ライフサイエンスコーパス: myeloblastic

1 PDGFRB-mediated factor-independent growth in myeloblastic 32D cells.

2 e impact of varying differentiation rates on myeloblastic accumulation.

3 le chromosomal translocations in human acute myeloblastic and B-cell lymphocytic leukemias.

4 n of C/EBP epsilon mRNA occurred in the late myeloblastic and promyelocytic cell lines (NB4, HL60, GF

5 SL expression was strongly associated with a myeloblastic (ANLL M0-M2) and monoblastic phenotype (M5)

6 ream of SEK and SAPK/JNK mediates UV-induced myeloblastic cell apoptosis.

7 lable concerning their function in mediating myeloblastic cell differentiation.

8 When this gene was expressed in the myeloblastic cell line 32Dcl3, it was found to abrogate

9 4ac were enriched at Mml1 and/or Mml2 in the myeloblastic cell line M1, which expresses c-myb.

10 n on the differentiation of the 32Dcl3 (32D) myeloblastic cell line to neutrophils in response to gra

11 increased adhesion nearly 2-fold between the myeloblastic cell line, 32D, and fibronectin compared to

12 er, we analyzed the expression of c-myc in a myeloblastic cell line, M1, expressing a conditionally a

13 ctical limitations, we evaluated two CD34(+) myeloblastic cell lines, KG-1 and Kasumi-3, for their ab

14 Expression of c-Maf in human immature myeloblastic cells inhibited CD13/APN-driven reporter ge

15 ional difference analysis (RDA) using 32Dcl3 myeloblastic cells that were deprived of IL-3 for 24h.

16 was performed using RNAs derived from 32Dcl3 myeloblastic cells that were proliferating in the presen

17 the apoptosis and differentiation of 32Dcl3 myeloblastic cells.

18 In contrast, immature (FAB class M1) and myeloblastic (FAB class M2) AML cells rarely expressed g

19 actic platelet-transfusion strategy in acute myeloblastic leukaemia have been published.

20 e strikingly opposite effects on human acute myeloblastic leukemia (AML) cells.

21 riteria for complete remission (CR) in acute myeloblastic leukemia (AML) require the absence of perip

22 overall survival (OS) and evolution to acute myeloblastic leukemia (AML) were FAB and WHO CMML subtyp

23 e critical steps for classification of acute myeloblastic leukemia (AML) which influences the selecti

24 d molecules is a well-known feature of acute myeloblastic leukemia (AML) with t(8;21).

25 lastic leukemia (ALL) and 418 cases of acute myeloblastic leukemia (AML)) with 30,000 contemporaneous

26 ood acute lymphoblastic leukemia (ALL)/acute myeloblastic leukemia (AML), for further postnatal expos

27 ts developed overt clinical MDS and 5, acute myeloblastic leukemia (AML).

28 pair capacity and its association with acute myeloblastic leukemia (AML).

29 lop a fatal disease analogous to human acute myeloblastic leukemia (AML-M2).

30 developed myelodysplastic syndrome and acute myeloblastic leukemia (MDS/AML), which raises the questi

31 that an early event in the cell membrane of myeloblastic leukemia (ML-1) cells was the vigorous acti

32 d in a small subset of cases with both acute myeloblastic leukemia and ALL.

33 ]/Abelson [ABL] kinase inhibitors in chronic myeloblastic leukemia and ATRA in acute promyelocytic le

34 e JNK/SAPK signaling pathway and resulted in myeloblastic leukemia cell apoptosis.

35 discovered as an early induction gene during myeloblastic leukemia cell differentiation.

36 ephosphorylation was determined in the human myeloblastic leukemia cell line HL-60 using subtype-sele

37 uced expression of CD38 protein in the human myeloblastic leukemia cell line HL-60.

