ライフサイエンスコーパス: blastic

1 ses with variant cytology (ie, anaplastic or blastic), 6 (28.6%) had p53 mutations as compared with o

2 in the metaphysis of long bones (62%) with a blastic appearance (53%).

3 astic large lymphocytes, some of which had a blastic appearance or resembled virocytes.

4 Conidia were blastic, aseptate, and formed in chains, with distinguis

5 Survival was compared for both lytic and blastic bone metastases and for patients with high and l

6 en compared to the more highly proliferative blastic cases or cell lines (mean arbitrary units: 58 ve

7 activation markedly accelerated leukemia and blastic crisis onset in Tec-p210bcr/abl transgenic mice

8 The patient with extramedullary blastic disease achieved complete response.

9 1 had a complete response in extramedullary blastic disease).

10 phase in 5 patients, accelerated in 15, and blastic in 8 (7 medullary, 1 extramedullary); median tim

11 ive p53 construct developed leukocytosis and blastic infiltration of lymph nodes, spleen, and liver w

12 macrophages, indicating that erythro-(myelo)-blastic islands are a site for terminal granulopoiesis a

13 eloid disorders, then the emergence of acute blastic leukemias; and treating malignant and nonmaligna

14 on primarily by mononuclear cells (including blastic lymphocytes), and increased crypt cell apoptosis

15 essed at variable levels in both typical and blastic MCLs.

16 mo2 and gata1 promoters exhibit an immature, blastic morphology and express only erythroid and myeloi

17 chromosome imbalances were observed in both blastic natural killer and cutaneous natural killer-like

18 vestigate comprehensively genomic changes in blastic natural killer and extranodal natural killer-lik

19 the RB1 gene at 13q14.2 was detected in one blastic natural killer cell lymphoma with 13q loss using

20 continuous infusion to 19 adults with CML in blastic or accelerated phase.

21 plete cytogenetic response in 8) and 43% for blastic phase (3 of 7 patients).

22 ronic phase (CP), accelerated phase (AP), or blastic phase (BP) were injected into preirradiated NOD/

23 In AML, accelerated phase (AP) and blastic phase (BP)-CML, basal TA was 10- to 50-fold high

24 se (CP), 175 accelerated phase (AP), and 246 blastic phase (BP).

25 es (MDS), or chronic myelogenous leukemia in blastic phase (CML-BP) were initially randomly assigned

26 The most advanced stage is CML blastic phase (CML-BP), characterized by the World Healt

27 es (MDS), or chronic myelogenous leukemia in blastic phase (CML-BP).

28 me (MDS; n = 8), chronic myeloid leukemia in blastic phase (CMLBP; n = 11), and acute lymphocytic leu

29 s leukemia (CML) in chronic, accelerated, or blastic phase and in 8 patients with myelofibrosis (MF)

30 tion of patients with CML in accelerated and blastic phase but not in chronic phase CML patients and

31 subclassified as either accelerated phase or blastic phase disease.

32 Progression to the accelerated or blastic phase of CML occurred in 5 patients who were rec

33 leukemic progenitors in the accelerated and blastic phase of CML.

34 Of 33 patients with the blastic phase of disease, 13 had a hematologic response

35 herapy (resistance/loss of response, n = 33; blastic phase on TKI therapy, n = 6; intolerance/toxicit

36 No patients progressed to accelerated or blastic phase or developed clonal chromosomal abnormalit

37 ith CML (93% chronic, 5% accelerated, and 2% blastic phase) corresponding to an annual incidence of 0

38 c phase, 17 in accelerated phase, and six in blastic phase).

39 phase, 41% in accelerated phase, and 34% in blastic phase).

40 months, 3% had progressed to accelerated or blastic phase.

41 no patient has progressed to accelerated or blastic phase.

42 hase, 83% for accelerated phase, and 43% for blastic phase.

43 ed by transformation into an accelerated and blastic phase.

44 ich inevitably terminates in a rapidly fatal blastic phase.

45 ted-phase (33.3%; 95% CI, 19.7% to 46.9%) or blastic-phase (16.7%; 95% CI, 1.9% to 31.9%) relapse.

46 SCT still remains an option for accelerated/blastic-phase and selected chronic-phase CML.

47 nly the chronic but also the accelerated and blastic phases of chronic myelogenous leukemia.

48 les from 184 (148 chronic and 36 accelerated/blastic phases) CML patients and found the levels to be

49 ients with CML (19 of them in accelerated or blastic phases) treated with dasatinib after treatment f

50 are made for patients in the accelerated and blastic phases, and for allogeneic stem cell transplanta

51 k of efficacy, progression to accelerated or blastic phases, or death at any time.

52 C(+) subset of DCs; the relationship between blastic plasmacytoid DC neoplasia cells and healthy DCs;

53 neoplasms, including a series of 45 cases of blastic plasmacytoid dendritic cell (BPDC) neoplasms and

54 Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDC

55 D4-dependent oncogenic regulatory network in blastic plasmacytoid dendritic cell neoplasm (BPDCN) and

56 Patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN) hav

57 Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is

58 Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is

59 Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is

60 Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is

61 primary end point has already been reported.Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is

62 Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is

63 Frankel et al describe a novel treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) usi

64 Historically, treatment options for blastic plasmacytoid dendritic cell neoplasm (BPDCN) wer

65 xpansion of pDCs and pDC precursors leads to blastic plasmacytoid dendritic cell neoplasm (BPDCN), an

66 spective study of treatment of patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN), an

67 Here we investigate the development of blastic plasmacytoid dendritic cell neoplasm (BPDCN)-an

68 s including acute myeloid leukemia (AML) and blastic plasmacytoid dendritic cell neoplasm (BPDCN).

69 ression and BCMA-targeted agents eradicate a blastic plasmacytoid dendritic cell neoplasm line, sugge

70 Blastic plasmacytoid dendritic-cell neoplasm (BPDCN) is

71 Cells in the colonies are very blastic, showing no cytoplasmic differentiation, and exp

72 Sudden blastic transformation (SBT) has been reported in 0.5% t

73 delphia-positive chronic myeloid leukemia in blastic transformation for treatment with the ABL tyrosi

74 Blastic transformation of chronic myelogenous leukemia (

75 wn about the molecular mechanisms leading to blastic transformation of CML and propose some novel the

76 Median survival from the date of blastic transformation was 5 months.

77 present follow-up, the survival and time to blastic transformation were similar.

78 tase 2A (PP2A) activity is important for CML blastic transformation.

79 Disease evolution does not generally involve blastic transformation.

80 natural killer (NK)-cell origin, CD4+ CD56+ blastic tumors (BTs) of skin have recently been proposed

81 15 of 50 cases of MCL: 7 of 10 (70%) in the blastic variant and 8 of 40 (20%) in the typical MCL (70

82 nhanced cell death, which was synergistic in blastic variant MCL cell lines.

83 Paradoxically, in the blastic variant of MCL, 8 of 10 (80%) cases showed expre

84 including 50 cases of MCL (40 typical and 10 blastic variants), 21 follicular lymphomas, 20 diffuse l

85 o patients had nodular, and two patients had blastic variants.