ライフサイエンスコーパス: lymphoid leukemia

1 approved to treat relapsed/refractory acute lymphoid leukemia.

2 As expected, these mice developed lymphoid leukemia.

3 infected WT animals developed predominantly lymphoid leukemia.

4 lly promote the development of an aggressive lymphoid leukemia.

5 r cells, including those in acute myeloid or lymphoid leukemia.

6 ia, myelodysplastic syndrome (MDS) and acute lymphoid leukemia.

7 CBFB-MYH11 association with myeloid but not lymphoid leukemia.

8 slocations associated with acute myeloid and lymphoid leukemia.

9 emia (CML) and in some patients with acute B-lymphoid leukemia.

10 loperoxidase or an antigen consistent with a lymphoid leukemia.

11 o distinguish megakaryoblastic leukemia from lymphoid leukemia.

12 combination for the treatment of myeloid and lymphoid leukemias.

13 60 (0.1%) Hodgkin lymphomas, and 126 (0.2%) lymphoid leukemias.

14 ator in the pathogenesis of myeloid and some lymphoid leukemias.

15 iant forms of MTHFR have a decreased risk of lymphoid leukemias.

16 ates were 36% in CLL and 60% in other B-cell lymphoid leukemias.

17 ion of malignant clones in acute myeloid and lymphoid leukemias.

18 o a selective GVL effect against myeloid and lymphoid leukemias after F-->M HSCT.

19 Analyses were performed separately for acute lymphoid leukemia (ALL) and acute nonlymphoid leukemia (

20 imary acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL), as well as normal hematopoietic

21 te megakaryocytic leukemia (AMKL), and acute lymphoid leukemia (ALL).

22 is of acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL).

23 requently in primary colon cancers and acute lymphoid leukemias (ALL), respectively, and methylation

24 oid leukemias (AMLs) and 8 (6%) of 131 acute lymphoid leukemias (ALLs), but not in other tumor types.

25 induced a mixture of acute myeloid and acute lymphoid leukemias (AML+ALL).

26 A total of 10 720 patients with acute lymphoid leukemia and 1323 patients with acute myeloid l

27 s to the development of a well-characterized lymphoid leukemia and a less well-defined non lymphoid d

28 sed in numerous tumor types, including acute lymphoid leukemia and acute myeloid leukemia (AML).

29 d with both acute myeloid leukemia and acute lymphoid leukemia and are usually associated with a rela

30 urately models human Philadelphia-positive B-lymphoid leukemia and chronic myeloid leukemia (CML).

31 as of diverse lineages ensued, most commonly lymphoid leukemia and erythroleukemia.

32 that is aberrantly expressed in myeloid and lymphoid leukemia and in this issue of Blood, Doubrovina

33 The lymphoid leukemias and macrophage tumors had provirus in

34 of primary human LSCs from both myeloid and lymphoid leukemias, and is also highly cytotoxic to bulk

35 s involved the pathogenesis of lymphomas and lymphoid leukemias are often based on the physiology of

36 uent targets of genetic alterations in human lymphoid leukemias are transcription factor genes with e

37 athogenesis of BCR-ABL1-positive myeloid and lymphoid leukemias are unknown.

38 ng, leukemia-initiating cells to result in B-lymphoid leukemia (B-ALL) in vivo.

39 en challenged with primary acute myeloid and lymphoid leukemia blasts; and (5) Vdelta2 cells are expa

40 pression induces the development of not only lymphoid leukemia but also erythro-megakaryocytic leukem

41 ifically, we determined that KDM2B maintains lymphoid leukemias, but restrains RAS-driven myeloid tra

42 alent cytotoxicity found between myeloid and lymphoid leukemia cell lines.

43 Using a combination of human B lymphoid leukemia cells and mouse models, we now show th

44 mpare the deformability of human myeloid and lymphoid leukemia cells and neutrophils at low deformati

45 These data indicate that lymphoid leukemia cells of different molecular subtypes

46 which adaphostin can damage both myeloid and lymphoid leukemia cells, but also indicate that this nov

47 In patients with chronic lymphoid leukemia (CLL) or small lymphocytic lymphoma (S

48 The human myeloid-lymphoid leukemia gene, MLL (also called ALL-1, Htrx, or

49 human MLL (mixed-lineage leukemia or myeloid-lymphoid leukemia) gene belongs to the trithorax gene fa

50 slocations associated with acute myeloid and lymphoid leukemia, has >50 known partner genes with whic

51 2 domain was not required for induction of B-lymphoid leukemia in mice by BCR/ABL.

52 1, which can induce both acute myeloid and T-lymphoid leukemia in mice.

53 Thus far, reports of engraftment of lymphoid leukemia in SCID mice have mainly been from pat

54 nct roles in the pathogenesis of myeloid and lymphoid leukemias induced by BCR-ABL1, validating NF-ka

55 increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation a

56 delay, with other recipients succumbing to B-lymphoid leukemia instead.

57 us genetic mechanisms of tumor initiation in lymphoid leukemias (LL) will lead to improvements in pro

58 is gene was recently identified as a myeloid/lymphoid leukemia (MLL) fusion protein partner in acute

59 BCR-ABL cases, de novo e13-e14a2/p210 Ph(+) lymphoid leukemia more frequently showed CML-type backgr

60 nts with CLL (n = 40) or other mature B-cell lymphoid leukemias (n = 10) were treated with four weekl

61 In contrast, among patients with acute lymphoid leukemia, no differences in cell depth were obs

62 ed by BCR/ABL, with mice developing B- and T-lymphoid leukemias of longer latency.

63 nts were children with newly diagnosed acute lymphoid leukemia or acute myeloid leukemia.

64 logic schemes used to classify lymphomas and lymphoid leukemias over the last several decades.

65 logic neoplasms, including lymphoma, chronic lymphoid leukemias, plasma cell neoplasms, acute leukemi

66 to play a role in the pathogenesis of human lymphoid leukemias through downregulation of the INK4A-A

67 histone methyltransferases Set1 and myeloid/lymphoid leukemia to these promoters, which was unaffect

68 likely explains the increased sensitivity of lymphoid leukemias to short-term exposure of MTX as comp

69 tic factors of myeloma, Hodgkin disease, and lymphoid leukemia using the United States Renal Data Sys

70 In patient 2, B cell acute lymphoid leukemia was diagnosed 10 months after liver tr

71 th a myeloproliferative disorder (MPD) and B-lymphoid leukemia, whereas BCR-ABL(P210)-transformed old

72 P190 BCR/ABL induced lymphoid leukemia with shorter latency than P210 or P230

73 n utilized in the treatment of lymphomas and lymphoid leukemias with impressive results.

74 emia (MLL) gene is described in B-cell acute lymphoid leukemia without structural cytogenetic abnorma