ライフサイエンスコーパス: remission induction

1 ived lipoATRA 90 mg/m(2) every other day for remission induction.

2 , prednisone, and asparaginase were used for remission induction.

3 minimal residual disease (MRD) levels during remission induction.

4 ne at a daily dose of 100 to 200 mg/m(2) for remission induction.

5 n AML may provide improved outcome following remission induction.

6 reated with escalated-dose cytarabine during remission induction.

7 urnover rapidly, and disappear rapidly after remission induction.

8 genes at nephritis onset that reverses with remission induction.

9 mg per kilogram of body weight per day) for remission induction.

10 paraginase (2500 IU/m(2)) over 1 hour during remission induction.

11 Following remission induction, 1018 patients were randomized to re

12 After remission induction, 2027 patients were randomized to re

13 rituximab was a well-tolerated and effective remission induction agent for severe refractory Wegener'

14 s with detectable leukaemic cells was 23% at remission induction and 17% at week 14 of continuation t

15 ous complications of LP occurring during the remission induction and consolidation treatment periods

16 eatment regimen was highly effective in both remission induction and disease-free survival for patien

17 II (M2b)-activated macrophage as a marker of remission induction and impending relapse and suggest th

18 ) regimen alone or with chemosensitizers for remission induction and interferon (IFN) versus IFN plus

19 an up-to-date summary of MMF and its use as remission induction and maintenance therapy for lupus ne

20 pt given in addition to standard therapy for remission induction and maintenance, more solid malignan

21 The use of CYC and glucocorticoids for remission induction and MTX for remission maintenance re

22 The use of CYC and glucocorticoids for remission induction and MTX for remission maintenance wa

23 performed using CYC and glucocorticoids for remission induction and MTX for remission maintenance.

24 ddress the distinction between therapies for remission induction and remission maintenance.

25 ents' minimal residual disease levels during remission induction and sequentially post-remission.

26 nal doses of intrathecal chemotherapy during remission induction and the first year of continuation t

27 disease levels measured on days 19 and 46 of remission induction, and on week 7 of maintenance treatm

28 y APL were treated with arsenic trioxide for remission induction at daily doses that ranged from 0.06

29 y, beginning 4 days after starting intensive remission induction chemotherapy and continuing until th

30 myelodysplasia-related) who had not received remission induction chemotherapy underwent allogeneic (n

31 The standard treatment paradigm for AML is remission induction chemotherapy with an anthracycline/c

32 All patients then received two courses of remission induction chemotherapy with daunorubicin, ara-

33 aluated angiogenesis after the completion of remission induction chemotherapy.

34 Cytarabine is a key constituent of remission induction chemotherapy.

35 n bone marrow samples collected on day 19 of remission-induction chemotherapy from 248 children with

36 ance of leukemic cells after 2 to 3 weeks of remission-induction chemotherapy, and these patients hav

37 with newly diagnosed ALL received 6 weeks of remission-induction chemotherapy.

38 o a phase 3 AML trial using intensive-timing remission induction/consolidation and related donor marr

39 Therapy included four- or five-agent remission induction; consolidation therapy with doxorubi

40 Detectable residual disease at the end of remission induction correlated with adverse genetic abno

41 cover neutrophils >/=1,000/microL during the remission induction course was 16 days (interquartile ra

42 of detectable residual disease at the end of remission induction (day 46).

43 igh risk of life-threatening events, such as remission induction failure, is a high priority in APL,

44 The purpose of this study was to determine remission induction frequency when bortezomib was combin

45 stent disease at day 15 and days 22 to 25 of remission induction in childhood acute lymphoblastic leu

46 ue to provide a valuable management tool for remission induction in mildly to moderately active dista

47 th autoimmune hepatitis (AIH) and results in remission induction in over 80% of patients.

48 Remission induction in patients with active primary SNV

49 effective differentiation-inducing agent for remission induction in patients with acute promyelocytic

50 X is the first proven alternative to CYC for remission induction in severe GPA and MPA.

51 ide (CYC) followed by azathioprine (AZA) for remission-induction in severe ANCA-associated vasculitis

52 of maintenance of glucocorticoids following remission induction is debatable.

53 Remission induction is the most important prognostic fac

54 The level of minimal residual disease during remission induction is the most important prognostic ind

55 al minimal residual disease monitoring after remission induction is warranted for patients with detec

56 gative minimal residual disease status after remission induction, minimal residual disease re-emerged

57 Carriers were more likely to fail remission induction (odds ratio = 4.22; 95% confidence i

58 DAC with standard-dose cytarabine (SDAC) for remission induction of previously untreated AML and to c

59 High-dose cytarabine applied during remission induction or as consolidation after attainment

60 In our study of children undergoing remission induction or consolidation therapy for acute l

61 After remission induction, patients were randomized to one of

62 ia of 0.01% or more at the end of the 6-week remission induction phase.

