ライフサイエンスコーパス: azacytidine

1 but not with the DNA demethylation agent, 5-azacytidine.

2 which could be reversed by treatment with 5-azacytidine.

3 by growth in the DNA methylation inhibitor 5-azacytidine.

4 s also achieved by treatment of cells with 5-Azacytidine.

5 on on treatment with a demethylating drug, 5-azacytidine.

6 presence of ribavirin and another mutagen, 5-azacytidine.

7 by treatment with the demethylating agent 5-azacytidine.

8 ter treatment with the demethylating agent 5-azacytidine.

9 ostatin A or the DNA methylation inhibitor 5-azacytidine.

10 all reexpressed hMLH1 after treatment with 5-azacytidine.

11 er the addition of the demethylating agent 5-azacytidine.

12 les, both of which could be reactivated by 5-azacytidine.

13 ssion by the inhibitor of DNA methylation, 5-azacytidine.

14 um butyrate or trichostatin A but not with 5-azacytidine.

15 by treatment with the demethylating agent 5-azacytidine.

16 thylating agents, 5-azacytidine or 2-deoxy-5-azacytidine.

17 5 controls with the hypomethylating agent 5-azacytidine.

18 was significantly decreased in response to 5-azacytidine.

19 iation of MSCs in culture was induced with 5-azacytidine.

20 s was restored with a demethylation agent, 5-azacytidine.

21 ession of GADD45alpha or pretreatment with 5-azacytidine.

22 epithelial cells by the demethylating drug 5-azacytidine.

23 ls, treatment with the demethylating agent 5-azacytidine (10 microM for 6 days) did not activate CYP1

24 ent of AML blasts with decitabine (DAC) or 5-azacytidine, 2 hypomethylating agents that show efficacy

25 ivision, we find that the 3 drugs studied, 5-azacytidine (5 micromol/L), hydroxyurea (40 micromol/L),

26 NA, and treatment of these cell lines with 5-azacytidine (5-AC), a demethylation reagent, induced p73

27 heavy metals only after demethylation with 5-azacytidine (5-AsaC).

28 5-azacytidine (5-Aza) is a potent inducer of fetal hemoglo

29 Cells primed to produce IFN by 5-azacytidine (5-aza) underwent endoplasmic reticulum (ER)

30 5-Azacytidine (5-Aza), a DNA demethylating agent, induces

31 by treatment with the demethylating agent 5-azacytidine (5-Aza).

32 CaP PCA cells: treatment of the cells with 5-azacytidine (5-aza-C), an inhibitor of DNA methyltransfe

33 pped when conducted on the cytosine analog 5-azacytidine (5-aza-C).

34 few CpG dinucleotides by brief exposure to 5-azacytidine (5-AzaC) but persisted even after prolonged

35 tly, TSA and the DNA demethylating reagent 5-azacytidine (5-AzaC) caused marked synergistic activatio

36 The cytosine analog 5-azacytidine (5-AzaC) is a demethylating agent that is al

37 5-Azacytidine (5-azaC) is an azanucleoside approved for my

38 ylation and that the methylation inhibitor 5-azacytidine (5-AzaC) potently blocks the increased cell

39 AMB468 with the DNA methylation inhibitor, 5-azacytidine (5-AzaC) results in growth arrest, whereas t

40 c acid (VPA) and DNA methylation inhibitor 5-azacytidine (5-azaC) specifically reversed the repressio

41 Following 5-azacytidine (5-azaC) treatment of siJKA, aberrant RNA sp

42 tes, such as the DNA-hypomethylating agent 5-azacytidine (5-AzaC), have been shown to lower malignant

43 y heavy metals only after demethylation by 5-azacytidine (5-AzaC).

44 Within this study, 5-azacytidine (5-azaC, a DNMT inhibitor) was used as a pos

45 also demonstrate resistance to the mutagen 5-azacytidine (5-AZC) and decreased accumulation of mutati

46 al mechanism for the ribonucleoside analog 5-azacytidine (5-AZC).

47 (HIV-1) by use of chemical mutagens [i.e., 5-azacytidine (5-AZC)] as well as by host factors with mut

48 r activity of the 5-azacytidine derivative 5-azacytidine-5'-elaidate (CP-4200), a nucleoside transpor

49 iated by preventing methylation, either by 5-azacytidine (5AC) treatment or by introduction of a muta

50 been treated with the demethylating agent, 5-azacytidine (5aC).

