ライフサイエンスコーパス: myelofibrosis

1 logeneic stem cell transplantation (SCT) for myelofibrosis.

2 essive myeloid neoplasms, in particular into myelofibrosis.

3 astic syndrome, acute myeloid leukaemia, and myelofibrosis.

4 These results are particularly relevant in myelofibrosis.

5 tients with high-risk or intermediate-2-risk myelofibrosis.

6 nic myelomonocytic leukaemia, and seven with myelofibrosis.

7 vera, essential thrombocythemia, and primary myelofibrosis.

8 act on survival or transformation to post-ET myelofibrosis.

9 themia vera (PV)-like disorder evolving into myelofibrosis.

10 gative essential thrombocythemia and primary myelofibrosis.

11 is the only potentially curative therapy for myelofibrosis.

12 regulate clonal dominance and progression to myelofibrosis.

13 t selection, timing, and outcomes of HSCT in myelofibrosis.

14 ythroid endogenous growth and progressing to myelofibrosis.

15 tial thrombocythemia, polycythemia vera, and myelofibrosis.

16 nformation from a total of 361 patients with myelofibrosis.

17 t of MPN-affected patients and prevention of myelofibrosis.

18 CSF, from defective platelet aggregation and myelofibrosis.

19 hrombocythemia and 88% of those with primary myelofibrosis.

20 th PMF, and 7/44 (16%) patients with post-ET myelofibrosis.

21 in patients with intermediate-2 or high-risk myelofibrosis.

22 ibrosis in a model of thrombopoietin-induced myelofibrosis.

23 nd 2, has clinically significant activity in myelofibrosis.

24 would be efficacious in Jak2-V617F-mediated myelofibrosis.

25 the treatment of high and intermediate risk myelofibrosis.

26 of STAT5 did not prevent the development of myelofibrosis.

27 the best available therapy, in patients with myelofibrosis.

28 e with essential thrombocythemia and primary myelofibrosis.

29 and a reduction in symptoms associated with myelofibrosis.

30 ce of thrombosis, and not to predict post-ET myelofibrosis.

31 ythroid ratio and significantly reversed the myelofibrosis.

32 otypical myeloproliferative neoplasm primary myelofibrosis.

33 h mild to moderate bleeding and many develop myelofibrosis.

34 rmine whether the same held true for primary myelofibrosis.

35 residual hematopoiesis and only grade 1 or 2 myelofibrosis.

36 ludes 8 risk factors for survival in primary myelofibrosis.

37 ated disorders such as polycythemia vera and myelofibrosis.

38 with polycythemia vera, and 96 patients with myelofibrosis.

39 OX as a new potential therapeutic target for myelofibrosis.

40 nd durable clinical benefit in patients with myelofibrosis.

41 s from clinical trials of JAK2 inhibitors in myelofibrosis.

42 (PV), essential thrombocythemia, and primary myelofibrosis.

43 extend survival of patients with higher-risk myelofibrosis.

44 proved therapy for patients with symptomatic myelofibrosis.

45 ons and is a central pathological feature of myelofibrosis.

46 ability to reduce disease burden or reverse myelofibrosis.

47 a JAK2-V617F knock-in mouse model of primary myelofibrosis.

48 olitinib-resistant or ruxolitinib-intolerant myelofibrosis.

49 treatment response after allogeneic SCT for myelofibrosis.

50 thrombocythemia (ET)/polycythemia vera (PV) myelofibrosis (0.701) improving prognostic ability in co

51 usefulness of the DIPSS in 170 patients with myelofibrosis, 12 to 78 years of age (median, 51.5 years

52 te the diagnostic value of this technique in myelofibrosis, (18)F-FLT PET imaging results were compar

53 more prone to develop post-polycythemia vera myelofibrosis (2.2 vs 0.8 per 100 patient-years; P = .01

54 mutated essential thrombocytemia and primary myelofibrosis, 2 myeloproliferative neoplasms in which m

55 frequency in PV (55%; n = 22; P = .0028) and myelofibrosis (35%; n = 20) patients than in NDs (9%; n

56 f 219 individuals, or 12%) and in those with myelofibrosis (4 out of 30 individuals, or 13%).

