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1 ythemia vera, essential thrombocythemia, and primary myelofibrosis.
2 of those with essential thrombocythemia and primary myelofibrosis.
3 cythemia vera, essential thrombocythemia and primary myelofibrosis.
4 have been devised for myelodysplasia and for primary myelofibrosis.
5 era (PV), essential thrombocythemia (ET), or primary myelofibrosis.
6 and 38 years), with a clinical phenotype of primary myelofibrosis.
7 vent in a JAK2-V617F knock-in mouse model of primary myelofibrosis.
8 ythemia vera, essential thrombocythemia, and primary myelofibrosis.
9 (MPL)-negative essential thrombocythemia and primary myelofibrosis.
10 ential thrombocythemia and 88% of those with primary myelofibrosis.
11 of those with essential thrombocythemia and primary myelofibrosis.
12 the prototypical myeloproliferative neoplasm primary myelofibrosis.
13 to determine whether the same held true for primary myelofibrosis.
14 lus) includes 8 risk factors for survival in primary myelofibrosis.
15 ia vera (PV), essential thrombocythemia, and primary myelofibrosis.
16 ythemia vera, essential thrombocythemia, and primary myelofibrosis.
17 or MPL-mutated essential thrombocytemia and primary myelofibrosis, 2 myeloproliferative neoplasms in
18 Methods: Twelve patients with MPNs (4 with primary myelofibrosis, 6 with essential thrombocythemia,
19 hermore, SMRT(mRID) mice develop spontaneous primary myelofibrosis, a chronic, usually idiopathic dis
20 oughly half of essential thrombocythemia and primary myelofibrosis acquire a unique somatic 1849G>T J
21 ations in this update include: patients with primary myelofibrosis and an intermediate-2 or high-risk
23 the challenges inherent in the management of primary myelofibrosis and presents an opportunity to add
24 dysplastic syndrome, acute myeloid leukemia, primary myelofibrosis, and T- and B-cell acute lymphocyt
25 cythemia vera, essential thrombocythemia and primary myelofibrosis are also caused by activated tyros
26 cythemia vera, essential thrombocytosis, and primary myelofibrosis are clonal disorders arising in a
27 tial thrombocythemia, polycythemia vera, and primary myelofibrosis are mainly caused by cardiovascula
28 cythemia vera, essential thrombocythemia and primary myelofibrosis are myeloproliferative neoplasms (
30 ythemia vera, essential thrombocythemia, and primary myelofibrosis, are hematopoietic stem cell disor
31 ntial thrombocytosis, polycythemia vera, and primary myelofibrosis--are acquired, clonal hematopoieti
32 AK2 mutation as essential thrombocytosis and primary myelofibrosis, but erythrocytosis only occurs in
34 f patients with essential thrombocythemia or primary myelofibrosis carry a mutation in the Janus kina
35 f patients with essential thrombocythemia or primary myelofibrosis carry a somatic mutation of the ca
36 oproliferative neoplasms (polycythemia vera, primary myelofibrosis, chronic myeloid leukemia); inflam
38 f of those with essential thrombocythemia or primary myelofibrosis do not, suggesting alternative mec
40 cythemia vera, essential thrombocythemia and primary myelofibrosis has diagnostic and pathogenetic im
41 ntial thrombocytosis, polycythemia vera, and primary myelofibrosis has ushered in a new era of scient
42 patients with essential thrombocythemia and primary myelofibrosis) has led the World Health Organiza
43 the bone marrow and spleen of patients with primary myelofibrosis have a mesenchymal phenotype, whic
50 patients with essential thrombocythemia and primary myelofibrosis, it has been hoped that targeted i
55 Smad2 levels were intrinsically increased in primary myelofibrosis-MSC along with enhanced expression
59 years or older with a confirmed diagnosis of primary myelofibrosis or post-polycythaemia vera or post
60 We found a high frequency of SF3B1-mutated primary myelofibrosis patients (14%) with distinct 3' sp
61 is study, we show that bone marrow MSCs from primary myelofibrosis patients exhibit unique molecular
62 n complements DIPSS-plus in the selection of primary myelofibrosis patients for high-risk treatment a
63 matopoietic and stromal cell compartments in primary myelofibrosis patients may heighten therapeutic
65 of JAK2 V617F- essential thrombocythemia and primary myelofibrosis patients, respectively, have "cano
66 The limited effects of current treatments of primary myelofibrosis (PM) led us to prospectively evalu
67 spectrum of plasma cytokine abnormalities in primary myelofibrosis (PMF) and examines their phenotypi
70 vera (PV), essential thombocytosis (ET), and primary myelofibrosis (PMF) as pathogenetically related
72 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) constitute the BCR-ABL1-nega
73 er-risk myelodysplastic syndromes (MDSs) and primary myelofibrosis (PMF) generally becomes resistant
75 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) have been extensively review
85 sporadic essential thrombocythemia (ET) and primary myelofibrosis (PMF) lacking JAK2 and MPL mutatio
87 system for transplantation-age patients with primary myelofibrosis (PMF) that integrates clinical, cy
88 tional Prognostic Scoring System (DIPSS) for primary myelofibrosis (PMF) uses five risk factors to pr
89 ia vera, essential thrombocythemia (ET), and primary myelofibrosis (PMF) whereas CALR and MPL mutants
90 ythemia (ET) compared with early/prefibrotic primary myelofibrosis (PMF) with presenting thrombocythe
91 designed to define neoplastic stem cells of primary myelofibrosis (PMF), a myeloproliferative neopla
92 e analyzed samples from patients affected by primary myelofibrosis (PMF), a well-known pathological s
93 longer duration than in patients with PV and primary myelofibrosis (PMF), and that "triple negative"
94 ntial thrombocythemia, polycythemia vera and primary myelofibrosis (PMF), are a heterogeneous group o
95 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), are diagnosed according to
96 s the only curative option for patients with primary myelofibrosis (PMF), but information on its net
97 ients with essential thrombocythemia (ET) or primary myelofibrosis (PMF), first investigating a cohor
98 ck of major improvements in the treatment of primary myelofibrosis (PMF), there are recent indication
117 oproliferative neoplasms defines 2 stages of primary myelofibrosis (PMF): prefibrotic/early (pre-PMF)
118 es including essential thrombocythemia (ET); primary myelofibrosis (PMF); and MPN, unclassifiable (MP
119 h JAK2 V617F-positive or JAK2 V617F-negative primary myelofibrosis, post-essential thrombocythemia my
120 rrent diagnosis of intermediate or high-risk primary myelofibrosis, post-polycythaemia vera myelofibr
121 19 patients with intermediate-2 or high-risk primary myelofibrosis, post-polycythemia vera myelofibro
122 ythemia vera, essential thrombocythemia, and primary myelofibrosis show an inherent tendency for tran
123 the bone marrow and spleen of patients with primary myelofibrosis show functional and morphologic ch
124 source of a critical osteogenic function in primary myelofibrosis that supports its pathophysiology,
125 t patients with essential thrombocythemia or primary myelofibrosis that was not associated with a JAK
126 cythemia vera, essential thrombocythemia and primary myelofibrosis, there likely are additional genet
128 f 884 karyotypically annotated patients with primary myelofibrosis, we sought to identify 1 or 2 para
129 nd extramedullary hematopoiesis characterize primary myelofibrosis, which is also associated with bon
130 t patients with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 and MPL.
131 g patients with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 or MPL, CALR
132 y acquired mutations in six patients who had primary myelofibrosis without mutations in JAK2 or MPL.