51 thyl-N'-nitro-N-nitrosoguanidine (NTG) and 5-azacytidine (5AZ).

52 es of action (methotrexate, actinomycin D, 5-azacytidine, 8-thioguanosine).

53 Treatment with 5-azacytidine, a demethylating agent, causes Th2 cells to

54 reatment of the hepatoma bearing rats with 5-azacytidine, a demethylating agent, induced basal as wel

55 Recently, azacytidine, a hypomethylating agent, was reported to in

56 nt of two of the resistant cell lines with 5-azacytidine, a known inhibitor of methylation, results i

57 Treatment with 5-azacytidine, a methylation inhibitor, partially reversed

58 nt of two clonal lines of Ku-80 cells with 5-azacytidine, a potent DNA demethylating agent, rendered

59 sure of proliferating 10T1/2 stem cells to 5-azacytidine, a potent DNA methylation inhibitor, gave ri

60 splanted hepatoma after demethylation with 5-azacytidine, a potent inhibitor of DNA methyltransferase

61 Decitabine, but not 5-azacytidine, also produced a G(2)/M cell-cycle arrest in

62 5'-Azacytidine, an inhibitor of DNA methylation that derepr

63 in the sibling cultures by treatment with 5-azacytidine, an inhibitor of DNA methylation, and the in

64 relieved upon treatment of the cells with 5-azacytidine, an inhibitor of DNA methyltransferase, with

65 genes that affect drug sensitivity, using 5-azacytidine and 2'-deoxy-5-azacytidine (DAC, decitabine)

66 ith the DNA methyltransferase inhibitors, 5'-azacytidine and 5'-aza-2'-deoxycytidine, activated basal

67 The cytidine analogues azacytidine and 5-aza-2'-deoxycytidine (decitabine) are

68 DNA methylation, led to widespread use of 5-azacytidine and 5-aza-2'-deoxycytidine (Decitabine) to d

69 The DNA-hypomethylating agents 5-azacytidine and 5-aza-2'-deoxycytidine are effective tre

70 concentrations of the pyrimidine analogues 5-azacytidine and 5-azacytosine.

71 Except for 5-azacytidine and 8-thioguanosine, all compounds examined

72 y, cytosine arabinoside, ethidium bromide, 5-azacytidine and aspirin all significantly reduced the ra

73 demonstrating that drugs like hydroxyurea, 5-azacytidine and butyric acid each yielded increases in g

74 s with the DNA methyltransferase inhibitor 5-azacytidine and comparing gene expression with oligonucl

75 Together, 5-azacytidine and decitabine exert growth-inhibitory and p

76 ned the effects of 2 demethylating agents, 5-azacytidine and decitabine on growth and survival of neo

77 uding in cancer stem cells, and two of them (azacytidine and decitabine) have been approved for treat

78 ents, cytarabine, or hypomethylating agents (azacytidine and decitabine).

79 eted a minimum of 4 cycles of therapy with 5-azacytidine and entinostat.

80 response to both methylation inhibition by 5-azacytidine and exposure to Pseudomonas aeruginosa lipop

81 omatoes to the methyltransferase inhibitor 5-azacytidine and find that they ripen prematurely.

82 ression and potency of nucleoside analogues, azacytidine and inosine-glycodialdehyde.

83 The cellular toxicity of 5-azacytidine and its DNA demethylating activity were stro

84 he mutational specificity of two mutagens, 5-azacytidine and N-methyl-N'-nitro-N-nitroso-guanidine.

85 d with 2 DNA methyltransferase inhibitors (5-azacytidine and procainamide) and 3 ERK pathway inhibito

86 h active lupus and in T cells treated with 5-azacytidine and procainamide.

87 d using two additional nucleoside analogs, 5-azacytidine and ribavirin.

88 tment with DNA demethylating agents, such as Azacytidine and several natural products.

