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1 aving a biological basis for their excessive myeloproliferation.
2 in AML, confer poor prognosis, and stimulate myeloproliferation.
3  transplantable hematopoietic neoplasms with myeloproliferation.
4 oimmune disease with hyperactive B cells and myeloproliferation.
5 RC contributes to the BM stromal response to myeloproliferation.
6 roper hematopoiesis and to prevent excessive myeloproliferation.
7 overall influence of overexpressed HoxA10 on myeloproliferation.
8 s not associated with an antecedent stage of myeloproliferation.
9  exaggerated cytokine responses that lead to myeloproliferation.
10 e biochemical abnormalities and relieves the myeloproliferation.
11  restored normal hematopoiesis and prevented myeloproliferation.
12 ne hematopoietic system resulted in profound myeloproliferation.
13 lls results in cytokine hypersensitivity and myeloproliferation.
14 ose-limiting mediators of TEL-PDGFRB-induced myeloproliferation.
15 creased differentiation of myeloid cells and myeloproliferation.
16  A20 in the myeloid lineage cells results in myeloproliferation.
17 rized by elevated inflammatory cytokines and myeloproliferation.
18 viral inhibition of Glut1 by shRNA prevented myeloproliferation and adipose tissue loss in mice with
19 (G12D) in the hematopoietic system developed myeloproliferation and cytopenia, which is reversed in K
20 a promising therapeutic target, with reduced myeloproliferation and fibrosis in vitro and in vivo and
21 eceptor blockade or NLRP3-inhibition reduces myeloproliferation and improves hematopoiesis.
22 rly interferon (IFN)- gamma, in the onset of myeloproliferation and lymphopenia of A20 deficient mice
23 vation in myeloid cells, and thus alleviated myeloproliferation and mice hypersensitivity to bacteria
24 l neoplastic disease characterized by clonal myeloproliferation and progressive bone marrow (BM) fibr
25 ET, and PMF include stem cell-derived clonal myeloproliferation and secondary stromal changes in the
26 nistration of SU11657 at 40 mg/kg suppressed myeloproliferation and significantly prolonged survival
27 tions, is at least partially responsible for myeloproliferation (and potentially vascular events) ass
28 ce dysregulation of kinase signaling, clonal myeloproliferation, and abnormal cytokine expression.
29  adults suffer from an extreme neutrophilia, myeloproliferation, and absence of leukocyte selectin li
30 al function (Yang) but also to autoimmunity, myeloproliferation, and cancer (Yin).
31 n the loss of normal HSC functions, a severe myeloproliferation, and death of the mice within weeks.
32 ontributes to confer the phenotype of excess myeloproliferation, and it cooperates with the JAK2V617F
33 ch as erythroid dysplasia, anemia, excessive myeloproliferation, and lymphomyeloid ratio shifts.
34  levels decreased Glut1 expression, dampened myeloproliferation, and prevented fat loss.
35 roangiopathy, obstructive nephropathy due to myeloproliferation, and urate nephropathy due to tumor l
36 f hematopoietic stem cells (HSCs), excessive myeloproliferation, and, ultimately, to HSC exhaustion a
37 insufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid prog
38                             Self-renewal and myeloproliferation become dependent on beta-catenin in I
39 ith these residues mutated showed no sign of myeloproliferation but instead developed T-cell lymphoma
40 that HoxA10 overexpression is sufficient for myeloproliferation but that differentiation block, and t
41 ting that ICSBP deficiency is sufficient for myeloproliferation, but additional genetic lesions are n
42 hey predict that JAK2 inhibitors may control myeloproliferation, but may have limited efficacy in era
43 ogenes, GM-CSF and IL-3 are not required for myeloproliferation by any of the oncogenes tested.
44 is essential to prevent megakaryocytosis and myeloproliferation by restricting the amount of TPO avai
45        In contrast, target genes involved in myeloproliferation due to HoxA10 overexpression have not
46 oliferative neoplasm characterized by clonal myeloproliferation, dysregulated kinase signaling, and r
47 y, we show that Dok1/Dok2 deficiency affects myeloproliferation even at a young age.
48 F) is characterized by bone marrow fibrosis, myeloproliferation, extramedullary hematopoiesis, spleno
49 ects of JAK2 inhibitors on MPLW515L-mediated myeloproliferation have not been investigated.
50     In the absence of Ifngamma, TIRAP drives myeloproliferation, implicating Ifngamma in suppressing
51 gly, hMRP8-NPMc(+) transgenic mice developed myeloproliferation in bone marrow and spleen, whereas no
52 -hematopoietic cells of the BM, resulting in myeloproliferation in SHIP-deficient animals.
53             The animals also exhibit chronic myeloproliferation in their bone marrow.
54 rovides a viable mechanism for the increased myeloproliferation in these animals.
55 hrough a NET/DC vaccine to treat NPMc-driven myeloproliferation in transgenic and transplantable mode
56 loaded with NPMc+ NET (NPMc+ NET/DC) reduced myeloproliferation in transgenic mice, favoring the deve
57 caused little inhibition of cytokine-induced myeloproliferation in wild type mice, decreased the numb
58 ES and were associated with other markers of myeloproliferation, including elevated B12 levels and sp
59 ty characterized by stem cell-derived clonal myeloproliferation, ineffective erythropoiesis, extramed
60              These findings demonstrate that myeloproliferation may result from perturbed interaction
61         We showed that PPARy agonists reduce myeloproliferation, modulate inflammation, and protect t
62 xpansion was not associated with evidence of myeloproliferation, more accurately reflecting the clini
63 d JNK mimics in wild type mice the increased myeloproliferation observed in GSTpi(-/-) animals.
64 lymphomas, chronic lymphocytic leukemia, and myeloproliferation over 18 months, thus resembling pheno
65  genetic CALR defects promote pre-neoplastic myeloproliferation, patients with myeloproliferative neo
66 oid differentiation, which progresses into a myeloproliferation phenotype.
67 associated with MLL-AF9 gene fusion and that myeloproliferation provides the pool of cells in which s
68 n haematopoietic differentiation involving a myeloproliferation resulting in accumulation of Mac-1/Gr
69 tic ablation of NF-kappaB p50 suppresses the myeloproliferation, showing that dysregulation of NF-kap
70 B cell-specific Lyn mutant mice also develop myeloproliferation, similar to the lyn(-/-) animals.
71 es against G-CSF only partially restored the myeloproliferation, suggesting that additional osteocyte
72 ibrosis in mice does not recapitulate clonal myeloproliferation that is fundamental to human MMM.
73  the progression of the indolent NPM1-driven myeloproliferation toward an exacerbated and proliferati
74 y, an additional role for DCs in suppressing myeloproliferation was discovered.
75                               Inversely, the myeloproliferation was driven by granulocyte colony-stim
76 tions are directly implicated in driving the myeloproliferation which characterizes essential thrombo
77 s that give rise to stem cell-derived clonal myeloproliferation, which is prone to leukemic and, in c
78 c myelopoiesis, and IL-1rn deletion promotes myeloproliferation, which relies on the bone marrow hema
79 osis with myeloid metaplasia (MMM) is clonal myeloproliferation with varying degrees of phenotypic di