38 In the ML-1 human myeloblastic leukemia cell line, a rapid and sustained i

39 The autonomously proliferating M1 myeloblastic leukemia cell line, which is null for p53 e

40 Retinoic acid (RA) causes HL-60 human myeloblastic leukemia cell myeloid differentiation that

41 tivated protein kinase (MAPK) of HL-60 human myeloblastic leukemia cells before causing myeloid diffe

42 protein synthesis following induction of M1 myeloblastic leukemia cells for terminal differentiation

43 eloid and monocytic differentiation of HL-60 myeloblastic leukemia cells in response to retinoic acid

44 zinc finger transcription factor Egr-1 in M1 myeloblastic leukemia cells promotes terminal differenti

45 identified based on increased expression in myeloblastic leukemia cells undergoing differentiation.

46 The ML-1 human myeloblastic leukemia cells used in this study prolifera

47 Ectopic expression of Egr-1 in M1 myeloblastic leukemia cells was observed to activate the

48 Using HL-60 human myeloblastic leukemia cells, a cell line that undergoes

49 In HL-60 human myeloblastic leukemia cells, it causes mitogen-activated

50 le arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present anal

51 radiation to induce DNA damage in human ML-1 myeloblastic leukemia cells, the promoter and intronic r

52 nduced terminal differentiation of murine M1 myeloblastic leukemia cells, where the cells growth arre

53 of genomic stability was determined in HL-60 myeloblastic leukemia cells.

54 n, is not induced upon differentiation of M1 myeloblastic leukemia cells.

55 primarily a 100-kD protein and a CD34+ acute myeloblastic leukemia expressing mainly 130-kD and 145-k

56 fferentiates between acute lymphoblastic and myeloblastic leukemia in blood films.

57 cdc25A during terminal differentiation using myeloblastic leukemia M1 cells, that can be induced to u

58 We have shown in human myeloblastic leukemia ML-1 cells that K+ channels are ac

59 present study, we found that the exposure of myeloblastic leukemia ML-1 cells to UV light (UVC) cause

60 igated in human lymphoblastoid CEM cells and myeloblastic leukemia ML-1 cells.

61 transformation of these disorders into acute myeloblastic leukemia probably relate to the underlying

62 dence rate of myelodysplastic syndrome/acute myeloblastic leukemia was 0.50% versus 0.07% in (90)Y-ib

63 n 40 patients (7 Hodgkin's Disease, 13 Acute Myeloblastic Leukemia, 5 Acute Lymphoblastic Leukemia, 8

64 iocytomas) and six other malignancies (acute myeloblastic leukemia, acute lymphoblastic leukemia, men

65 the colony-forming capacity of primary acute myeloblastic leukemia, but not normal CD34+ cells.

66 secondary myelodysplasia and secondary acute myeloblastic leukemia, resulting in 15 patient deaths.

67 HM (75%), particularly acute myeloblastic leukemia, was frequent in patients with Asp

68 ic blasts obtained from a patient with acute myeloblastic leukemia.

69 Abl oncogene, which is causative for chronic myeloblastic leukemia.

70 enic CD40L to protect against the CD40- WEHI myeloblastic leukemia.

71 cluding pancreas carcinomas, lymphocytic and myeloblastic leukemias, and thyroid carcinomas.

72 d highly in some karyotypically normal acute myeloblastic leukemias.

73 of ectopic expression of Egr-1 on the murine myeloblastic leukemic cell line M1, which is induced for

74 HP-1, and U-937) but was weakly expressed in myeloblastic leukemic cells (KG-1 and HL-60).

75 duction of myeloid differentiation, using M1 myeloblastic leukemic cells and normal cells from bone m

76 verexpression impairs differentiation of the myeloblastic M1 cell line following interleukin (IL)-6 s

77 Human myeloblastic ML-1 can be induced to differentiate into m

78 ve patients receiving chemotherapy for acute myeloblastic or lymphoblastic leukemia.

79 ine lymphoblastic (A20) leukemia and a CD40- myeloblastic (WEHI-3) leukemia in a tumor treatment mode