ライフサイエンスコーパス: myelofibrosis

1 extend survival of patients with higher-risk myelofibrosis.

2 ons and is a central pathological feature of myelofibrosis.

3 vera, essential thrombocythemia, and primary myelofibrosis.

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

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

6 gative essential thrombocythemia and primary myelofibrosis.

7 is the only potentially curative therapy for myelofibrosis.

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

9 ythroid endogenous growth and progressing to myelofibrosis.

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

11 CSF, from defective platelet aggregation and myelofibrosis.

12 hrombocythemia and 88% of those with primary myelofibrosis.

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

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

15 ibrosis in a model of thrombopoietin-induced myelofibrosis.

16 nd 2, has clinically significant activity in myelofibrosis.

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

18 the treatment of high and intermediate risk myelofibrosis.

19 of STAT5 did not prevent the development of myelofibrosis.

20 the best available therapy, in patients with myelofibrosis.

21 e with essential thrombocythemia and primary myelofibrosis.

22 and a reduction in symptoms associated with myelofibrosis.

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

24 ythroid ratio and significantly reversed the myelofibrosis.

25 ability to reduce disease burden or reverse myelofibrosis.

26 otypical myeloproliferative neoplasm primary myelofibrosis.

27 h mild to moderate bleeding and many develop myelofibrosis.

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

29 rmine whether the same held true for primary myelofibrosis.

30 residual hematopoiesis and only grade 1 or 2 myelofibrosis.

31 ludes 8 risk factors for survival in primary myelofibrosis.

32 ated disorders such as polycythemia vera and myelofibrosis.

33 with polycythemia vera, and 96 patients with myelofibrosis.

34 OX as a new potential therapeutic target for myelofibrosis.

35 nd durable clinical benefit in patients with myelofibrosis.

36 s from clinical trials of JAK2 inhibitors in myelofibrosis.

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

38 mia myelofibrosis, or post-polycythemia vera myelofibrosis.

39 vera, essential thrombocythemia, and primary myelofibrosis.

40 tory cytokines that are commonly elevated in myelofibrosis.

41 ide and lenalidomide can alleviate anemia in myelofibrosis.

42 olitinib-resistant or ruxolitinib-intolerant myelofibrosis.

43 treatment response after allogeneic SCT for myelofibrosis.

44 logeneic stem cell transplantation (SCT) for myelofibrosis.

45 essive myeloid neoplasms, in particular into myelofibrosis.

46 astic syndrome, acute myeloid leukaemia, and myelofibrosis.

47 These results are particularly relevant in myelofibrosis.

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

49 proved therapy for patients with symptomatic myelofibrosis.

50 nic myelomonocytic leukaemia, and seven with myelofibrosis.

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 alf of essential thrombocythemia and primary myelofibrosis acquire a unique somatic 1849G>T JAK2 muta

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

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

62 rednisone is well tolerated in patients with myelofibrosis and active in the treatment of anemia.

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

69 lenges inherent in the management of primary myelofibrosis and presents an opportunity to address the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 vera, essential thrombocytosis, and primary myelofibrosis are clonal disorders arising in a pluripot

91 Treatment options for myelofibrosis are limited.

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

93 vera, essential thrombocythemia and primary myelofibrosis are myeloproliferative neoplasms (MPN) cha

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

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

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

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

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

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

100 Eighty-four patients with myelofibrosis-associated anemia were randomly assigned t

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

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

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

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

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

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

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

108 About half of patients with myelofibrosis carry a gain-of-function mutation in the J

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

110 7q acquired uniparental disomy and in 2 of 2 myelofibrosis cases with focal 17q11 deletions.

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

112 otential therapeutic target to block primary myelofibrosis disease progression.

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

114 se with essential thrombocythemia or primary myelofibrosis do not, suggesting alternative mechanisms

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 with normal megakaryopoiesis and absence of myelofibrosis in histopathology.

