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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
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.

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