ライフサイエンスコーパス: azacitidine

1 for azacitidine plus vorinostat ( P = .16 v azacitidine).

2 syndromes is hypomethylating agents such as azacitidine.

3 rapies such as donor lymphocyte infusion and azacitidine.

4 solidation treatment followed by 4 cycles of azacitidine.

5 responders who received >/= 6 cycles of oral azacitidine.

6 ubcutaneously once weekly during 4 cycles of azacitidine.

7 n days 1 to 3) with the same two agents plus azacitidine (250 mg/m2/d on days 4 to 50) for the therap

8 ths), the ORR was 38% for patients receiving azacitidine, 49% for azacitidine plus lenalidomide ( P =

9 ed a phase 1/2 study of the combination of 5-azacitidine (5-AZA), valproic acid (VPA), and ATRA in pa

10 proved median overall survival compared with azacitidine (5.5 vs 8.8 months, respectively, P = .03).

11 her for azacitidine plus lenalidomide versus azacitidine (68% v 28%, P = .02) but similar for all arm

12 a Bayesian adaptive design to receive either azacitidine 75 mg/m(2) intravenously/subcutaneously dail

13 The go-forward dose is azacitidine 75 mg/m(2) on days 1 through 5 and lenalidom

14 icacy and safety of combination therapy with azacitidine (75 mg/m(2)/d for 5 days) and lenalidomide (

15 onic myelomonocytic leukemia (CMML) 1:1:1 to azacitidine (75 mg/m(2)/day on days 1 to 7 of a 28-day c

16 cted with either intravenous or subcutaneous azacitidine (75 mg/m2/d for 7 days every 28 days).

17 egimen consisting of hydroxyurea followed by azacitidine, 75 mg/m(2) for 7 days, and gemtuzumab ozoga

18 Of 277 patients from 90 centers, 92 received azacitidine, 93 received azacitidine plus lenalidomide,

19 Primary T cells treated with 5-azacitidine, a DNA methyltransferase inhibitor, showed i

20 proved in myelodysplastic syndromes (MDS): 5-azacitidine and 5-aza-2'-deoxycitidine (decitabine).

21 16, 113 patients were treated: 40 (35%) with azacitidine and 73 (65%) with decitabine.

22 The hypomethylating drugs azacitidine and decitabine have shown efficacy in myelod

23 5-Azacitidine and decitabine were approved in the United S

24 her-risk MDS include hypomethylating agents (azacitidine and decitabine), intensive chemotherapy (ICT

25 therapies include the hypomethylating agents azacitidine and decitabine, which should be administered

26 lating agents in hematology, with a focus on azacitidine and decitabine.

27 d active sequential treatment combination of azacitidine and lenalidomide for patient with myelodyspl

28 We aimed to assess azacitidine and lenalidomide in patients with high-risk

29 or azacitidine plus lenalidomide ( P = .14 v azacitidine), and 27% for azacitidine plus vorinostat (

30 Lenalidomide, azacitidine, and decitabine are all FDA-approved agents

31 Lenalidomide, azacitidine, and decitabine, each recently approved by t

32 Lenalidomide and azacitidine are active in patients with lower- and highe

33 he DNA methylation inhibitors decitabine and azacitidine are efficacious for hematological neoplasms

34 However, responses to azacitidine are generally temporary, and outcomes after

35 We previously reported that azacitidine (Aza C) was active in patients with high-ris

36 sent study, we report a comparative study of azacitidine (AZA) and decitabine (DAC) in combination wi

37 Although azacitidine (AZA) improves survival in patients with hig

38 Azacitidine (AZA) is effective treatment for myelodyspla

39 Azacitidine (AZA) is the current standard of care for hi

40 MDS patients collected before treatment with azacitidine (AZA) or decitabine (DEC).

41 Azacitidine (AZA) up-regulates the expression of tumor A

42 eated with the methyltransferase inhibitor 5-azacitidine (aza-CR) followed by the histone deacetylase

43 Azacitidine (AzaC) mitigates graft-versus-host disease (

44 hypomethylating agents, decitabine (Dec) and azacitidine (AzaC), induce FOXP3 expression in CD4(+)CD2

45 Combination treatment strategies using an azacitidine backbone are demonstrating promising early r

46 clinical trials of novel targeted therapies, azacitidine-based combination therapeutic strategies, an

47 n Patients with higher-risk MDS treated with azacitidine-based combinations had similar ORR to azacit

48 Whether azacitidine-based combinations with lenalidomide or vori

49 treatment with the DNA-demethylating agent, azacitidine, causes increased mRNA levels in embryonic c