89 n the presence of the epigenetic modifiers 5-azacytidine and suberoyl bis-hydroxamic acid and under c

90 A combination of the DNMT inhibitor 5-azacytidine and the HDAC inhibitor butyrate markedly red

91 L) patients enrolled in a phase 1 trial of 5-azacytidine and the histone deacetylase inhibitor entino

92 Treatment of breast cancer MCF7 cells with 5'azacytidine and Trichostatin A resulted in expression of

93 stological origins with the epigenetic drugs azacytidine and valproate, and tested tumor and self-rea

94 had relapsed disease or were refractory to 5-azacytidine and/or lenalidomide, and 3 had received inte

95 using three nucleoside analogs, ribavirin, 5-azacytidine, and 5-fluorouracil.

96 f cNJ101 cells with a demethylating agent, 5-azacytidine, and a histone deacetylase inhibitor, tricho

97 as achieved using the demethylating agent, 5-azacytidine, and the HDAC inhibitor, valproic acid.

98 5-Azacytidine- and 5-aza-deoxycytidine (5-aza-CdR)-mediate

99 Finally, we identified 5'-azacytidine as a new P-TEFb-releasing agent.

100 The impact of azacytidine (Aza C) on the quality of life of 191 patien

101 Patients received 5-azacytidine (AZA) 75 mg/m(2) intravenously daily for 7 d

102 5-Azacytidine (AZA) is a nucleoside analog that is used to

103 correlation (R = 0.44, P = .11) to that of 5-azacytidine (AZA), but a good correlation to that of cyt

104 using the DNA methyltransferase inhibitor 5-azacytidine (Aza).

105 vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA).

106 5-Azacytidine (aza-C) and its derivatives are cytidine ana

107 Anticancer drug 5-azacytidine (aza-C) induces DNA-protein cross-links (DPC

108 iting DNA methyltransferase activity using 5-azacytidine (Aza; a cytosine analog) to limit HSV-1-indu

109 e transcriptase activity was produced with 5-azacytidine (AzaC) and with 5'-iodo-2'-deoxyuridine (IUd

110 R2 seedlings germinated in the presence of 5-azacytidine (AzaC) were herbicide-resistant and also con

111 SA), and the DNA methyltransferase inhibitor azacytidine (AzaCdR) promote lytic reactivation.

112 TGF-beta) cytokine, a demethylating agent (5-azacytidine), B cell receptor engagement with anti-IgG a

113 erived by treating 10T1/2 fibroblasts with 5-azacytidine, but not in parental 10T1/2 cells.

114 hat clinically relevant, nontoxic doses of 5-azacytidine can restore erythropoietin production and am

115 Treatment of LNCaP-LN3 cells with 5'-azacytidine caused re-expression of LDHB transcripts.

116 that gemcitabine and doxorubicin (but not 5-azacytidine, cis-platinum, or 5-fluorouracil) induce lyt

117 d whether the demethylating agent 2'-deoxy-5-azacytidine (DAC) can be used in vivo to sensitize MMR-d

118 GPC3 expression was restored after 2-deoxy 5-azacytidine (DAC)-mediated demethylation of its promoter

119 sitivity, using 5-azacytidine and 2'-deoxy-5-azacytidine (DAC, decitabine) as demethylating agents.

120 DNA methylation is reversible, drugs like 5'-azacytidine, decitabine, and histone deacetylase inhibit

121 Demethylation agent 5'-azacytidine decreased BMPER expression in fibroblasts, a

122 Transport assays using [(1)(4)C]5-azacytidine demonstrated Na(+)-independent uptake of the

123 Deoxy-azacytidine derepressed miR-487b and attenuated CSC-medi

124 In contrast, the cellular activity of the 5-azacytidine derivative 5-azacytidine-5'-elaidate (CP-420

125 ar carcinoma (HCC) cell lines treated with 5-azacytidine (DNA hypomethylating agent) and/or trichosta

126 ty was maximally rescued by treatment with 5-azacytidine (DNA methyltransferase inhibitor) compared w

127 te to a myofibroblast-like phenotype using 5-azacytidine do not promote tumor cell growth as efficien

128 ent with the DNA demethylating agent 5-deoxy-azacytidine does not increase Xi expression ahead of rep

129 exposure to the DNA methylation inhibitor 5-azacytidine, enforces astrocyte dedifferentiation.

130 on of egg production and egg maturation by 5-azacytidine establishes an essential role for 5-methylcy

131 n could be turned on, off, and on again by 5-azacytidine exposure, washout, and reexposure.

