinophilia and nonspecific cytogenetic/molecu

286 In patients with MPN, the HRs of death from hematologic malignancies and

287 trioxide cured a large fraction of mice with MPNs.

288 was 5.2 (95% CI, 4.6-5.9) for patients with MPNs (2628 with essential thrombocythemia, 3063 with pol

289 A total of 7958 patients with MPNs (4279 women [53.8%] and 3679 men [46.2%]; mean [SD]

290 AMD was increased overall for patients with MPNs (adjusted HR, 1.3; 95% CI, 1.1-1.5), with adjusted

291 s 2.4% (95% CI, 2.1%-2.8%) for patients with MPNs and 2.3% (95% CI, 2.2%-2.4%) for the controls.

292 Our results suggest that patients with MPNs are at increased risk of AMD, supporting the possib

293 g may be effective in treating patients with MPNs associated with alternative JAK2 mutations, allowin

294 In addition, patients with MPNs had a higher risk of neovascular AMD (adjusted HR,

295 the megakaryocyte genome in 12 patients with MPNs to determine whether there are somatic variants and

296 To compare the risk of AMD in patients with MPNs with the risk of AMD in matched controls from the g

297 For patients with MPNs, detection of the BCR-ABL1 fusion delineates chroni

298 of morbidity and mortality in patients with MPNs, the events causing these clotting abnormalities re

299 of mouse models of MPNs and in patients with MPNs.

300 bination) in the management of patients with MPNs.