50 The lenalidomide/azacitidine combination is well-tolerated and highly act

51 US regulatory approval of azacitidine, decitabine, and lenalidomide between 2004 a

52 Oral and SC azacitidine decreased DNA methylation in blood, with max

53 Furthermore, azacitidine did not increase the rate of infection or bl

54 Lenalidomide and azacitidine each have activity in myelodysplastic syndro

55 Azacitidine exposure increased with escalating oral dose

56 l report a phase 2 study of lenalidomide and azacitidine for higher risk myelodysplastic syndromes (M

57 Decitabine (DAC) and 5-azacitidine have recently been approved for the treatmen

58 potent, more specific drugs that behave like azacitidine imperative.

59 That azacitidine improves survival in patients with high-risk

60 ted dose of lenalidomide in combination with azacitidine in patients with acute myeloid leukaemia and

61 efficacy of low-dose decitabine vs low-dose azacitidine in this group of patients.

62 epigenetic modifier drugs, panobinostat and azacitidine, increased CD33 expression in some cell line

63 ce superior overall response rates (ORRs) to azacitidine is not known.

64 Purpose Azacitidine is standard, first-line therapy in higher-ri

65 Although azacitidine is the mainstay of treatment in MDS, only ha

66 The combination of lenalidomide and azacitidine is well tolerated with encouraging clinical

67 Low-dose decitabine and azacitidine may have broad applicability for cancer mana

68 Overall, 41 patients received SC and oral azacitidine (MDSs, n = 29; CMML, n = 4; AML, n = 8).

69 tidine-based combinations had similar ORR to azacitidine monotherapy, although patients with CMML ben

70 All participants received 75 mg/m(2) azacitidine once a day for days 1-5 for each 28 day cycl

71 yndromes with excess blasts after failure of azacitidine or decitabine treatment.

72 val after failure of intensive chemotherapy, azacitidine, or decitabine was more favorable in patient

73 010 with intensive chemotherapy (n = 557) or azacitidine- or decitabine-based therapy (n = 114).

74 The pharmacodynamic effects of DAC and 5-azacitidine outside their known activity as inhibitors o

75 t compared with 16% of patients treated with azacitidine (P = .2).

76 for patients receiving azacitidine, 49% for azacitidine plus lenalidomide ( P = .14 v azacitidine),

77 /m(2)/day on days 1 to 7 of a 28-day cycle); azacitidine plus lenalidomide (10 mg/day on days 1 to 21

78 For patients with CMML, ORR was higher for azacitidine plus lenalidomide versus azacitidine (68% v

79 enters, 92 received azacitidine, 93 received azacitidine plus lenalidomide, and 92 received azacitidi

80 although patients with CMML benefitted from azacitidine plus lenalidomide.

81 domide ( P = .14 v azacitidine), and 27% for azacitidine plus vorinostat ( P = .16 v azacitidine).

82 lenalidomide (10 mg/day on days 1 to 21); or azacitidine plus vorinostat (300 mg twice daily on days

83 acitidine plus lenalidomide, and 92 received azacitidine plus vorinostat.

84 well tolerated in outpatient settings, with azacitidine prolonging survival and decreasing time to a

85 Azacitidine prolongs survival by a median of only 9.5 mo

86 Azacitidine provides important clinical benefits for pat

87 ths for patients treated with decitabine and azacitidine, respectively (P = .1).

88 03) for patients treated with decitabine and azacitidine, respectively.

89 ment of patients with higher risk MDS with 5-azacitidine results in significant improvement in overal

90 sk myelodysplastic syndromes (MDS) receiving azacitidine therapy.

91 ide clinical benefits in MDS patients during azacitidine therapy.

92 ents with relapsed leukemia, the addition of azacitidine to etoposide and amsacrine did not improve r

93 mplete remissions were seen in 10% to 17% of azacitidine-treated patients; partial remissions were ra

94 oses of ABBV-075 coupled with bortezomib and azacitidine treatment, despite the lack of in vitro syne

95 utated hematopoietic cells were sensitive to azacitidine treatment.

96 usly reported clinical trials (n = 309) with azacitidine using the WHO classification system for MDS

97 alysis of the international phase 3 study of azacitidine vs conventional care regimens in older (>/=6

98 for the 27 AML patients randomly assigned to azacitidine was 19.3 months compared with 12.9 months fo

99 Oral azacitidine was bioavailable and demonstrated biologic a

100 Cross-over to SC azacitidine was permitted for nonresponders who received

101 tial Cancer and Leukemia Group B trials with azacitidine were recollected and reanalyzed as part of t