132 e-passage clones only by pretreatment with 5-azacytidine followed by trichostatin A, suggesting that

133 8 h to the DNA methyltransferase inhibitor 5-azacytidine, followed by a three-step protocol for the i

134 hylated cells with the demethylating agent 5-azacytidine had a modest effect on COX-2 expression, but

135 inhibition of beta-globin mRNA levels, and 5-azacytidine had little effect on beta-globin mRNA levels

136 t were unmethylated at the COX-2 promoter, 5-azacytidine had no effect on H. pylori-stimulated COX-2

137 mple, we have previously demonstrated that 5-azacytidine has its greatest antiviral potency during re

138 with inhibitors of DNA methyltransferases (5-Azacytidine), histone deacetylases (valproic acid), and

139 We examine trials of agents, including 5-azacytidine, hydroxyurea, and short-chain fatty acids.

140 Treatment of mice with 5-azacytidine (i.p.) resulted in a significant dose-depend

141 ated using the methylation-inhibitor 5-deoxy-azacytidine in all three lines.

142 key transporter for the cellular uptake of 5-azacytidine in leukemia cells and raise the possibility

143 t with the DNA methyltransferase inhibitor 5-azacytidine in the context of a mouse containing the ent

144 Demethylation of DNA with 5-azacytidine in two cell lines induced expression of hTER

145 d by treatment with a demethylation agent (5-azacytidine) in two NSCLC cell lines lacking DMBT1 expre

146 in expression was induced upon exposure to 5-azacytidine, in cells derived from -117 Greek hereditary

147 but differentiate in vitro in response to 5'-azacytidine, in part depending on Bmpr1a, a receptor for

148 concentrations of the demethylating agent 5-azacytidine increased basal expression and hypoxic induc

149 iously observed that the nucleoside analog 5-azacytidine increased the spleen necrosis virus (SNV) mu

150 ter in vivo by treatment of the cells with 5-azacytidine increased transglutaminase expression and hy

151 rostatic carcinoma cell line cultures with 5-azacytidine induced ETB mRNA expression, suggesting that

152 se, treatment with the demethylating agent 5-azacytidine induced expression of the absent hMLH1 prote

153 Treatment with the hypomethylating agent 5-azacytidine induced PLS3 expression in Jurkat cells and

154 with the DNA methyltransferase inhibitor, 5 azacytidine induced RI expression and restored TGF-beta

155 ts with CEF culture supernatants from both 5-azacytidine-induced and noninduced CEF led to ALV infect

156 A strong dependence of 5-azacytidine-induced DNA demethylation on hENT1 activity

157 n HD cells relative to control, as well as 5-azacytidine-induced hypomethylation.

158 se in vitiliginous SL101 birds and also in 5-Azacytidine-induced vitiliginous BL101 parental control

159 , treatment with the hypomethylating agent 5-azacytidine induces chromosome breakage in root tips.

160 Finally, treatment of MBD2-null mice with 5-azacytidine induces only a small, nonadditive induction

161 cp70 with the demethylating agent 2-deoxy-5'-azacytidine induces resensitization to cisplatin and re-

162 Demethylation agent 5-azacytidine inhibited the deletion of the penultimate ex

163 responsible proteins for the transport of 5-azacytidine into MDS/AML cells are unknown.

164 The nucleoside analog 5-azacytidine is an archetypical drug for epigenetic cance

165 sy over the mechanism of Hb F induction by 5-azacytidine led to the identification of hydroxyurea as

166 Here we describe 5-azacytidine-mediated RNA immunoprecipitation (Aza-IP), a

167 Neither 5-azacytidine nor decitabine induced substantial apoptosis

168 treated with the DNA demethylating agents, 5-azacytidine or 2-deoxy-5-azacytidine.

169 Similarly, inhibiting methylation with 5-azacytidine or knocking down the DNA methyltransferase D

170 3- cell subpopulations were cultured with 5'-azacytidine or vascular endothelial growth factor (VEGF1

171 RNA-seq analysis of CSCs treated with 5-azacytidine plus butyrate provided evidence that inhibit

172 itive cells with the methylation inhibitor 5-azacytidine prevented the emergence of resistant cells,

173 ely, global inhibition of methylation with 5-azacytidine promoted eotaxin-3 production in association

174 xpression by demethylation treatment using 5-azacytidine reduced the proliferation and colony formati

175 for the modulation of transporter-related 5-azacytidine resistances.