57 SMRT(mRID) mice develop spontaneous primary myelofibrosis, a chronic, usually idiopathic disorder ch

58 which has been approved for the treatment of myelofibrosis, a rare myeloproliferative neoplasm (MPN),

59 ythemia vera, essential thrombocythemia, and myelofibrosis and 252 637 population controls unselected

60 months, no patient had developed leukemia or myelofibrosis and 5% had thrombosis; the miscarriage rat

61 b-B results in severe macrothrombocytopenia, myelofibrosis and aberrant platelet function in mice and

62 pparent from early multipotent stem cells in myelofibrosis and associated aberrant molecular signatur

63 MK growth and proliferation results in rapid myelofibrosis and establishes a previously unrecognized

64 eoplasms (MPN), and in particular those with myelofibrosis and extensive splenomegaly and symptomatic

65 ched in more advanced phases of MPNs such as myelofibrosis and leukemic transformation, suggesting th

66 ications, and bone marrow failure because of myelofibrosis and leukemic transformation.

67 Abnormal cytokine expression accompanies myelofibrosis and might be a therapeutic target for Janu

68 eloproliferative neoplasms (MPNs), including myelofibrosis and polycythemia vera.

69 ith JAK inhibitors used for the treatment of myelofibrosis and polycythemia vera/essential thrombocyt

70 Patients who had myelofibrosis and previous ruxolitinib treatment for at

71 ncluding their implications for evolution to myelofibrosis and secondary acute myeloid leukemia.

72 nhibitors are valuable therapeutic agents in myelofibrosis and show promising results in graft-versus

73 s, which include normalization of life span (myelofibrosis and some patients with PV), reduction of c

74 lly, they have the propensity to progress to myelofibrosis and transform to acute myeloid leukemia.

75 r of unknown primary, acute myeloid leukemia/myelofibrosis and Waldenstrom macroglobulinemia/myeloma.

76 polycythemia vera, 1.7 (95% CI, 0.8-4.0) for myelofibrosis, and 1.5 (95% CI, 1.1-2.1) for unclassifia

77 hemia, 3063 with polycythemia vera, 547 with myelofibrosis, and 1720 with unclassifiable MPNs) and 4.

78 c stem and progenitor cells, MK hyperplasia, myelofibrosis, and consequent extramedullary hematopoies

79 tic stem cell transplantation is curative in myelofibrosis, and current prognostic scoring systems ai

80 hat G6 is efficacious in Jak2-V617F-mediated myelofibrosis, and given its bone marrow efficacy, it ma

81 c myelofibrosis represents an early phase of myelofibrosis, and is characterized by granulocytic/mega

82 ation of these together with splenomegaly or myelofibrosis, and it can take years for a true panmyelo

83 of thrombosis, hemorrhage, transformation to myelofibrosis, and leukemia.

84 (MPNs), including essential thrombocythemia, myelofibrosis, and polycythemia vera (PV).

85 tive for a large proportion of patients with myelofibrosis, and post-HCT success was dependent on pre

86 manifesting by neutropenia, thrombasthenia, myelofibrosis, and progressive bone marrow failure.

87 latelet and neutrophil counts, more advanced myelofibrosis, and reduced survival.

88 GPS is associated with a bleeding tendency, myelofibrosis, and splenomegaly.

89 ic syndrome, acute myeloid leukemia, primary myelofibrosis, and T- and B-cell acute lymphocytic leuke

90 tors in only a select group of patients with myelofibrosis, and their potential value in polycythemia

91 be a useful tool to measure the severity of myelofibrosis, and to monitor noninvasively the patients

92 ial and venous complications, progression to myelofibrosis, and transformation to acute leukemia.

