ライフサイエンスコーパス: myeloproliferation

1 rized by elevated inflammatory cytokines and myeloproliferation.

2 aving a biological basis for their excessive myeloproliferation.

3 oimmune disease with hyperactive B cells and myeloproliferation.

4 RC contributes to the BM stromal response to myeloproliferation.

5 roper hematopoiesis and to prevent excessive myeloproliferation.

6 overall influence of overexpressed HoxA10 on myeloproliferation.

7 in AML, confer poor prognosis, and stimulate 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 transplantable hematopoietic neoplasms with myeloproliferation.

16 viral inhibition of Glut1 by shRNA prevented myeloproliferation and adipose tissue loss in mice with

17 l neoplastic disease characterized by clonal myeloproliferation and progressive bone marrow (BM) fibr

18 ET, and PMF include stem cell-derived clonal myeloproliferation and secondary stromal changes in the

19 nistration of SU11657 at 40 mg/kg suppressed myeloproliferation and significantly prolonged survival

20 tions, is at least partially responsible for myeloproliferation (and potentially vascular events) ass

21 ce dysregulation of kinase signaling, clonal myeloproliferation, and abnormal cytokine expression.

22 adults suffer from an extreme neutrophilia, myeloproliferation, and absence of leukocyte selectin li

23 al function (Yang) but also to autoimmunity, myeloproliferation, and cancer (Yin).

24 n the loss of normal HSC functions, a severe myeloproliferation, and death of the mice within weeks.

25 ontributes to confer the phenotype of excess myeloproliferation, and it cooperates with the JAK2V617F

26 ch as erythroid dysplasia, anemia, excessive myeloproliferation, and lymphomyeloid ratio shifts.

27 levels decreased Glut1 expression, dampened myeloproliferation, and prevented fat loss.

28 f hematopoietic stem cells (HSCs), excessive myeloproliferation, and, ultimately, to HSC exhaustion a

29 insufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid prog

30 Self-renewal and myeloproliferation become dependent on beta-catenin in I

31 ith these residues mutated showed no sign of myeloproliferation but instead developed T-cell lymphoma

32 that HoxA10 overexpression is sufficient for myeloproliferation but that differentiation block, and t

33 ting that ICSBP deficiency is sufficient for myeloproliferation, but additional genetic lesions are n

34 hey predict that JAK2 inhibitors may control myeloproliferation, but may have limited efficacy in era

35 ogenes, GM-CSF and IL-3 are not required for myeloproliferation by any of the oncogenes tested.

36 is essential to prevent megakaryocytosis and myeloproliferation by restricting the amount of TPO avai

37 In contrast, target genes involved in myeloproliferation due to HoxA10 overexpression have not

38 oliferative neoplasm characterized by clonal myeloproliferation, dysregulated kinase signaling, and r

39 y, we show that Dok1/Dok2 deficiency affects myeloproliferation even at a young age.

40 F) is characterized by bone marrow fibrosis, myeloproliferation, extramedullary hematopoiesis, spleno

41 ects of JAK2 inhibitors on MPLW515L-mediated myeloproliferation have not been investigated.

42 gly, hMRP8-NPMc(+) transgenic mice developed myeloproliferation in bone marrow and spleen, whereas no

43 -hematopoietic cells of the BM, resulting in myeloproliferation in SHIP-deficient animals.

44 The animals also exhibit chronic myeloproliferation in their bone marrow.

45 rovides a viable mechanism for the increased myeloproliferation in these animals.

46 caused little inhibition of cytokine-induced myeloproliferation in wild type mice, decreased the numb

47 ES and were associated with other markers of myeloproliferation, including elevated B12 levels and sp

48 ty characterized by stem cell-derived clonal myeloproliferation, ineffective erythropoiesis, extramed

49 These findings demonstrate that myeloproliferation may result from perturbed interaction

50 xpansion was not associated with evidence of myeloproliferation, more accurately reflecting the clini

51 d JNK mimics in wild type mice the increased myeloproliferation observed in GSTpi(-/-) animals.

52 oid differentiation, which progresses into a myeloproliferation phenotype.

53 associated with MLL-AF9 gene fusion and that myeloproliferation provides the pool of cells in which s

54 n haematopoietic differentiation involving a myeloproliferation resulting in accumulation of Mac-1/Gr

55 tic ablation of NF-kappaB p50 suppresses the myeloproliferation, showing that dysregulation of NF-kap

56 B cell-specific Lyn mutant mice also develop myeloproliferation, similar to the lyn(-/-) animals.

57 ibrosis in mice does not recapitulate clonal myeloproliferation that is fundamental to human MMM.

58 the progression of the indolent NPM1-driven myeloproliferation toward an exacerbated and proliferati

59 tions are directly implicated in driving the myeloproliferation which characterizes essential thrombo

60 osis with myeloid metaplasia (MMM) is clonal myeloproliferation with varying degrees of phenotypic di