ライフサイエンスコーパス: lymphoid tumor

1 World Health Organization Classification of Lymphoid Tumors.

2 tential to cause cellular transformation and lymphoid tumors.

3 erate in the development of both myeloid and lymphoid tumors.

4 ate agent for treating refractory ATM mutant lymphoid tumors.

5 could serve as a marker for certain types of lymphoid tumors.

6 ath of lymphoid cells, and in the genesis of lymphoid tumors.

7 30% of the MN1-TEL-positive mice developed T-lymphoid tumors.

8 amily, may also contribute to a variety of B lymphoid tumors.

9 ion, immunodeficiency, and high incidence of lymphoid tumors.

10 lays an important role in the progression of lymphoid tumors.

11 r some chromosomal translocations present in lymphoid tumors.

12 mary cells isolated from 2 patients having B-lymphoid tumors.

13 n herpesvirus associated with epithelial and lymphoid tumors.

14 d incidence of malignancy and, particularly, lymphoid tumors.

15 chromosomal translocations of their genes in lymphoid tumors.

16 or in primary prostate, lung, lens, ovary or lymphoid tumors.

17 in neuroendocrine, breast, liver, colon, and lymphoid tumors.

18 n found to be involved in the progression of lymphoid tumors.

19 the role of such lesions in both myeloid and lymphoid tumors.

20 of p53 (p53(+/-)) spontaneously developed a lymphoid tumor (6%), whereas 88% of UV-irradiated p53(+/

21 as a novel therapeutic agent to treat human lymphoid tumors and ameliorate graft-versus-host disease

22 A-T) patients, including a high incidence of lymphoid tumors and immune defects characterized by defe

23 e of the DNA-binding domains of Rpa1 develop lymphoid tumors, and their homozygous littermates succum

24 sequencing reads were generated from primary lymphoid tumors, cancer cell lines and an EBV-transforme

25 n of primary PHA-activated T cells (72%) and lymphoid tumor cell line (e.g., YT; 74%) within 24 h, as

26 und constitutively phosphorylated in several lymphoid tumor cell lines as well as primary leukemia an

27 genous soluble DPPIV enhanced sensitivity of lymphoid tumor cell lines to doxorubicin, suggesting a p

28 ed on the surface of three different Xenopus lymphoid tumor cell lines, each derived from a different

29 tensive apoptosis in lymphoid as well as non-lymphoid tumor cell lines.

30 programmed cell death (PCD) signals to human lymphoid tumor cells as well as peripheral blood mononuc

31 The interaction of lymphoid tumor cells with components of the extracellula

32 us that maintains its genome as a plasmid in lymphoid tumor cells.

33 broblastic and B-lymphoid cells but not to T-lymphoid tumor cells.

34 se mb1-cre:Tp53(flox/flox) mice succumbed to lymphoid tumors containing Ig gene rearrangements and im

35 lacking clonal translocations but develop B lymphoid tumors containing immunoglobulin (Ig) transloca

36 We previously established that lymphoid tumors could be induced in cats by intradermal

37 that implicates aberrant RAG1/2 activity in lymphoid tumor development and premature immunosenescenc

38 e potential role of MCT-1 in promoting human lymphoid tumor development.

39 r UV-irradiated p53 wild-type mice developed lymphoid tumors during the 60-week observation period.

40 tent antitumor activity against solid murine lymphoid tumors (even when the drug was administered ora

41 In human lymphoid tumors expression of MCT-1 is constant througho

42 Non-SCT patients with lymphoid tumors had a significantly higher rate of antig

43 l SRS 19-6 MuLV were analyzed, most of the T-lymphoid tumors had similar enhancer alterations in the

44 The development of Myc-induced lymphoid tumors has been well studied and supports this

45 advances in the management of ocular adnexal lymphoid tumors have been based on the distinction betwe

46 M-MuLV normally induces T-lymphoid tumors in all infected mice.

47 ed or virally transduced forms of Myc induce lymphoid tumors in animals, and deregulated expression o

48 )) rapidly developed thymic lymphomas and/or lymphoid tumors in spleen or liver.

49 88% of UV-irradiated p53(+/-) mice developed lymphoid tumors in the spleen or liver.

50 t account for the accelerated development of lymphoid tumors in UV-irradiated p53(+/-) mice, deletion

51 a variety of lymphoid lineages), 65 primary lymphoid tumors (including 24 lymphoblastic leukemia/lym

52 ical cell survival signals for certain human lymphoid tumors, indicating that nonhyperactive STATs sh

53 charide- or Con A-stimulated lymphoblasts or lymphoid tumor lines, whereas MLC-elicited effectors eff

54 nsferred to stromal cells that reside in the lymphoid tumor microenvironment (TME), promoting the rep

55 nd a control, UV-irradiated MV using a human lymphoid tumor model in immunodeficient mice.

56 similar to that of endogenous Blk induced B lymphoid tumors of limited clonality, whose phenotypes a

57 ansferase inhibitor L-744,832 in mammary and lymphoid tumors overexpressing the N-ras proto-oncogene

58 MN1-TEL-positive T-lymphoid tumors showed elevated expression of the Notch-

59 All of the lymphoid tumors tested were of T cell type.

60 ct Myc binding targets in a model of human B lymphoid tumor using ChIP coupled with pair-end ditag se

61 Health Organization classification of human lymphoid tumors while recognizing differences that may b

62 c translocations occur frequently in human B lymphoid tumors, while N-myc gene amplification is frequ

63 cilitated the development of a wide range of lymphoid tumors, with prominent B cell infiltration obse