93 Other existing therapies for myelofibrosis appear no more effective than placebo.

94 Treatment options for myelofibrosis are limited.

95 ombocythemia, polycythemia vera, and primary myelofibrosis are mainly caused by cardiovascular diseas

96 tution experiments indicate that MPN/MDS and myelofibrosis are of hematopoietic rather than stromal o

97 re congenital neutropenia as well as primary myelofibrosis are rare in infancy.

98 investigating the role of transplantation in myelofibrosis are unlikely to occur, thus current decisi

99 cythemia vera, essential thrombocytosis, and myelofibrosis, are disorders characterized by abnormal h

100 rombocytosis, polycythemia vera, and primary myelofibrosis--are acquired, clonal hematopoietic stem c

101 rare CALRins5-, transduced mice developed a myelofibrosis associated with a splenomegaly and a marke

102 stat was found to be active in patients with myelofibrosis but also had the potential to cause clinic

103 radioresistant BM stroma compartment impairs myelofibrosis but, at the same time, associates with an

104 tion as essential thrombocytosis and primary myelofibrosis, but erythrocytosis only occurs in PV.

105 constitutional symptoms and splenomegaly in myelofibrosis, but the effect of these agents on the nat

106 JAK1/2 improve symptoms and prolong life in myelofibrosis, but their use is limited by cost.

107 gnificant clinical benefits in patients with myelofibrosis by reducing spleen size, ameliorating debi

108 In essential thrombocythemia and primary myelofibrosis, CALR mutations and JAK2 and MPL mutations

109 Available therapies for myelofibrosis can exacerbate cytopenias and are not indi

110 ts with essential thrombocythemia or primary myelofibrosis carry a mutation in the Janus kinase 2 gen

111 ts with essential thrombocythemia or primary myelofibrosis carry a somatic mutation of the calreticul

112 7q acquired uniparental disomy and in 2 of 2 myelofibrosis cases with focal 17q11 deletions.

113 paves the way for selective targeting of the myelofibrosis clone and illustrates the power of single-

114 antly higher in patients with PMF or post-ET myelofibrosis compared with those with ET.

115 otential therapeutic target to block primary myelofibrosis disease progression.

116 ycythemia vera and chronic myeloid leukemia, myelofibrosis displays high patient morbidity and mortal

117 ief Fatigue Inventory) to assess symptoms of myelofibrosis, essential thrombocythemia, and polycythem

118 d durable clinical benefits in patients with myelofibrosis for whom no approved therapies existed.

119 fibrosis, or post-essential thrombocythaemia myelofibrosis, found to be ruxolitinib resistant or into

120 In particular, contributions to primary myelofibrosis from mesenchymal stromal cells (MSC) have

121 c sclerosis, hypertrophic cardiomyopathy, or myelofibrosis from Stanford (Jan 01, 2008, to Dec 31, 20

122 However, its efficacy in Jak2-mediated myelofibrosis has not previously been examined.

123 Among these myeloproliferative neoplasms, myelofibrosis has the most unfavorable prognosis.

124 c agents in patients with MYH9-RDs; however, myelofibrosis has to be considered as a potential severe

125 rombocytosis, polycythemia vera, and primary myelofibrosis has ushered in a new era of scientific dis

126 e marrow and spleen of patients with primary myelofibrosis have a mesenchymal phenotype, which is sug

127 Most patients with primary myelofibrosis have elevated levels of JAK-dependent proi

128 rthermore, currently available therapies for myelofibrosis have little to no efficacy in the bone mar

129 introduction of Janus kinase inhibitors for myelofibrosis have ushered in a new era for treatment of

130 he contribution of MKs to the progression of myelofibrosis, highlighting the newly identified role of

131 akaryocytes is an established feature of and myelofibrosis; however, the exact mechanism responsible

132 with normal megakaryopoiesis and absence of myelofibrosis in histopathology.

