ライフサイエンスコーパス: myeloblastic leukemia

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

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

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

4 d highly in some karyotypically normal acute myeloblastic leukemias.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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