ライフサイエンスコーパス: B-cell tumor

1 lification of the specific Ig genes from the B-cell tumor.

2 within hours of cloning the Ig genes from a B-cell tumor.

3 f the first reports of CD40L expression in a B-cell tumor.

4 large B cell lymphoma (DLBCL) and additional B cell tumors.

5 iverse and heterogeneous group of high-grade B cell tumors.

6 constitutively active in abl/myc induced pre-B cell tumors.

7 egion (IGHV) genes, and is emerging in other B cell tumors.

8 gs the survival of mice with implanted human B-cell tumors.

9 o the poor outcome reported in all MHC II(-) B-cell tumors.

10 efficacy should be examined in patients with B-cell tumors.

11 activity in p37(Ing1b)/p53-null B cells and B-cell tumors.

12 enter B cells and in germinal center-derived B-cell tumors.

13 s is a frequent event in the pathogenesis of B-cell tumors.

14 n was more common in cHL compared with other B-cell tumors and emerged as a prognostic biomarker for

15 noncoding region of the bcl-6 gene, in both B-cell tumors and in normal germinal center B cells.

16 helps explain oncogene mutations observed in B-cell tumors, and further, that many oncogenes are vuln

17 ession was validated in Ewing sarcoma cells, B-cell tumors, and human keratinocytes where NOTCH dysre

18 novel marker for this lymphoma across mature B-cell tumors, and support the distinction of NMZL as an

19 eric antigen receptors (CAR) specific to the B cell tumor antigen CD19 can successfully eradicate sys

20 We hypothesized that B cell tumor antigen escape may be overcome by a chimeri

21 stigations of VH gene mutational patterns in B-cell tumors are often performed at an arbitrary time p

22 Follicular lymphoma (FL) is a B-cell tumor arising in germinal centers and retaining f

23 Oncogenes are often dysregulated in B cell tumors as a result of a reciprocal translocation

24 patients may not have any increased risk for B-cell tumors at all or even to all T-cell types but onl

25 lonal translocations, nearly all analyzed CP B-cell tumors carried clonal translocations.

26 icantly increases CD20 levels in established B-cell tumor cell lines and primary malignant cells.

27 ing NKG2D ligands had increased incidence of B cell tumors, confirming that the inability to clear NK

28 This differential expression of CXCR3 in B-cell tumors contrasts with that of another B-cell-asso

29 Among B-cell tumors, deletion of 7q and NOTCH2 mutations are a

30 in human lymphoma cell lines and in primary B-cell tumors demonstrated a predominant TIMP-1 expressi

31 mice also succumb reproducibly to progenitor B cell tumors, demonstrating that Artemis is a tumor sup

32 g is not constitutive in raf/myc induced pre-B cell tumors, demonstrating that subversion of this com

33 We also profiled the microRNA of B-cell tumors derived from diffuse large B-cell lymphoma

34 ave now addressed whether Ink4c loss impacts B-cell tumor development in the Emu-Myc transgenic mouse

35 howed that BCL-6 mutations are restricted to B cell tumors displaying GC or post-GC phenotype and car

36 A subset of B-cell tumors exhibits recurrent translocations of Bcl-3

37 several human B cell cancer lines, and human B cell tumors expressing AID at high levels have genomic

38 growth, were enriched in NMZL across mature B-cell tumors, functionally caused the loss of the phosp

39 y using a safe idiotypic (Id) antigen from a B cell tumor fused to a fragment C (FrC) sequence from t

40 lymphocytic leukemia (CLL) and other related B-cell tumors have been described in the literature and

41 has been found to be mutated in a variety of B cell tumors, here we sought to determine whether p53 a

42 lling the malignant growth of this incurable B cell tumor in patients.

43 and rapid targeting to lymphoid tissues and B cell tumors in mice.

44 J(H) probe was consistent with a monoclonal B-cell tumor in 13 cases.

45 redisposition to T-cell tumors compared with B-cell tumors in A-T patients may be related to a prefer

46 ncertainty concerning the ratio of T-cell to B-cell tumors in A-T, but this could be clarified by the

47 BLV infection is strongly associated with B-cell tumors in cattle.

48 In this study, we characterized the B-cell tumors in MSH6-deficient mice and describe their

49 ll lines in vitro as well as in EBV-positive B-cell tumors in SCID mice.

