ライフサイエンスコーパス: MPN

1 MPN-projecting PA(Esr1+) cells are activated during mati

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

3 monitoring well samples had 0.38 mean log(10)MPN fewer E. coli (95% CI: 0.16, 0.59; p = 0.001) and 0.

4 0.16, 0.59; p = 0.001) and 0.38 mean log(10)MPN fewer thermotolerant coliforms (95% CI: 0.14, 0.62;

5 We determined the difference in mean log(10)MPN FIB counts/100 mL in monitoring well samples between

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

7 In this study of 113 MPN patients, we aimed to comprehensively characterize t

8 ases and 1,152,977 controls), we identify 17 MPN risk loci (P < 5.0 x 10(-8)), 7 of which have not be

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

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

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

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

13 revealed a novel molecular basis of adverse MPN progression that may be therapeutically exploitable

14 lethal myelofibrosis, recapitulating adverse MPN disease progression and revealing a novel genetic in

15 Thrombotic events after MPN and before second cancer were higher in cases than i

16 patients experiencing arterial events after MPN diagnosis deserve careful clinical surveillance for

17 and melanoma diagnosed concurrently or after MPN diagnosis.

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

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

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

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

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

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

24 age at MPN diagnosis, date of diagnosis, and MPN disease duration were included (n = 1234).

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

26 opting treatment strategies used for MDS and MPN.

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

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

29 While key inhibitory inputs to the VMHvl and MPN have been identified, the extrahypothalamic excitato

30 tched with each case for center, sex, age at MPN diagnosis, date of diagnosis, and MPN disease durati

31 ere is a shared genetic architecture between MPN risk and several haematopoietic traits from distinct

32 ria was assumed to be the difference between MPN(rpf) and CFU.

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

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

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

36 blood cell counts in accordance with current MPN diagnostic criteria.

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

38 the biology underpinning mutant CALR-driven MPNs, discuss clinical implications, and highlight futur

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

40 eted therapies effective enough to eliminate MPN cells are still missing.

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

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

43 ibition is a viable therapeutic approach for MPN patients.

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

45 Cases were comparable to controls for MPN type, driver mutations and cardiovascular risk facto

46 ct lineages; that there is an enrichment for MPN risk variants within accessible chromatin of HSCs; a

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

48 cability of immunotherapeutic strategies for MPN patients.

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

50 nts who began treatment with ruxolitinib for MPNs from January 2010 to March 2017.

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

52 unpublished MPL exon 10 sequencing data from MPN patients, demonstrating that some, if not all, of th

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

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

55 %) mutation positives of which 16 (2.5%) had MPN at baseline.

56 n successfully suppresses MAPK activation in MPN cell lines and primary MPN cells in vitro, and the f

57 inhibition suppressed MEK/ERK activation in MPN cell lines in vitro, but not in Jak2V617F and MPLW51

58 We describe a critical role for CDK6 in MPN evolution.

59 iclib, showing that the functions of CDK6 in MPN pathogenesis are largely kinase independent.

60 us provide a rationale for targeting CDK6 in MPN.

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

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

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

64 ata indicate that higher CXCL4 expression in MPN has profibrotic effects and is a mediator of the cha

65 wed that the predicted time to 2 log fall in MPN(rpf) in a Phase 2a setting using in vitro pre-clinic

66 Hypoglycemia in MPN mouse models correlated with hyperactive erythropoie

67 on when considering using Ezh2 inhibitors in MPN.

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

69 esult, rarely induce molecular remissions in MPN patients.

70 nvestigated the role of MEK/ERK signaling in MPN cell survival in the setting of JAK inhibition.

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

72 oliferation and its clinical consequences in MPNs.

73 rtunity for improved therapeutic efficacy in MPNs and in other malignancies driven by aberrant JAK-ST

74 lecular events governing clonal evolution in MPNs, the cell-intrinsic and -extrinsic mechanisms drivi

75 er mutations in JAK2 have been identified in MPNs, most notably exon 12 mutations in PV.

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

77 offer an unexplored neoantigen repertoire in MPNs.

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

79 he development of leukemic transformation in MPNs, recent progress made in our understanding of the m

80 ssible chromatin of HSCs; and that increased MPN risk is associated with longer telomere length in le

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

82 th the thrombopoietin receptor MPL to induce MPNs.

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

84 iously unappreciated mechanism for inherited MPN risk through the modulation of HSC function.

