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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
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
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
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
81 tive for a large proportion of patients with myelofibrosis, and post-HCT success was dependent on pre
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.
90 vera, essential thrombocytosis, and primary myelofibrosis are clonal disorders arising in a pluripot
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
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
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
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
109 ts with essential thrombocythemia or primary myelofibrosis carry a mutation in the Janus kinase 2 gen
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
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
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
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
147 s with essential thrombocythemia and primary myelofibrosis, it has been hoped that targeted inhibitio
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
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
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
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
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
189 zations, incidence of cancer, 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
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
198 From 2007 to 2011, 66 patients with primary myelofibrosis or myelofibrosis (MF) preceded by essentia
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.
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
211 ted in platelets from JAK2 inhibitor-treated myelofibrosis patients that express the JAK2 V617F mutan
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
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
231 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 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
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
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
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,
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
275 ks) of the efficacy and safety of Controlled Myelofibrosis Study With Oral Janus-associated Kinase (J
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,
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
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
298 ts with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 or MPL, CALR mutation
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