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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 (
24     Severe congenital neutropenia as well as primary myelofibrosis are rare in infancy.
25 ntial thrombocytosis, polycythemia vera, and primary myelofibrosis--are acquired, clonal hematopoieti
26             In essential thrombocythemia and primary myelofibrosis, CALR mutations and JAK2 and MPL m
27 f patients with essential thrombocythemia or primary myelofibrosis carry a mutation in the Janus kina
28 n be a potential therapeutic target to block primary myelofibrosis disease progression.
29 f of those with essential thrombocythemia or primary myelofibrosis do not, suggesting alternative mec
30              In particular, contributions to primary myelofibrosis from mesenchymal stromal cells (MS
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
35 rs, and potentially useful animal models for primary myelofibrosis have been developed.
36                           Most patients with primary myelofibrosis have elevated levels of JAK-depend
37                                              Primary myelofibrosis is a myeloproliferative neoplasm t
38                       We conclude that MK in primary myelofibrosis is associated with extremely poor
39                                              Primary myelofibrosis is characterized by the developmen
40                                              Primary myelofibrosis is the rarest of the myeloprolifer
41  patients with essential thrombocythemia and primary myelofibrosis, it has been hoped that targeted i
42                      Among 200 patients with primary myelofibrosis, karyotype at diagnosis was abnorm
43       Significant disease components include primary myelofibrosis, leukemia, histiocytic sarcoma, an
44       The latter line of mice also developed primary myelofibrosis-like symptoms as they aged.
45 Smad2 levels were intrinsically increased in primary myelofibrosis-MSC along with enhanced expression
46                                              Primary myelofibrosis-MSC overexpressed heparin-binding
47          From 2007 to 2011, 66 patients with primary myelofibrosis or myelofibrosis (MF) preceded by
48                                              Primary myelofibrosis or myelofibrotic transformation pr
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
52                                    Among 793 primary myelofibrosis patients seen at our institution,
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
55                                              Primary myelofibrosis (PMF) and polycythemia vera (PV) a
56           Essential thrombocythemia (ET) and primary myelofibrosis (PMF) are chronic diseases charact
57 vera (PV), essential thombocytosis (ET), and primary myelofibrosis (PMF) as pathogenetically related
58      Treatment of polycythemia vera (PV) and primary myelofibrosis (PMF) CD34(+) cells with low doses
59 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) constitute the BCR-ABL1-nega
60                     Furthermore, even though primary myelofibrosis (PMF) has a markedly worse prognos
61                                Patients with primary myelofibrosis (PMF) have substantially reduced l
62                                              Primary myelofibrosis (PMF) is a clonal hematologic mali
63                                              Primary myelofibrosis (PMF) is a fatal neoplastic diseas
64                                              Primary myelofibrosis (PMF) is a myeloproliferative neop
65                                              Primary myelofibrosis (PMF) is characterized by bone mar
66                                              Primary myelofibrosis (PMF) is characterized by fibrosis
67  sporadic essential thrombocythemia (ET) and primary myelofibrosis (PMF) lacking JAK2 and MPL mutatio
68                                      Because primary myelofibrosis (PMF) originates at the level of t
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
79 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).
80 ients with essential thrombocythemia (ET) or primary myelofibrosis (PMF).
81 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).
82 rotein 3) in mice leads to an MPN resembling primary myelofibrosis (PMF).
83 es reliable risk assessment in patients with primary myelofibrosis (PMF).
84 unmutated essential thrombocythemia (ET) and primary myelofibrosis (PMF).
85 ransformation, and survival of patients with primary myelofibrosis (PMF).
86 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).
87 cance for SF3B1 mutations in both MDS-RS and primary myelofibrosis (PMF).
88 enotype and progression in 499 patients with primary myelofibrosis (PMF).
89 ra (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).
90 ents with essential thrombocythemia (ET) and primary myelofibrosis (PMF).
91 of CD34+ cells is a unique characteristic of primary myelofibrosis (PMF).
92 ot included in current prognostic scores for primary myelofibrosis (PMF).
93 era (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF).
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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