133 ings recapitulate the development of post-PV myelofibrosis in human myeloproliferative neoplasms.

134 , and in patients with systemic sclerosis or myelofibrosis in two of the three cohorts.

135 s for myeloproliferative neoplasm-associated myelofibrosis, including Janus kinase (JAK) inhibitors,

136 ould be a treatment option for patients with myelofibrosis, including those with baseline cytopenias

137 on than activated JAK2 alone and accelerated myelofibrosis, indicating that Lnk directly inhibits onc

138 rsus best available therapy in patients with myelofibrosis irrespective of baseline cytopenias.

139 Myelofibrosis is a chronic myeloproliferative neoplasm c

140 Myelofibrosis is a hematological malignancy with a media

141 Myelofibrosis is a myeloid malignancy associated with an

142 Primary myelofibrosis is a myeloproliferative neoplasm that is a

143 Myelofibrosis is a rare hematologic malignancy with limi

144 Myelofibrosis is a severe myeloproliferative neoplasm ch

145 As myelofibrosis is an extremely rare disease, randomized c

146 We conclude that MK in primary myelofibrosis is associated with extremely poor overall

147 Primary myelofibrosis is characterized by the development of fib

148 Diagnosis of post-PV myelofibrosis is established according to the Internatio

149 The only approved JAK2 inhibitor for myelofibrosis is the dual JAK1 and JAK2 inhibitor, ruxol

150 brotic diseases, including IPF; scleroderma; myelofibrosis; kidney-, pancreas-, and heart-fibrosis; a

151 gnificant disease components include primary myelofibrosis, leukemia, histiocytic sarcoma, and vascul

152 brosis patients' BM cells developed a lethal myelofibrosis-like phenotype.

153 A sub-fraction of myelofibrosis megakaryocyte progenitors (MkPs) are trans

154 ia vera (PV), essential thrombocythemia, and myelofibrosis (MF) (both primary and secondary), are rec

155 n CALR are frequently found in patients with myelofibrosis (MF) and essential thrombocythemia (ET) wi

156 (IWG-MRT) criteria for treatment response in myelofibrosis (MF) and represents a collaborative effort

157 Although most patients with myelofibrosis (MF) derive benefit from ruxolitinib, some

158 ) and other hematologic malignancies such as myelofibrosis (MF) in mice.

159 Myelofibrosis (MF) is a BCR-ABL-negative myeloproliferat

160 Myelofibrosis (MF) is a BCR-ABL1-negative myeloprolifera

161 Myelofibrosis (MF) is a devastating blood disorder.

162 Myelofibrosis (MF) is characterized by cytopenias, const

163 Myelofibrosis (MF) is characterized by hematopoiesis occ

164 Patients with myelofibrosis (MF) often develop anemia and frequently b

165 It is currently assumed that myelofibrosis (MF) originates from acquired mutations th

166 hylation profiles of sorted blood cells from myelofibrosis (MF) patients and healthy controls.

167 s constitutional symptoms and spleen size of myelofibrosis (MF) patients by mechanisms distinct from

168 we show the clonal evolution structure in 15 myelofibrosis (MF) patients while receiving treatment wi

169 1, 66 patients with primary myelofibrosis or myelofibrosis (MF) preceded by essential thrombocythemia

170 nt of acute promyelocytic leukemia (APL) and myelofibrosis (MF) samples, and identified LICs in these

171 stem and progenitor cells from patients with myelofibrosis (MF) to the Janus kinase (JAK) inhibitor,

172 and spleen of the Gata1(low) mouse model of myelofibrosis (MF) was profiled and the consequences of

173 ort that in JAK2V617F positive patients with myelofibrosis (MF), a proportion of endothelial cells (E

174 ved to become the centerpiece of therapy for myelofibrosis (MF), and its use in patients with hydroxy

175 nt improvements in the signs and symptoms of myelofibrosis (MF), and possible prolongation of patient

176 urden and improved survival in patients with myelofibrosis (MF), irrespective of their JAK2 mutation

177 contributes to dysregulated JAK signaling in myelofibrosis (MF), polycythemia vera (PV), and essentia

178 on of myeloproliferative neoplasms including myelofibrosis (MF).

