ライフサイエンスコーパス: DLCL

1 ade (12 MALT, 16 CLL/SLL) and high-grade (19 DLCL) lymphomas.

2 we have cloned the breakpoint region from a DLCL patient with t(14;15)(q32;q11-13) and the correspon

3 minal-centre-derived lymphomas, suggesting a DLCL-associated malfunction of somatic hypermutation.

4 than in classical MCL (s-MCL; 13 of 103) and DLCL (8 of 19).

5 In MCL and DLCL, the percentage of E2F-1+ nuclei was high, correlat

6 Most MCLs (91 of 112) and DLCLs (12 of 19) showed a loss of p27; MALT and CLL/SLL,

7 B cell diffuse large cell lymphoma (B-DLCL) is a heterogeneous group of tumors, based on signi

8 as revealed two distinct tumor subtypes of B-DLCL: germinal center B cell-like DLCL and activated B c

9 Fourteen primary B-DLCL cases were studied by gene expression profiling usi

10 In a separate study, we determined that B-DLCL can also be subdivided into two groups based on the

11 we evaluated the correlation between these B-DLCL subtypes established by the two different methods.

12 differential diagnosis between HD and CD30+ DLCL.

13 notypic differences were found between CD30+ DLCL and HD.

14 The cases of B-cell CD30+ DLCL had a characteristic immunophenotype.

15 All cases of CD30+ DLCL were positive for one or more common or lineage-spe

16 In patients with CD30+ DLCL, a T-cell phenotype was found in 60%, a null-cell t

17 clinical features of 52 patients with CD30+ DLCL.

18 on-PCR analysis of RNA extracted from frozen DLCL samples and lymphoma cell lines, BCL8 expression wa

19 uding 262 in the pre-HAART (HIV-BL, 117; HIV-DLCL, 145) and 101 in the HAART era (HIV-BL, 18; HIV-DLC

20 5) and 101 in the HAART era (HIV-BL, 18; HIV-DLCL, 83).

21 Compared with HIV-BL, HIV-DLCL was associated with significantly lower CD4 counts

22 L in the HAART era (HIV-BL, 5.7 months v HIV-DLCL, 43.2 months; P = .0003).

23 the pre-HAART era (HIV-BL, 6.4 months v HIV-DLCL, 8.3 months; P = .43), survival was significantly w

24 Clinical outcomes in patients with HIV-DLCL are now approaching the outcomes of patients with d

25 Survival of patients with HIV-DLCL has improved in the HAART era, along with CD4 count

26 of the promoters found juxtaposed to BCL6 in DLCL and FL during B-lineage differentiation.

27 ate was 94% (76% CR) in MCL, 37% (31% CR) in DLCL, and 90% (50% CR) in FL.

28 ctivities of five Pim1 mutants identified in DLCL patients have been determined.

29 omal translocation or by other mechanisms in DLCL.

30 own for other B cell malignancies, including DLCL.

31 types of B-DLCL: germinal center B cell-like DLCL and activated B cell-like DLCL.

32 es classified as germinal center B cell-like DLCL by gene expression showed the presence of ongoing m

33 by gene expression as activated B cell-like DLCL had no ongoing somatic mutations, whereas, in the r

34 ted to the rest of the activated B cell-like DLCL tumors by gene expression.

35 r B cell-like DLCL and activated B cell-like DLCL.

36 inant subtypes, diffuse large-cell lymphoma (DLCL) (n = 233) and follicular lymphoma (n = 173), were

37 d KI-1 positive diffuse large cell lymphoma (DLCL) cell line (KIS-1).

38 an aggressive diffuse large B-cell lymphoma (DLCL) occurs in 60% to 80% of cases, and this transforma

39 a (PMBL) is a diffuse large B cell lymphoma (DLCL) postulated to arise from noncirculating thymic B l

40 (FL), 16 with diffuse large B-cell lymphoma (DLCL), and 17 with mantle cell lymphoma (MCL).

41 ypermutation in diffuse large cell lymphoma (DLCL), the most common form of non-Hodgkin's lymphoma.

42 0 patients with diffuse large cell lymphoma (DLCL).

43 with primary diffuse large B-cell lymphoma (DLCL).

44 rticularly with diffuse large cell lymphoma (DLCL; OR = 0.29; 0.10-0.82).

45 primary CD30+ diffuse large-cell lymphomas (DLCL) and 128 cases of Hodgkin's disease (HD) and discus

46 imately 40% of diffuse large cell lymphomas (DLCL) and approximately 14% of follicular lymphomas (FL)

47 e recurrent in diffuse large-cell lymphomas (DLCL).

48 10 of 12 (83%) diffuse large cell lymphomas (DLCLs) and 2 of 3 diffuse mixed B-cell lymphomas (DMs).

49 re than 50% of diffuse large-cell lymphomas (DLCLs), which are tumours derived from germinal centres.

50 ome 15 is clonally rearranged in about 4% of DLCL in agreement with the frequency of 15q11-13 translo

51 l NHL (OR = 0.68, 95% CI: 0.48, 0.98) and of DLCL (OR = 0.50, 95% CI: 0.30, 0.85).

52 rval (CI): 0.55, 1.2; p-trend = 0.06) and of DLCL (OR = 0.53, 95% CI: 0.31, 0.90; p-trend = 0.01).

53 The associations of DLCL and FL with TYMS 1494del6 and MTHFR 677TT genotypes

54 ssion of BCL8 in a significant proportion of DLCL suggests an important role for this gene in the mol

55 pe and are associated with a reduced risk of DLCL in women.

56 PMBLs do not represent a distinct subtype of DLCL.

57 the bcl-6 gene is rearranged in up to 45% of DLCLs, rearrangement of the bcl-6 gene was detected in o

58 When compared with six other DLCL cell lines lacking t(9;14)(p13;q32), the KIS-1 cell

59 ement in PMBLs distinguishes them from other DLCLs of B cell origin, suggesting that PMBLs do not rep

60 (OR = 0.68, 95% CI: 0.49, 0.94), and perhaps DLCL (OR = 0.79, 95% CI: 0.51, 1.2), and of follicular l

61 Five of the 9 progressed DLCL cases showed p16 expression and demonstrated retent

62 the 9 matched pairs of LGFCL and progressed DLCL with interpretable immunohistochemical staining, 9

63 of LGFCL and their corresponding progressed DLCL biopsies for loss of heterozygosity and homozygous

64 istochemically evaluable cases of progressed DLCL showed loss of or, in 1 case, markedly diminished p

65 ere identified exclusively in the progressed DLCL biopsies.

66 of deletions involving p16 in the progressed DLCLs suggests that genetic loss at 9p21 targeting p16 a

67 The case of refractory DLCL had identifiable transcripts from IgM, IgD, IgA, Ig

68 egimen for patients with relapsed/refractory DLCL.

69 sequences of both the FCL and the refractory DLCL remained heterogeneous.

70 ities and in a fraction of randomly selected DLCL patients.

71 A cosmid library was prepared from SKI-DLCL-1, and Cgamma-positive clones spanning the breakpoi

72 d thrombospondin 3) are overexpressed in SKI-DLCL-1.

73 A novel cell line, SKI-DLCL-1, was established from ascitic fluid that carries

74 The VH sequences of the DLCL which responded to treatment became homogeneous at

75 ding domain by analysis of BCL6 cDNAs in two DLCL cases and one mixed follicular lymphoma (MxFL).

76 The patient with FCL and one patient with DLCL both achieved clinical remission, although this was

77 uently relapsed, and the second patient with DLCL was refractory to radiotherapy and chemotherapy.