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1 rom alpha-granules drives the development of bone marrow fibrosis.
2 nules within blood platelets and progressive bone marrow fibrosis.
3 pathic disorder characterized by progressive bone marrow fibrosis.
4 dly reduced extramedullary hematopoeisis and bone marrow fibrosis.
5 a significant regression of splenomegaly and bone marrow fibrosis.
6 they do not offer significant improvement of bone marrow fibrosis.
7  appear to be associated with progression to bone marrow fibrosis.
8 LeukemiaNet criteria, and change in grade of bone marrow fibrosis according to the European consensus
9 egakaryocyte proliferation is accompanied by bone marrow fibrosis and characterizes PMF, while the cl
10 arameters, particularly ADC, correlated with bone marrow fibrosis and disease severity in MF.
11  of some molecules showed an early effect on bone marrow fibrosis and on variant allele frequencies o
12 ropoiesis, extramedullary hematopoiesis, and bone marrow fibrosis and osteosclerosis.
13 transforming growth factor beta1 in inducing bone marrow fibrosis and stromal cell-derived osteoprote
14 oclax-based combination treatment, including bone marrow fibrosis and variant allele frequency, in pa
15 acterized by megakaryocyte (MK) hyperplasia, bone marrow fibrosis, and abnormal stem cell trafficking
16 m characterised by splenomegaly, cytopenias, bone marrow fibrosis, and debilitating symptoms includin
17 der that leads to ineffective hematopoiesis, bone marrow fibrosis, and extramedullary hematopoiesis.
18  patients results in congenital neutropenia, bone marrow fibrosis, and extramedullary renal hematopoi
19 who had neutropenia, neutrophil dysfunction, bone marrow fibrosis, and nephromegaly.
20  improves hematologic parameters, attenuates bone marrow fibrosis, and synergizes with JAK inhibitor
21                                Biomarker and bone marrow fibrosis assessments suggested selective eff
22                                              Bone marrow fibrosis (BMF) develops in various hematolog
23 t week 24, hemoglobin improvement, change in bone marrow fibrosis (BMF) grade, and safety.
24 vidence of extramedullary hematopoiesis, and bone marrow fibrosis, but no lymphoproliferative disease
25 locytosis, extramedullary hematopoiesis, and bone marrow fibrosis, but not thrombocytosis.
26 olonies, larger spleen size, and accelerated bone marrow fibrosis compared with heterozygous Jak2V617
27 ed blood counts, spleen weights, and reduced bone marrow fibrosis compared with ruxolitinib alone.
28 criminant analysis to classify the extent of bone marrow fibrosis for each participant based on ADC v
29 s secondary polycythemia, thrombocytosis, or bone marrow fibrosis from other causes.
30  < 100 x 10(9)/L, circulating blasts >/= 2%, bone marrow fibrosis grade >/= 2, constitutional symptom
31 een implicated in the etiology of idiopathic bone marrow fibrosis (IMF).
32  mg/kg led to a median OS of 29.9 months and bone marrow fibrosis improvement in 40.5% and variant al
33 expansion and accelerates the development of bone marrow fibrosis in heterozygous Jak2V617F mice.
34 ukocytosis and splenomegaly, and ameliorates bone marrow fibrosis in homozygous Jak2V617F mice.
35 counts, reduces splenomegaly and ameliorates bone marrow fibrosis in homozygous Jak2V617F mouse model
36  leukocytosis and splenomegaly and inhibited bone marrow fibrosis in Jak2V617F and MPLW515L mouse mod
37  reduction of spleen size, and abrogation of bone marrow fibrosis in murine models of myelofibrosis.
38  mass in PV, a high platelet count in ET and bone marrow fibrosis in PMF, respectively.
39 okines, reduced disease burden, and reversed bone marrow fibrosis in vivo.
40                                              Bone marrow fibrosis is a maladaptive feature of primary
41                                              Bone marrow fibrosis is the result of a complex and not
42 highest correlation with pathologic grade of bone marrow fibrosis (Kendall tau(B) = 0.44, P = .01).
43 mary myelofibrosis (PMF) is characterized by bone marrow fibrosis, myeloproliferation, extramedullary
44 cidence, degree, and prognostic relevance of bone marrow fibrosis obtained at time of initial diagnos
45 ites correlated with increased risk of overt bone marrow fibrosis (odds ratio = 5.81, P = .01).
46                   No improvement was seen in bone marrow fibrosis or JAK2(V617F) allele burden.
47 athologic or cytogenetic remissions, reverse bone marrow fibrosis, or improve survival over best supp
48 ge, with cytopenia, splenomegaly, and severe bone marrow fibrosis, posing challenges in managing them
49 CXCL8/CXCR2 signaling in MF pathogenesis and bone marrow fibrosis progression.
50  megakaryocytic dysplasia, splenomegaly, and bone marrow fibrosis, prompting us to investigate SETBP1
51                                              Bone marrow fibrosis remains an area of active study, al
52 lostim produced a dose-dependent increase in bone marrow fibrosis that resolved after treatment withd
53                                    Extensive bone marrow fibrosis was found in 23 patients (62%).
54                                              Bone marrow fibrosis was reversed in all 4 patients who
55 e events (eg, thrombosis, hepatobiliary, and bone marrow fibrosis) were infrequent.
56 knockout diminished leukemic engraftment and bone marrow fibrosis while extending survival.