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

86 In conclusion, JAK2V617F MPNs are characterized by exacerbated vasoconstrictor re

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

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

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

90 chronic myeloid leukemia (aCML; n = 71), MDS/MPN with ring sideroblasts and thrombocytosis (MDS/MPN-R

91 s and clonal architecture differed among MDS/MPN subtypes.

92 rombocytosis (MDS/MPN-RS-T; n = 71), and MDS/MPN unclassifiable (MDS/MPN-U; n = 106).

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

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

95 n impact on the outcome of the different MDS/MPN subtypes, which may be relevant for clinical decisio

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

97 tions that were associated with distinct MDS/MPN subtypes and that were mutually exclusive with most

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

99 ASXL1-SETBP1 in aCML, and SF3B1-JAK2 in MDS/MPN-RS-T).

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

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

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

103 odysplastic/myeloproliferative neoplasm (MDS/MPN).

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

105 can be of use in the clinical setting of MDS/MPN.

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

107 that mimicked the ones observed in other MDS/MPN subtypes and that had an impact on the outcome of th

108 th ring sideroblasts and thrombocytosis (MDS/MPN-RS-T; n = 71), and MDS/MPN unclassifiable (MDS/MPN-U

109 proliferative neoplasms, unclassifiable (MDS/MPN-U) are a group of rare and heterogeneous myeloid dis

110 -T; n = 71), and MDS/MPN unclassifiable (MDS/MPN-U; n = 106).

111 terized cohort including 367 adults with MDS/MPN subtypes, including chronic myelomonocytic leukemia

112 Patients with MDS/MPN-U were the most heterogeneous and displayed differen

113 e the diagnostic boundaries between MDS, MDS/MPNs, sAML, clonal hematopoiesis of indeterminate potent

114 dysplastic/myeloproliferative neoplasms (MDS/MPNs).

115 ysplastic/myeloproliferative neoplasms (MDSs/MPNs) harbor somatic mutations in myeloid-related genes,

116 tually exclusive with most of the other MDSs/MPNs (eg, TET2-SRSF2 in CMML, ASXL1-SETBP1 in aCML, and

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

118 de new avenues for designing a range of meso-MPN particles for various applications.

119 ed mesoporous metal-phenolic particles (meso-MPN particles) with a large-pore (~40 nm) single cubic n

120 e, we show that HRP, when loaded in the meso-MPN particles (486 mg g(-1)), retained ~82% activity of

121 network and the phenolic groups in the meso-MPN particles enable high loadings of various proteins (

122 For example, GOx loading in the meso-MPN particles was 362 mg g(-1), which is ~6-fold higher

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

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

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

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

127 In Mks from patients with CALR-mutated MPNs, defective interactions between mutant calreticulin

128 butes to the pathophysiology of CALR-mutated MPNs.

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

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

131 known as monolayer-protected nanoparticles (MPNs).

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

133 ereditary thrombocytosis and triple-negative MPNs.

134 aematopoiesis, myeloproliferative neoplasia (MPN) and leukaemia.

135 m an antecedent myeloproliferative neoplasm (MPN) are characterized by a unique set of cytogenetic an

136 elphia-negative myeloproliferative neoplasm (MPN) are prone to the development of second cancers, but

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

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

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

140 g is central to myeloproliferative neoplasm (MPN) pathogenesis and results in activation of STAT, PI3

141 central role in myeloproliferative neoplasm (MPN) pathogenesis.

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

143 osis (PMF) is a myeloproliferative neoplasm (MPN) that leads to progressive bone marrow (BM) fibrosis

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

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

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

147 drome (MDS) and myeloproliferative neoplasm (MPN).

148 patients with a myeloproliferative neoplasm (MPN).

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

150 are drivers of myeloproliferative neoplasm (MPN).

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

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

153 terogeneity in myeloproliferative neoplasms (MPN) stem and progenitor cells, providing insights into

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

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

156 "early-stage" myeloproliferative neoplasms (MPN).

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

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

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

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

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

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

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

164 Myeloproliferative neoplasms (MPNs) are blood cancers that are characterized by the ex

165 Ph-negative myeloproliferative neoplasms (MPNs) are hematological cancers that can be subdivided i

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

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

168 patients with myeloproliferative neoplasms (MPNs) harbor the acquired somatic JAK2 (V617F) mutation.

169 -initiating in myeloproliferative neoplasms (MPNs) has led to new and effective therapies for these d

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

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

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

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

174 ver in several myeloproliferative neoplasms (MPNs), including essential thrombocythemia, myelofibrosi

175 used to treat myeloproliferative neoplasms (MPNs), including myelofibrosis and polycythemia vera.

