ライフサイエンスコーパス: aggressive lymphoma

1 cell lymphoma risk-related gene named BAL (B aggressive lymphoma).

2 KSHV is the etiologic agent of PEL-an aggressive lymphoma.

3 tial remission in 52 patients with poor-risk aggressive lymphoma.

4 nd frequently undergoes transformation to an aggressive lymphoma.

5 ntial chemoimmunotherapy (R-HDS) in relapsed aggressive lymphoma.

6 ity analysis to compare PP to SP for diffuse aggressive lymphoma.

7 ical evaluation in patients with indolent or aggressive lymphoma.

8 FDG uptake is lower in indolent than in aggressive lymphoma.

9 ubgroup with a higher risk to transform into aggressive lymphoma.

10 mparable to any prior risk-based analysis in aggressive lymphoma.

11 advanced-stage (III or IV) or bulky stage II aggressive lymphoma.

12 alternative for primary therapy of high-risk aggressive lymphoma.

13 sment of prognosis and treatment response in aggressive lymphomas.

14 eems clinically active in both B- and T-cell aggressive lymphomas.

15 microenvironment's pathogenic role in these aggressive lymphomas.

16 perspectives regarding MYC dysregulation in aggressive lymphomas.

17 inical activity of this targeted strategy in aggressive lymphomas.

18 ecific agents based on the cell of origin in aggressive lymphomas.

19 that was able to distinguish MCL from other aggressive lymphomas.

20 allo-SCT) in the management of patients with aggressive lymphomas.

21 AT3 may be a new therapeutic target in these aggressive lymphomas.

22 ized to glucose for classifying indolent and aggressive lymphomas.

23 as a strong prognostic tool in patients with aggressive lymphomas.

24 ation chemotherapy capable of curing diffuse aggressive lymphomas.

25 tients may possibly be cured when treated as aggressive lymphomas.

26 sign risk-adapted therapies in patients with aggressive lymphomas.

27 generation regimens for primary treatment of aggressive lymphomas.

28 BAL1 (B-aggressive lymphoma 1) was originally identified as a ri

29 mas and 8 follicular lymphomas, grade 3), 24 aggressive lymphomas (14 large-B-cell lymphomas and 10 a

30 entral nervous system, and transformation to aggressive lymphoma (4%), requiring long-term follow-up.

31 plastic large-cell lymphomas), and 15 highly aggressive lymphomas (7 lymphoblastic lymphomas and 8 Bu

32 ar lymphomas, grades 1 and 2), 16 moderately aggressive lymphomas (8 mantle cell lymphomas and 8 foll

33 Prophylactic CSF for patients with diffuse aggressive lymphoma aged 65 years and older treated with

34 hs, we observed 3 cases of transformation to aggressive lymphoma and 3 cases of myelodysplastic syndr

35 FL known to have subsequently transformed to aggressive lymphoma and an additional 64 FL samples from

36 r therapy to HIV-1-infected individuals with aggressive lymphoma and leukemia.

37 Aurora A kinase (AAK) is overexpressed in aggressive lymphomas and can correlate with more histolo

38 motherapy, is strongly prognostic in certain aggressive lymphomas and provides information independen

39 e use of CSFs in older patients with diffuse aggressive lymphoma, and addition of recommendations aga

40 Prognostic risk systems for aggressive lymphomas are useful for FLCL.

41 We selected aggressive lymphomas as a platform for the discussion of

42 ibose)polymerase (PARP)14--a member of the B aggressive lymphoma (BAL) family of macrodomain-containi

43 Primary CNS lymphoma (PCNSL) is an aggressive lymphoma but clinically validated biologic ma

44 r the staging and restaging of patients with aggressive lymphoma, but less is known about the utility

45 ven informative founder HMG-I mice developed aggressive lymphoma by a mean age of 4.8 months.

46 ensify therapies for patients with high-risk aggressive lymphoma by utilizing hematopoietic growth fa

47 Acute hematological diseases (leukemias and aggressive lymphomas) can be cured in approximately half

48 est that NR4A1 has proapoptotic functions in aggressive lymphoma cells and define NR4A1 as a novel ge

49 In aggressive lymphomas, CHOP (cyclophosphamide, doxorubici

50 Plasmablastic lymphoma (PBL) is an aggressive lymphoma commonly associated with HIV infecti

51 ailor therapy for subgroups of patients with aggressive lymphoma depends on the continued identificat

52 In aggressive lymphomas (DLBCL and FL grade 3), low NR4A1 e

53 ficantly increases the survival of mice with aggressive lymphoma due to a genetic defect of the lafor

54 FDG uptake was lower in indolent than in aggressive lymphoma for patients with new (SUV, 7.0 +/-

55 Aggressive lymphomas frequently carry additional oncogen

56 rming FDG PET/CT before SCT in patients with aggressive lymphoma has prognostic value.