179 s commonly found in patients with late-stage myelofibrosis (MF).

180 udies in patients with primary and secondary myelofibrosis (MF).

181 signaling is central to the pathogenesis of myelofibrosis (MF).

182 o abnormal BM and spleen microenvironment in myelofibrosis (MF).

183 ymptoms and quality of life in patients with myelofibrosis (MF).

184 olitinib, for the treatment of patients with myelofibrosis (MF).

185 hibitor with established clinical benefit in myelofibrosis (MF).

186 een found in approximately 50% patients with myelofibrosis (MF).

187 olitinib-resistant or ruxolitinib-intolerant myelofibrosis might achieve significant clinical benefit

188 vels were intrinsically increased in primary myelofibrosis-MSC along with enhanced expression of the

189 Primary myelofibrosis-MSC overexpressed heparin-binding cytokine

190 zations, incidence of cancer, progression to myelofibrosis, myelodysplasia or leukemic transformation

191 Progression to myelofibrosis, myelodysplasia or leukemic transformation

192 utcomes: thrombosis and disease evolution to myelofibrosis, myelodysplastic syndrome, or acute myeloi

193 al infarction (n = 2), headache (n = 2), and myelofibrosis (n = 2) occurred in more than 1 patient; t

194 %) receiving BAT (lung adenocarcinoma [n=1], myelofibrosis [n=1], and sepsis [n=2]).

195 Transformation to myelofibrosis occurred in 1 CMR patient, presumably beca

196 nd Treatment (IWG-MRT) response criteria for myelofibrosis or for other myeloproliferative neoplasms

197 lar complications and progression to post-PV myelofibrosis or leukemia.

198 From 2007 to 2011, 66 patients with primary myelofibrosis or myelofibrosis (MF) preceded by essentia

199 be ambiguous; for example, with prefibrotic myelofibrosis or reactive monocytosis.

200 Disease transformation into myelofibrosis or secondary leukemia was not reported.

201 imary myelofibrosis, post-polycythaemia vera myelofibrosis, or post-essential thrombocythaemia myelof

202 rimary myelofibrosis, post-polycythemia vera myelofibrosis, or post-essential thrombocythemia myelofi

203 ssential thrombocythemia, polycythemia vera, myelofibrosis, or unclassifiable MPNs.

204 Myelofibrosis, panleukopenia, anemia, and thrombocytopen

205 nd a high frequency of SF3B1-mutated primary myelofibrosis patients (14%) with distinct 3' splicing p

206 , we show that bone marrow MSCs from primary myelofibrosis patients exhibit unique molecular and func

207 ments DIPSS-plus in the selection of primary myelofibrosis patients for high-risk treatment approache

208 l Working Group showed that the prognosis of myelofibrosis patients is predicted by the Dynamic Inter

209 tic and stromal cell compartments in primary myelofibrosis patients may heighten therapeutic efficacy

210 Among 793 primary myelofibrosis patients seen at our institution, 62 displ

211 ted in platelets from JAK2 inhibitor-treated myelofibrosis patients that express the JAK2 V617F mutan

212 Immunodeficient mice transplanted with myelofibrosis patients' BM cells developed a lethal myel

213 V617F- essential thrombocythemia and primary myelofibrosis patients, respectively, have "canonical" M

214 n about 30% of essential thrombocythemia and myelofibrosis patients.

215 herapeutic modality that provides a cure for myelofibrosis patients.

216 ucing splenomegaly and improving symptoms in myelofibrosis patients.

217 d improvement in constitutional symptoms, in myelofibrosis patients.