50 n site 3 (Evi3), has been implicated in most B-cell tumors in the AKXD-27 strain.

51 uency of T-cell tumors compared with that of B-cell tumors in these patients.

52 and slows the growth of these "addicted" pre-B-cell tumors in vivo, suggesting a promising therapeuti

53 whereas single-transgenic Myc mice developed B cell tumors infrequently (4 of 43, 9.3%).

54 Chronic lymphocytic leukemia (CLL) is a B-cell tumor involving small lymphocytes that generally

55 In B cell tumors, it can provide information on the cell of

56 sarcoma (KS) and is also linked to the rare B-cell tumor known as primary effusion lymphoma (PEL).

57 nally active in the latently infected murine B-cell tumor line S11.

58 ion treatment of TRAF3-deficient B cells and B cell tumor lines with c-Myc inhibitors enhanced their

59 ssion also has been seen in many established B cell tumor lines.

60 se data indicate that TC-PTP is required for B-cell tumor maintenance.

61 to spontaneous translocations in other mouse B-cell tumor models, CP B-cell tumor translocations were

62 known as HHV8) is the causative agent of two B cell tumors, multicentric Castleman disease (MCD) and

63 or immune modulation as well as treatment of B cell tumors of GC origin.

64 Multiple myeloma is a clonal B-cell tumor of slowly proliferating plasma cells within

65 Compared to our knowledge of B-cell tumors, our understanding of T-cell leukemia and

66 B2 mutant p80HT, which develop predominantly B cell tumors, p52 transgenic mice are not prone to lymp

67 BALB/c mice predominantly develop late stage B cell tumors (plasmacytomas) and less frequently develo

68 ffective in controlling these EBV-associated B-cell tumors.Recently the demonstration that EBV transc

69 Fourteen of sixteen B cell tumors removed from spleens of five such hu-SPL-S

70 otch activation in multiple murine and human B-cell tumors, representing both immature and mature sub

71 is a partner in recurrent translocations in B cell tumors, resulting in deregulated expression.

72 Human germinal center B cell tumors retain the ability of their nontransformed

73 (2) such peptides can be used to generate a B-cell tumor-specific vaccine; and (3) a vaccine targeti

74 -catalyzed DNA-dependent p53 acetylation and B-cell tumor suppression.

75 sion of human carcinomas, e.g. diffuse large B cell tumors, T cell lymphomas, etc.

76 beverage type and were slightly stronger for B-cell tumors than for T-cell tumors.

77 nal zone lymphoma (NMZL) is a rare, indolent B-cell tumor that is distinguished from splenic marginal

78 als, which may explain the high incidence of B-cell tumors that arise from oncogene translocation int

79 sociated lymphoid tissue (MALT) are indolent B-cell tumors that have a predilection for epithelial si

80 passes a closely related group of aggressive B-cell tumors that includes sporadic, endemic, and human

81 AIDS-PCNSL biopsy samples and in EBV+ human B-cell tumors that spontaneously developed in severe com

82 examined DNA methylation patterns in TCL1-tg B-cell tumors to discover tumor-associated epigenetic ch

83 tions in other mouse B-cell tumor models, CP B-cell tumor translocations were not recurrent and did n

84 n SYK credentials as a therapeutic target in B-cell tumors, we explored the role of PDE4B in these re

85 s lymphoma, and, by extension, for the other B cell tumors with which EBV is associated.

86 An unusual group of human B-cell tumors with cellular features of chronic lymphocy

87 here exists a wide spectrum of IgM-secreting B-cell tumors with different clinical behavior.

88 oplastic transformation, imprints V genes of B-cell tumors with the mutational history of the cell of

89 Knock-in mice developed IgM-positive B-cell tumors, with most being typical of eBL by histolo

90 GN529 was highly active against subcutaneous B-cell tumor xenografts in severe combined immunodeficie