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

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

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

179 patients with myeloproliferative neoplasms (MPNs).

180 nt JAK2-driven myeloproliferative neoplasms (MPNs).

181 T signaling in myeloproliferative neoplasms (MPNs).

182 nt fraction of myeloproliferative neoplasms (MPNs).

183 of CALR-mutant myeloproliferative neoplasms (MPNs).

184 h CALR-mutated myeloproliferative neoplasms (MPNs).

185 l stenosis and myeloproliferative neoplasms (MPNs).

186 patients with myeloproliferative neoplasms (MPNs).

187 m signaling in myeloproliferative neoplasms (MPNs).

188 with JAK2V617F myeloproliferative neoplasms (MPNs).

189 ssociated with myeloproliferative neoplasms (MPNs).

190 requent within myeloproliferative neoplasms (MPNs).

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

192 e micro-dissect malignant pulmonary nodules (MPNs) into paired pre-invasive and invasive components f

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

194 The impact of additional non-MPN driver mutations (NDM) on the risk of disease compli

195 Mutation-positive non-MPNs with elevated blood cell counts raise concerns of M

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

197 The medial preoptic nucleus (MPN) and ventrolateral part of the ventromedial hypothal

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

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

200 forming unit (CFU) and most probable number (MPN) with Rpf supplementation were quantified.

201 ermotolerant coliforms most probable number (MPN).

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

203 to predict 149 unique neoantigens in 62% of MPN patients.

204 ugmented and subverted metabolic activity of MPN cells, resulting in systemic metabolic changes in vi

205 04 and MPLY591 mutants in a bigger cohort of MPN.

206 elevated blood cell counts raise concerns of MPN underdiagnosis in the population.

207 ribute synergistically to the development of MPN.

208 The odds ratio for a diagnosis of MPN per percentage allele burden was 1.14 (95% CI, 1.09-

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

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

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

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

213 herapeutic efficacy in the in vivo models of MPN.

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

215 etter understand the precise pathogenesis of MPN.

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

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 l mechanisms that lead to the acquisition of MPNs remain unclear.

220 ndicate a substantial heritable component of MPNs that is among the highest known for cancers(1).

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

222 and reduced hematopoietic manifestations of MPNs.

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

224 metabolic alterations to the pathogenesis of MPNs and suggest that metabolic dependencies of mutant c

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

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

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

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

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

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 Recognizing this new PV/CEL-overlap MPN has significant clinical implications, as both PV an

233 ), previously associated with V617F-positive MPN.

234 Patient-derived, post-MPN, CD34+ sAML blasts exhibiting relative resistance to

235 ting preclinical efficacy against human post-MPN sAML cells.

236 human postmyeloproliferative neoplasm (post-MPN) secondary AML (sAML) cells demonstrated accessible

237 The frequency of thrombosis preceding MPN was similar for cases and controls (P = .462).

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

239 APK activation in MPN cell lines and primary MPN cells in vitro, and the finding that it failed to co

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

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

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 s the magnitude of force exerted on a single MPN.

245 the HSC compartment observed in early-stage MPN, with a small number of JAK2V617F HSC competing with

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

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

255 idence interval, 1.14-3.41), suggesting that MPN patients experiencing arterial events after MPN diag

256 opoietic states-collectively suggesting that MPN risk is associated with the function and self-renewa

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

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

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

260 sence of hematopoietic CXCL4 ameliorates the MPN phenotype, reduces stromal cell activation and BM fi

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

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

263 val, whereas high-glucose diet augmented the MPN phenotype.

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

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

266 to its complementary oligonucleotide on the MPN.

267 These MPN sensing materials distinctively stand out from other

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

269 identify modulators of HSC biology linked to MPN risk, and show through targeted variant-to-function

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

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

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

273 rabilities that can be targeted for treating MPNs.

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

275 hemia vera, myelofibrosis, or unclassifiable MPNs.

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

277 for complete characterization of this unique MPN.

278 evated IL-1beta production in the JAK2-V617F MPN model.

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

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

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

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

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

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

285 sed approach and validation in patients with MPN, we determined that the differential spatial express

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

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

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

289 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.

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

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

292 stenosis or atherosclerosis in patients with MPNs suggests that vascular function is altered.

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

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

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

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

297 es of ruxolitinib treatment in patients with MPNs.

298 JAK2 V617F positives with and without MPN presented elevated odds for prevalent venous thrombo

299 tation-positive individuals with and without MPN.

300 pants, and 42% of mutation positives without MPN presented elevation of >=1 blood cell counts; 80 (13