218 ted effects of current treatments of primary myelofibrosis (PM) led us to prospectively evaluate reco

219 of plasma cytokine abnormalities in primary myelofibrosis (PMF) and examines their phenotypic correl

220 Essential thrombocythemia (ET) and primary myelofibrosis (PMF) are chronic diseases characterized b

221 atment of polycythemia vera (PV) and primary myelofibrosis (PMF) CD34(+) cells with low doses of RG71

222 essential thrombocythemia (ET), and primary myelofibrosis (PMF) constitute the BCR-ABL1-negative mye

223 myelodysplastic syndromes (MDSs) and primary myelofibrosis (PMF) generally becomes resistant to avail

224 Furthermore, even though primary myelofibrosis (PMF) has a markedly worse prognosis than

225 Patients with primary myelofibrosis (PMF) have substantially reduced life expe

226 Primary myelofibrosis (PMF) is a clonal hematologic malignancy c

227 Primary myelofibrosis (PMF) is a fatal neoplastic disease charac

228 Primary myelofibrosis (PMF) is a myeloproliferative neoplasm (MP

229 Primary myelofibrosis (PMF) is a myeloproliferative neoplasm cha

230 Primary myelofibrosis (PMF) is characterized by bone marrow fibr

231 Primary myelofibrosis (PMF) is characterized by fibrosis, ineffe

232 c essential thrombocythemia (ET) and primary myelofibrosis (PMF) lacking JAK2 and MPL mutations.

233 or transplantation-age patients with primary myelofibrosis (PMF) that integrates clinical, cytogeneti

234 essential thrombocythemia (ET), and primary myelofibrosis (PMF) whereas CALR and MPL mutants are fou

235 (ET) compared with early/prefibrotic primary myelofibrosis (PMF) with presenting thrombocythemia.

236 d to define neoplastic stem cells of primary myelofibrosis (PMF), a myeloproliferative neoplasm chara

237 ed samples from patients affected by primary myelofibrosis (PMF), a well-known pathological situation

238 uration than in patients with PV and primary myelofibrosis (PMF), and that "triple negative" mutation

239 rombocythemia, polycythemia vera and primary myelofibrosis (PMF), are a heterogeneous group of myeloi

240 ly curative option for patients with primary myelofibrosis (PMF), but information on its net advantag

241 th essential thrombocythemia (ET) or primary myelofibrosis (PMF), first investigating a cohort of 892

242 jor improvements in the treatment of primary myelofibrosis (PMF), there are recent indications that t

243 ble risk assessment in patients with primary myelofibrosis (PMF).

244 d essential thrombocythemia (ET) and primary myelofibrosis (PMF).

245 ation, and survival of patients with primary myelofibrosis (PMF).

246 essential thrombocythemia (ET), and primary myelofibrosis (PMF).

247 r SF3B1 mutations in both MDS-RS and primary myelofibrosis (PMF).

248 and progression in 499 patients with primary myelofibrosis (PMF).

249 essential thrombocythemia (ET), and primary myelofibrosis (PMF).

250 ) in mice leads to an MPN resembling primary myelofibrosis (PMF).

251 h essential thrombocythemia (ET) and primary myelofibrosis (PMF).

252 essential thrombocythemia (ET), and primary myelofibrosis (PMF).

253 llmark of bone marrow (BM) milieu in primary myelofibrosis (PMF).

254 rative neoplasms defines 2 stages of primary myelofibrosis (PMF): prefibrotic/early (pre-PMF) and ove

255 ding essential thrombocythemia (ET); primary myelofibrosis (PMF); and MPN, unclassifiable (MPN,U).

