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

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

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

5 inflection point when FL transforms into an aggressive lymphoma.

6 se avidity, and analyzed for the presence of aggressive lymphoma.

7 hese processes to promote the gut tropism of aggressive lymphoma.

8 lymphocytic leukemia (CLL), typically to an aggressive lymphoma.

9 ion of chronic lymphocytic leukemia (CLL) to aggressive lymphoma.

10 nd frequently undergoes transformation to an aggressive lymphoma.

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

12 MYC contributes to poor prognosis in aggressive lymphoma.

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

14 ical evaluation in patients with indolent or aggressive lymphoma.

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

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

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

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

19 generation regimens for primary treatment of aggressive lymphomas.

20 rigger genomic instability and cell death in aggressive lymphomas.

21 new therapeutic strategies for this group of aggressive lymphomas.

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

23 sment of prognosis and treatment response in aggressive lymphomas.

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

25 microenvironment's pathogenic role in these aggressive lymphomas.

26 erefore, an attractive target for therapy in aggressive lymphomas.

27 perspectives regarding MYC dysregulation in aggressive lymphomas.

28 inical activity of this targeted strategy in aggressive lymphomas.

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

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

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

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

33 ized to glucose for classifying indolent and aggressive lymphomas.

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

35 ation chemotherapy capable of curing diffuse aggressive lymphomas.

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

37 re was significant difference between ADC in aggressive lymphoma (0.65 +/- 0.1, 0.67 +/- 0.13 x 10(-3

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

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

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

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

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

43 In mice with aggressive lymphoma, a single, local injection of the sc

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

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

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

47 ning to investigate venetoclax resistance in aggressive lymphoma and high-risk CLL patients.

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

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

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

51 able responses in patients with indolent and aggressive lymphomas and the RP2D was preliminarily iden

52 e deployed rationally to treat BCR-dependent aggressive lymphomas and used to construct mechanistical

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

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

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

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

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

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

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

60 as an initiator of CLL transformation toward aggressive lymphoma by inducing Notch signaling between

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

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

63 The risk of misdiagnosis as more aggressive lymphomas, causing patient overtreatment, nee

64 (miRNA) genes that are targeted by PRMT5 in aggressive lymphoma cell lines.

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

66 an S100 protein-defined subcluster of highly aggressive lymphoma cells that developed from CLL cells,

67 In aggressive lymphomas, CHOP (cyclophosphamide, doxorubici

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

69 among 931 children with Burkitt lymphoma, an aggressive lymphoma commonly characterized by immunoglob

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

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

72 lymphoma (DLBCL) is a heterogeneous group of aggressive lymphomas driven by distinct biological pathw

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

74 Richter transformation (RT) is defined as an aggressive lymphoma emerging in patients with chronic ly

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

76 Aggressive lymphomas frequently carry additional oncogen

77 tify imaging-based markers of distinguishing aggressive lymphoma from indolent lymphoma.

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

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

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

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

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

83 rmation (RT) refers to the development of an aggressive lymphoma in patients with underlying chronic

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

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

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

87 d enhanced glofitamab-mediated regression of aggressive lymphomas in humanized mice.

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

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

90 Clinical studies in aggressive lymphomas, including RS, are under way.

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

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

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

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

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

96 The therapeutic landscape for aggressive lymphoma is rapidly evolving, and there is a

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

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

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

100 ew reference segmentation threshold for most aggressive lymphomas may homogenize volume-based metrics

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

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

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

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

105 ular basis of the transformation of CLL into aggressive lymphoma, or Richter syndrome (RS), has remai

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

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

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

109 T with significantly reduced survival and an aggressive lymphoma phenotype.

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

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

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

113 ver, early progression and transformation to aggressive lymphoma remain key issues requiring further

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

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

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

117 blastic lymphoma (PBL) represents a rare and aggressive lymphoma subtype frequently associated with i

118 s a novel strategy for the treatment of this aggressive lymphoma subtype.

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

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

121 ormation (RT) reflects the development of an aggressive lymphoma that is associated with poor respons

122 Richter's transformation (RT) is an aggressive lymphoma that occurs upon progression from ch

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

124 Among aggressive lymphomas, the association between diffuse la

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

126 h CLL who present with signs and symptoms of aggressive lymphoma transformation.

127 Burkitt lymphoma (BL) is an aggressive lymphoma type that is currently treated by in

128 Patients with aggressive lymphoma underwent allogeneic or autologous S

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

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

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

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

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

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

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

136 37-year-old patient with HIV-1 infection and aggressive lymphoma who had disease progression after fi

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

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

139 lf-renewal properties, ultimately leading to aggressive lymphomas with an increased repopulating pote

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

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

142 t in the treatment of patients with systemic aggressive lymphomas, with emerging data also demonstrat