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

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

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

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

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

135 Myelofibrosis is a chronic myeloproliferative neoplasm c

136 Myelofibrosis is a hematological malignancy with a media

137 Myelofibrosis is a myeloid malignancy associated with an

138 Primary myelofibrosis is a myeloproliferative neoplasm that is a

139 Myelofibrosis is a Philadelphia chromosome-negative myel

140 Myelofibrosis is a rare hematologic malignancy with limi

141 As myelofibrosis is an extremely rare disease, randomized c

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

143 Primary myelofibrosis is characterized by the development of fib

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

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

146 Primary myelofibrosis is the rarest of the myeloproliferative ne

147 s with essential thrombocythemia and primary myelofibrosis, it has been hoped that targeted inhibitio

148 Among 200 patients with primary myelofibrosis, karyotype at diagnosis was abnormal in 83

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

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

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

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

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

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

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

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

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

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

159 Myelofibrosis (MF) is a devastating blood disorder.

160 Myelofibrosis (MF) is characterized by cytopenias, const

161 Myelofibrosis (MF) is characterized by hematopoiesis occ

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

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

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

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

166 1, 66 patients with primary myelofibrosis or myelofibrosis (MF) preceded by essential thrombocythemia

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

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

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

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

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

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

173 ew treatment options exist for patients with myelofibrosis (MF), and their survival is significantly

174 Managing patients with myelofibrosis (MF), either those with primary MF or thos

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

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

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

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

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

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

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

182 reviously reported responses in persons with myelofibrosis (MF).

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

184 on of myeloproliferative neoplasms including myelofibrosis (MF).

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

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

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

188 Primary myelofibrosis-MSC overexpressed heparin-binding cytokine

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

190 Progression to myelofibrosis, myelodysplasia or leukemic transformation

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

192 %) receiving BAT (lung adenocarcinoma [n=1], myelofibrosis [n=1], and sepsis [n=2]).

193 hrombocythemia, n = 78, P = 8.2 x 10(-9) and myelofibrosis, n = 41, P = 8.0 x 10(-5)).

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

195 ogressive nature of the thrombocytopenia and myelofibrosis of GPS resulting in fatal hemorrhages in s

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 Primary myelofibrosis or myelofibrotic transformation preceded a

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

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

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

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

204 yelofibrosis, post-essential thrombocythemia myelofibrosis, or post-polycythemia vera myelofibrosis.

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

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 herapeutic modality that provides a cure for myelofibrosis patients.

214 ucing splenomegaly and improving symptoms in myelofibrosis patients.

215 d improvement in constitutional symptoms, in myelofibrosis patients.

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

217 preceded by mutation(s) that give rise to a "myelofibrosis" phenotype.

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 Primary myelofibrosis (PMF) and polycythemia vera (PV) are chron

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

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

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

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 cha

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

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

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

232 Because primary myelofibrosis (PMF) originates at the level of the pluri

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

234 rognostic Scoring System (DIPSS) for primary myelofibrosis (PMF) uses five risk factors to predict su

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

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

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

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

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

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

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

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

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

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

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

251 cells is a unique characteristic of primary myelofibrosis (PMF).

252 ded in current prognostic scores for primary myelofibrosis (PMF).

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

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

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

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

257 617F-positive or JAK2 V617F-negative primary myelofibrosis, post-essential thrombocythemia myelofibro

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

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

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

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

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

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

264 Prefibrotic myelofibrosis represents an early phase of myelofibrosis

265 %) using the International Working Group for Myelofibrosis Research and Treatment (IWG-MRT)-defined c

266 rding to the International Working Group for Myelofibrosis Research and Treatment consensus criteria,

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

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

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

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

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

272 In myelofibrosis, stem cell transplant is the current treat

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

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

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

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

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

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

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

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

281 vera, essential thrombocythemia and primary myelofibrosis, there likely are additional genetic event

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

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

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

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

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

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

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

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

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.