256 agnosis of intermediate or high-risk primary myelofibrosis, post-polycythaemia vera myelofibrosis, or

257 nts with intermediate-2 or high-risk primary myelofibrosis, post-polycythemia vera myelofibrosis, or

258 INTERPRETATION: In patients with myelofibrosis previously treated with ruxolitinib, momel

259 ion led to accelerated development of lethal myelofibrosis, recapitulating adverse MPN disease progre

260 hieved clinically meaningful improvements in myelofibrosis-related symptoms and QoL, but patients rec

261 tinib experienced improvements in individual myelofibrosis-related symptoms, although patients receiv

262 ucing spleen size, ameliorating debilitating myelofibrosis-related symptoms, and improving overall su

263 fever/elevated C-reactive protein, reticulin myelofibrosis, renal dysfunction, organomegaly (TAFRO) c

264 Prefibrotic myelofibrosis represents an early phase of myelofibrosis

265 International Working Group for Myelofibrosis Research and Treatment criteria for progno

266 ythemia vera, essential thrombocythemia, and myelofibrosis, respectively.

267 tial thrombocythemia, polycythemia vera, and myelofibrosis, respectively.

268 vera, essential thrombocythemia, and primary myelofibrosis show an inherent tendency for transformati

269 e marrow and spleen of patients with primary myelofibrosis show functional and morphologic changes th

270 In myelofibrosis, stem cell transplant is the current treat

271 In the phase 3 Controlled Myelofibrosis Study with Oral JAK Inhibitor Treatment-I

272 COMFORT-I (Controlled Myelofibrosis Study With Oral JAK Inhibitor Treatment-I)

273 ks) of the efficacy and safety of Controlled Myelofibrosis Study With Oral Janus-associated Kinase (J

274 l symptom score, assessed using the modified Myelofibrosis Symptom Assessment Form).

275 of a critical osteogenic function in primary myelofibrosis that supports its pathophysiology, suggest

276 ts with essential thrombocythemia or primary myelofibrosis that was not associated with a JAK2 or MPL

277 ll adverse events (thrombosis, bleeding, and myelofibrosis), the rate was significantly different (1.

278 gh JAK inhibitors have important benefits in myelofibrosis therapy, their role in polycythemia vera/e

279 ofibrosis, or post-essential thrombocythemia myelofibrosis to receive oral ruxolitinib or the best av

280 ed patients with intermediate-2 or high-risk myelofibrosis to twice-daily oral ruxolitinib (155 patie

281 aining cohort to create a clinical-molecular myelofibrosis transplant scoring system (MTSS), which wa

282 domide and lenalidomide in 125 patients with myelofibrosis treated in 3 consecutive phase 2 trials: 4

283 e use of the International Working Group for Myelofibrosis Treatment and Research consensus criteria,

284 come of patients with primary and post-ET/PV myelofibrosis undergoing allogeneic stem cell transplant

285 Twelve patients with myelofibrosis underwent (18)F-FDG PET/CT before and afte

286 Progression to overt myelofibrosis was 3% in ET and 9% in early PMF, but no t

287 ally in the spleen, and a slight increase in myelofibrosis was noted.

288 ed clinical trials for treating lymphoma and myelofibrosis-was prepared by RCM carried out at a subst

289 cular basis for aberrant megakaryopoiesis in myelofibrosis, we performed single-cell transcriptome pr

290 xolitinib improves symptoms in patients with myelofibrosis, we postulated that ruxolitinib would impr

291 ryotypically annotated patients with primary myelofibrosis, we sought to identify 1 or 2 parameters t

292 Fifteen patients with histology-proven myelofibrosis were included consecutively in the study.

293 cquired mutations, particularly prevalent in myelofibrosis, where their presence carries prognostic i

294 medullary hematopoiesis characterize primary myelofibrosis, which is also associated with bone marrow

295 est available therapy (BAT) in patients with myelofibrosis who had suboptimal responses or haematolog

296 ytic leukaemia, myelodysplastic syndrome, or myelofibrosis who were refractory, resistant, or intoler

297 ts with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 and MPL.

298 ts with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 or MPL, CALR mutation

299 Patients with higher-risk myelofibrosis (with no exclusions for baseline anaemia o

300 ed mutations in six patients who had primary myelofibrosis without mutations in JAK2 or MPL.