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1 of those with essential thrombocythemia and primary myelofibrosis.
2 cythemia vera, essential thrombocythemia and primary myelofibrosis.
3 have been devised for myelodysplasia and for primary myelofibrosis.
4 ythemia vera, essential thrombocythemia, and primary myelofibrosis.
5 (MPL)-negative essential thrombocythemia and primary myelofibrosis.
6 ential thrombocythemia and 88% of those with primary myelofibrosis.
7 of those with essential thrombocythemia and primary myelofibrosis.
8 the prototypical myeloproliferative neoplasm primary myelofibrosis.
9 to determine whether the same held true for primary myelofibrosis.
10 vent in a JAK2-V617F knock-in mouse model of primary myelofibrosis.
11 lus) includes 8 risk factors for survival in primary myelofibrosis.
12 ia vera (PV), essential thrombocythemia, and primary myelofibrosis.
13 ythemia vera, essential thrombocythemia, and primary myelofibrosis.
14 ythemia vera, essential thrombocythemia, and primary myelofibrosis.
15 or MPL-mutated essential thrombocytemia and primary myelofibrosis, 2 myeloproliferative neoplasms in
16 hermore, SMRT(mRID) mice develop spontaneous primary myelofibrosis, a chronic, usually idiopathic dis
17 oughly half of essential thrombocythemia and primary myelofibrosis acquire a unique somatic 1849G>T J
18 the challenges inherent in the management of primary myelofibrosis and presents an opportunity to add
19 dysplastic syndrome, acute myeloid leukemia, primary myelofibrosis, and T- and B-cell acute lymphocyt
20 cythemia vera, essential thrombocythemia and primary myelofibrosis are also caused by activated tyros
21 cythemia vera, essential thrombocytosis, and primary myelofibrosis are clonal disorders arising in a
22 tial thrombocythemia, polycythemia vera, and primary myelofibrosis are mainly caused by cardiovascula
23 cythemia vera, essential thrombocythemia and primary myelofibrosis are myeloproliferative neoplasms (
25 ntial thrombocytosis, polycythemia vera, and primary myelofibrosis--are acquired, clonal hematopoieti
27 f patients with essential thrombocythemia or primary myelofibrosis carry a mutation in the Janus kina
29 f of those with essential thrombocythemia or primary myelofibrosis do not, suggesting alternative mec
31 cythemia vera, essential thrombocythemia and primary myelofibrosis has diagnostic and pathogenetic im
32 ntial thrombocytosis, polycythemia vera, and primary myelofibrosis has ushered in a new era of scient
33 patients with essential thrombocythemia and primary myelofibrosis) has led the World Health Organiza
34 the bone marrow and spleen of patients with primary myelofibrosis have a mesenchymal phenotype, whic
41 patients with essential thrombocythemia and primary myelofibrosis, it has been hoped that targeted i
45 Smad2 levels were intrinsically increased in primary myelofibrosis-MSC along with enhanced expression
49 is study, we show that bone marrow MSCs from primary myelofibrosis patients exhibit unique molecular
50 n complements DIPSS-plus in the selection of primary myelofibrosis patients for high-risk treatment a
51 matopoietic and stromal cell compartments in primary myelofibrosis patients may heighten therapeutic
53 The limited effects of current treatments of primary myelofibrosis (PM) led us to prospectively evalu
54 spectrum of plasma cytokine abnormalities in primary myelofibrosis (PMF) and examines their phenotypi
57 vera (PV), essential thombocytosis (ET), and primary myelofibrosis (PMF) as pathogenetically related
59 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) constitute the BCR-ABL1-nega
67 sporadic essential thrombocythemia (ET) and primary myelofibrosis (PMF) lacking JAK2 and MPL mutatio
69 system for transplantation-age patients with primary myelofibrosis (PMF) that integrates clinical, cy
70 tional Prognostic Scoring System (DIPSS) for primary myelofibrosis (PMF) uses five risk factors to pr
71 ia vera, essential thrombocythemia (ET), and primary myelofibrosis (PMF) whereas CALR and MPL mutants
72 ythemia (ET) compared with early/prefibrotic primary myelofibrosis (PMF) with presenting thrombocythe
73 designed to define neoplastic stem cells of primary myelofibrosis (PMF), a myeloproliferative neopla
74 longer duration than in patients with PV and primary myelofibrosis (PMF), and that "triple negative"
75 ntial thrombocythemia, polycythemia vera and primary myelofibrosis (PMF), are a heterogeneous group o
76 s the only curative option for patients with primary myelofibrosis (PMF), but information on its net
77 ients with essential thrombocythemia (ET) or primary myelofibrosis (PMF), first investigating a cohor
78 ck of major improvements in the treatment of primary myelofibrosis (PMF), there are recent indication
94 oproliferative neoplasms defines 2 stages of primary myelofibrosis (PMF): prefibrotic/early (pre-PMF)
95 es including essential thrombocythemia (ET); primary myelofibrosis (PMF); and MPN, unclassifiable (MP
96 h JAK2 V617F-positive or JAK2 V617F-negative primary myelofibrosis, post-essential thrombocythemia my
97 rrent diagnosis of intermediate or high-risk primary myelofibrosis, post-polycythaemia vera myelofibr
98 19 patients with intermediate-2 or high-risk primary myelofibrosis, post-polycythemia vera myelofibro
99 ythemia vera, essential thrombocythemia, and primary myelofibrosis show an inherent tendency for tran
100 the bone marrow and spleen of patients with primary myelofibrosis show functional and morphologic ch
101 source of a critical osteogenic function in primary myelofibrosis that supports its pathophysiology,
102 t patients with essential thrombocythemia or primary myelofibrosis that was not associated with a JAK
103 cythemia vera, essential thrombocythemia and primary myelofibrosis, there likely are additional genet
104 f 884 karyotypically annotated patients with primary myelofibrosis, we sought to identify 1 or 2 para
105 nd extramedullary hematopoiesis characterize primary myelofibrosis, which is also associated with bon
106 t patients with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 and MPL.
107 g patients with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 or MPL, CALR
108 y acquired mutations in six patients who had primary myelofibrosis without mutations in JAK2 or MPL.
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