63 The remission induction rate was 40% in Flt3/ITD-positive pa

64 The remission induction rate was similar in the non-DS-Frenc

65 Preliminary results indicated a high remission induction rate with the human CD52 antibody, C

66 h normal karyotype, FLT3/ITD mutations, high remission induction rates, and improved survival (partic

67 For remission induction, recent randomized trial data sugges

68 The remission induction regimen consisted of oral prednisone

69 erapy when oral etoposide is used as part of remission induction regimens for relapsed or refractory

70 Remission-induction regimens were RTX at 375 mg/m(2) x 4

71 gether with the increasing clinical drive to remission induction, requires that further therapeutic t

72 Remission induction, survival, and event-free survival r

73 had a higher CR rate and fewer deaths during remission induction than did those receiving placebo (P

74 atment for 2 years: 2 doses of 1 gm each for remission induction, then 1 gm every 6 months (total of

75 re likely to die during the first 8 weeks of remission induction therapy (hazard ratio = 7.26; 95% co

76 rates (n = 629) were collected at the end of remission induction therapy and at 3 intervals thereafte

77 nants of the early cytoreductive response to remission induction therapy and subsequent clinical outc

78 e who had peripheral blood MRD at the end of remission induction therapy but only 13.3% +/- 9.1% for

79 eukaemia and 0.01% or more MRD at the end of remission induction therapy could benefit from augmented

80 monoclonal antibody, has proven efficacy in remission induction therapy for AAV, and two trials with

81 Rituximab was effective remission induction therapy for refractory ANCA-associat

82 levels of MRD (0.001%-< 0.01%) at the end of remission induction therapy have prognostic significance

83 nitoring residual T-LL cells in blood during remission induction therapy identified patients with slo

84 After 45 days of remission induction therapy on Eastern Cooperative Oncol

85 ony-stimulating factor (G-CSF) following ALL remission induction therapy prompted us to examine this

86 and of these, 111 were randomized to receive remission induction therapy with all-trans retinoic acid

87 gh-risk presenting features (85.7%) received remission induction therapy with dexamethasone, vincrist

88 e: one, rate of complete response (CR) after remission induction therapy with methotrexate, temozolom

89 Patients received standard remission induction therapy, and responding patients wer

90 l trials evaluating mycophenolate mofetil as remission induction therapy, gusperimus, belimumab and c

91 vated minimal residual disease at the end of remission induction therapy.

92 mouse model of acute myeloid leukemia (AML) remission induction therapy.

93 negative for minimal residual disease after remission induction therapy.

94 poorer leukemia cell clearance on day 19 of remission induction therapy.

95 daunomycin, cytarabine, and etoposide (DAV) remission induction therapy.

96 , prednisone, and asparaginase were used for remission induction therapy.

97 ), beginning one day after the completion of remission-induction therapy and continuing until the neu

98 Three-drug remission-induction therapy combined with MRD-based risk

99 All patients received the same intensive, remission-induction therapy followed by 120 weeks of ris

100 glucocorticoids have been the cornerstone of remission-induction therapy for severe antineutrophil cy

101 Failure of remission-induction therapy is a rare but highly adverse

102 Minimal residual disease (MRD) at the end of remission-induction therapy predicts relapse in acute ly

103 ed thirty-three patients were registered for remission-induction therapy with VAD or VAD plus the che

104 ny extramedullary site after 4 to 6 weeks of remission-induction therapy, in 1041 of 44,017 patients

105 mal residual disease during or at the end of remission induction; they were less likely to have the t

106 Minimal residual disease levels during remission induction treatment have important prognostic

107 sk cytogenetic features, or poor response to remission induction treatment), and for the estimated 2%

108 FLAG-Ida is an effective remission induction treatment, with a high complete remi

109 disease (MRD) results obtained on day 19 of remission induction treatment.

110 al disease (MRD) levels on days 19 and 46 of remission induction treatment.

111 the level of minimal residual disease after remission-induction treatment.

112 This 12-month double-blind study attempted remission induction using standard therapy with or witho

113 Remission induction utilized non-cross-resistant regimen

114 nts with and without detectable leukaemia at remission induction was 32.5% (10.6) and 7.5% (4.0), res

115 The rate of remission induction was 60.5%, with a 48% rate of subseq

116 ce of lymphoblasts (even 1%-4%) on day 15 of remission induction was associated with a poor prognosis

117 esidual disease (> or = 1%) after 6 weeks of remission induction were significantly associated with p

118 at initial diagnosis was selected for during remission induction with glucocorticoids and contributed

119 Remission induction with infliximab plus MTX provided a

120 V and renal involvement respond similarly to remission induction with RTX plus glucocorticoids or CYC

121 nal and/or biologic immunosuppressants after remission-induction with anti-B cell antibodies.