57 ollicular lymphoma and its transformation to aggressive lymphoma have been well described, the underl

58 rted a low income, stage >/= 2 at diagnosis, aggressive lymphoma, having received chemotherapy, and g

59 ith risk factors) and II adults with diffuse aggressive lymphoma in CR after eight cycles of cyclopho

60 to an environmental PAH can induce a highly aggressive lymphoma in mice and raises the possibility t

61 Lig4), another key NHEJ factor, succumbed to aggressive lymphoma in the absence of tumor suppressor p

62 family of transcription factors and induces aggressive lymphomas in chickens and transgenic mice.

63 fe and effective in influencing remission of aggressive lymphomas in HCV patients.

64 For patients with relapsed or refractory aggressive lymphoma, in comparison with DHAP, treatment

65 rast to the cases of indolent and moderately aggressive lymphoma, in which their expression was inter

66 led to good long-term survival prospects for aggressive lymphoma; introduction of novel approaches, i

67 Transformation to aggressive lymphoma is a critical event in the clinical

68 Histologic transformation (HT) to an aggressive lymphoma is a well-described event in the nat

69 (BM) and lymph nodes (LNs), where typically aggressive lymphoma is found in a LN biopsy with indolen

70 The prognosis of relapsed or refractory aggressive lymphoma is poor.

71 The major cause of death in aggressive lymphoma is relapse or nonresponse to initial

72 Progression of follicular lymphoma to a more aggressive lymphoma is seen in the majority of patients,

73 The strong prognostic value of PET for aggressive lymphomas is established, whether the imaging

74 f chronic lymphocytic leukemia (CLL) into an aggressive lymphoma, most commonly diffuse large B-cell

75 f chronic lymphocytic leukemia (CLL) into an aggressive lymphoma, most commonly of the diffuse large

76 deposits were found mostly in patients with aggressive lymphoma (nine of 26 patients with Hodgkin ly

77 explain the clinical activity of TGR-1202 in aggressive lymphoma not found with idelalisib.

78 increased cumulative incidence of secondary aggressive lymphoma (P = .014) providing a rationale for

79 In the diffuse aggressive lymphoma patients, the 1-year FFS for patient

80 dvances in the therapy of HIV-associated and aggressive lymphomas, patients with PBL for the most par

81 y of PARP-like proteins also designated as B aggressive lymphoma proteins (BAL1, 2a/2b, 3, or PARP-9,

82 Transplantation of an aggressive lymphoma (RcsX) was used to induce tumor form

83 laxis (SP) for elderly patients with diffuse aggressive lymphoma receiving chemotherapy.

84 secondary CNS dissemination in patients with aggressive lymphomas remains an important, unmet clinica

85 Most cases of aggressive and highly aggressive lymphomas showed strong expression of initiat

86 iffuse large B-cell lymphoma (ABC-DLBCL), an aggressive lymphoma subgroup defined by gene expression

87 orable clinical features of the indolent and aggressive lymphoma subtypes, as it is generally incurab

88 diffuse large B cell lymphoma (DLBCL) is an aggressive lymphoma that is addicted to NF-kappaB signal

89 called "double-hit" lymphomas (HGBL-DH), are aggressive lymphomas that form a separate provisional en

90 Among aggressive lymphomas, the association between diffuse la

91 For patients with aggressive lymphomas, the presence of FDG-avid lesions a

92 Patients with aggressive lymphoma underwent allogeneic or autologous S

93 ates, allogeneic transplantation in relapsed aggressive lymphoma warrants further investigation.

94 the ProMACE-CytaBOM regimen in patients with aggressive lymphoma was 200%.

95 ession of the antiapoptotic protein bcl-2 on aggressive lymphomas was shown to be associated with inf

96 h also includes the development of secondary aggressive lymphoma, was inferior in NLPHL (10-year, 63%

97 For patients with relapsed or refractory aggressive lymphoma, we hypothesized that gemcitabine-ba

98 umor-biopsy specimens from 303 patients with aggressive lymphomas were profiled for gene expression a

99 used to identify a novel gene, termed BAL (B-aggressive lymphoma), which is expressed at significantl

100 37-year-old patient with HIV-1 infection and aggressive lymphoma who had disease progression after fi

101 d, risk-adapted approach to the treatment of aggressive lymphomas will be feasible.

102 tage IIB to IV) and Sezary syndrome (SS) are aggressive lymphomas with a median survival of 1 to 5 ye

103 atures with Burkitt lymphoma (BL) are highly aggressive lymphomas with poor clinical outcome.

104 erapy has been evaluated in the treatment of aggressive lymphomas with promising results, but it rema