176 ment of cells with the methylase inhibitor 5-azacytidine restored CREB binding to the Wnt10b gene pro

177 ment of R2 progeny of silenced plants with 5-azacytidine resulted in demethylation of the Ubi1 promot

178 Experimental DNA demethylation with 5'-azacytidine results in a similar increase of H3-K4me.

179 tudinal analysis in a patient treated with 5-azacytidine revealed that karyotypically abnormal HSCs p

180 116 cells with the DNA demethylating agent 5-azacytidine reverses promoter methylation, promotes norm

181 Azacytidine-reverted xrs-5 cells that acquired nuclear D

182 When seedlings are treated with 5-azacytidine, root growth of epi-lines is restored to wil

183 However, because of 5-azacytidine's general toxicity, other nucleoside analogs

184 s with the DNA methyltransferase inhibitor 5-azacytidine selectively demethylated this area and incre

185 level, and the DNA methylation inhibitor, 5-Azacytidine, significantly elevated the Drg-1 gene expre

186 5-Azacytidine, the first such agent in clinical use, was p

187 After these cells were treated with 5-azacytidine, they regained the ability to clone in hypox

188 methyltransferase and the cytidine analog 5-azacytidine to recover RNA targets by immunoprecipitatio

189 Clonogenic assays demonstrate that the 5-azacytidine treated cells show increased sensitivity to

190 odest effect on COX-2 expression, but when 5-azacytidine-treated cells were subsequently stimulated w

191 Stroma derived from 5-azacytidine-treated patients lacked aberrant methylation

192 Furthermore, 5-azacytidine treatment activated CIITA expression in clas

193 5'-azacytidine treatment additionally regulated BMPER expre

194 methylated and silenced mir-124 gene loci, 5-azacytidine treatment allowed miR-124 re-expression and

195 Similar to mouse NPC1L1, 5-azacytidine treatment also increased the level of human

196 Rescue of DNA repair gene expression by 5-azacytidine treatment identified DNA methylation as a me

197 Bisulfite analysis of cells in which 5-azacytidine treatment induced GFP expression revealed me

198 Increasing dosages of 5-azacytidine treatment led to higher levels of firefly lu

199 Demethylation of the gene by deoxy-5-azacytidine treatment led to its reactivation in a lung

200 2-Deoxy-5-azacytidine treatment of cell lines with aberrant methyl

201 The 5-azacytidine treatment of OSCC cells led to an up-regulat

202 Last, although 5-azacytidine treatment of Rael cells results in a G1 arre

203 Experimental demethylation by either 5-azacytidine treatment or DNMT1 depletion diminished both

204 ressive cells by promoter methylation, but 5-azacytidine treatment reactivated the expression.

205 rectal carcinoma cells, RKO, with or without azacytidine treatment to reexpress hMLH1.

206 a-globin gene at a level commensurate with 5-azacytidine treatment, 10- to 20-fold over that observed

207 en methylation of the MITEs was blocked by 5-azacytidine treatment, a threefold increase in the endog

208 beta RII message, which was reversed upon 5'-azacytidine treatment, indicating that the promoter meth

209 Following 5-azacytidine treatment, RA and trichostatin A markedly in

210 pericytes; these effects were prevented by 5-azacytidine treatment.

211 des were demethylated in Ku-80 cells after 5-azacytidine treatment.

212 5-Azacytidine treatments also resulted in stabilization of

213 ful biomarker to predict the efficiency of 5-azacytidine treatments.

214 tion of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2'-deoxycyti

215 lation of MGMT in HeLa S3 cells induced by 5-azacytidine was accompanied by progressive demethylation

216 5-Azacytidine was first synthesized almost 40 years ago.

217 The finding that 5-azacytidine was incorporated into DNA and that, when pre

218 Cells treated with 5-azacytidine were monitored for 2 wk compared with 1 wk f

219 associated with RIP by taking advantage of 5-azacytidine, which prevents most methylation in Neurospo

220 did not occur when conidia were plated on 5-azacytidine, which reduces DNA methylation.

221 2 after the treatment of HCT116 cells with 5-azacytidine, which resulted in differential expression o