ライフサイエンスコーパス: azacytidine

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

2 ession of GADD45alpha or pretreatment with 5-azacytidine.

3 epithelial cells by the demethylating drug 5-azacytidine.

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

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

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

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

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

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

10 by treatment with the demethylating agent 5-azacytidine.

11 ter treatment with the demethylating agent 5-azacytidine.

12 clinical response to decitabine, but not to azacytidine.

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

14 all reexpressed hMLH1 after treatment with 5-azacytidine.

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

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

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

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

19 by treatment with the demethylating agent 5-azacytidine.

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

21 ription, as well as decreased sensitivity to azacytidine.

22 ls from female donors and were reversed by 5-azacytidine.

23 ed Kawasaki disease mice were treated with 5-azacytidine.

24 5 controls with the hypomethylating agent 5-azacytidine.

25 was significantly decreased in response to 5-azacytidine.

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

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

28 sponse with eprenetapopt and venetoclax with azacytidine; 15 (38%, 23-55) had a complete response.

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

30 treatment naive or who had R/R PTCL received azacytidine 300 mg once per day on days 1 to 14, and rom

31 n before, during, and after treatment with 5-azacytidine (40 patients; 15 nonresponders, 25 responder

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

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

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

35 5-azacytidine (5-Aza) is a potent inducer of fetal hemoglo

36 of DNA methyltransferase (Dnmt) inhibitor 5-azacytidine (5-aza) to generate outer hair cells (OHCs)

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

38 5-Azacytidine (5-Aza), a DNA demethylating agent, induces

39 In contrast to 5-azacytidine (5-aza), allogeneic stem-cell transplantatio

40 reatment with the DNA demethylating agent, 5-azacytidine (5-aza), was significantly more toxic to TET

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

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

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

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

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

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

47 5-Azacytidine (5-azaC) is an azanucleoside approved for my

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

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

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

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

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

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

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

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

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

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

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

59 ved DNA hypomethylating agents (DHAs) like 5-azacytidine (5AC) and decitabine (DAC) demonstrate effic

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

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

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

63 vious work has demonstrated that the DNMTi 5-Azacytidine (5AZA-C) activates type I interferon signali

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

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

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

67 Treatment of CP myoblasts with 5-azacytidine, a DNA hypomethylating agent, reduced this e

68 Treatment with 5-Azacytidine, a DNMT1 inhibitor, led to demethylation of

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

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

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

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

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

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

75 n combination with the hypomethylating agent azacytidine, achieves complete remission with or without

76 in this myeloid model could be reversed with azacytidine, albeit without significant improvement of n

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

78 class switch, and inhibition of RNA 5mC by 5-azacytidine ameliorated progression of IgA nephropathy.

79 5'-Azacytidine, an inhibitor of DNA methylation that derepr

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

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

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

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

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

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

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

87 de DNA methyltransferase (DNMT) inhibitors 5-azacytidine and 5-aza-2'-deoxycytidine lack selectivity

88 e DNA methyltransferase inhibitors (DNMTi) 5-azacytidine and 5-aza-2-deoxycytidine have been approved

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

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

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

92 ells treated with the small molecule drugs 5-azacytidine and bisperoxovanadium (HOpic), which inhibit

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

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

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

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

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

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

99 ferase and histone deacetylase inhibitors, 5-azacytidine and entinostat, disrupts the premetastatic n

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

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

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

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

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

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

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

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

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

109 Combined azacytidine and romidepsin are highly active in PTCL pat

110 In a phase 1 trial, we found oral 5-azacytidine and romidepsin to be safe and effective, wit

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

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

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

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

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

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

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

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

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

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

121 5-Azacytidine- and 5-aza-deoxycytidine (5-aza-CdR)-mediate

122 Hypomethylating agents decitabine and azacytidine are regarded as interchangeable in the treat

123 DNA hypomethylating agents decitabine and 5-azacytidine are the only two drugs approved for treatmen

124 The 5-azacytidines are approved inhibitors of DNMT1, but their

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

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

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

128 dels, we conducted a phase 1 study of oral 5-azacytidine (AZA) and romidepsin (ROMI) in patients with

129 5-Azacytidine (AZA) is a nucleoside analog that is used to

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

131 he DNA methyltransferase inhibitor (DNMTi) 5-azacytidine (AZA), have profound effects on transcriptio

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

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

134 5-Azacytidine (aza-C) and its derivatives are cytidine ana

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

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

137 t using a DNA methyltransferase inhibitor (5-azacytidine, AZA), methylation-specific PCR (MSP) and bi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 Methylation inhibitor 5-azacytidine diminishes the differences between memory an

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

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

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

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

159 d with the DNA methyltransferase inhibitor 5-Azacytidine during seed germination and early growth.

160 DNA methylation inhibitor 5-azacytidine effectively reverses expression of the TSGs

161 n targets (TE) activated by the same drug (5-azacytidine) elicit an immune response, which may be imp

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

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

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

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

166 8 h to the DNA methyltransferase inhibitor 5-azacytidine, followed by a three-step protocol for the i

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

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

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

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

171 rter mouse embryonic stem cells (mESCs) to 5-Azacytidine, HDAC inhibitors, BET inhibitors or GSK-J4 (

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

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

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

175 Inhibition of DNA methyltransferase by 5-azacytidine in 786-O and Caki-2 cells resulted in Wnt-5a

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

177 Demethylation with azacytidine in cultured sympathetic ganglia cells led to

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

179 ase 1 study of romidepsin combined with oral azacytidine in patients with relapsed/refractory (R/R) l

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

181 iated mechanism of action for venetoclax and azacytidine in the treatment of AML and highlights a pot

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

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

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

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

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

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

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

189 In addition, azacytidine induced a viral mimicry response in AML cell

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

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

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

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

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

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

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

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

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

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

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

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

202 uces wound-edge gene methylation and that 5'-azacytidine, inhibitor of methylation, improved wound cl

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

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

205 rospinal fluid, alone or in combination with azacytidine, is a highly effective therapy for multiple

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

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

208 ory acute myeloid leukemia patients pre/post azacytidine+nivolumab treatment that the disease-related

209 Neither 5-azacytidine nor decitabine induced substantial apoptosis

210 PegIFN-alpha combined with 5-azacytidine only partially overcame resistance in VF;DmD

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

212 ia directly with DNA methylation inhibitors (Azacytidine or Dnmt1-siRNA), prevented Mfn2 and Mlh1 hyp

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

214 3- cell subpopulations were cultured with 5'-azacytidine or vascular endothelial growth factor (VEGF1

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

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

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

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

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

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

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

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

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

224 116 cells with the DNA demethylating agent 5-azacytidine reverses promoter methylation, promotes norm

225 Treatment with 5-azacytidine reverted DNA hypermethylation but did not re

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

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

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

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

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

231 5-Azacytidine, the first such agent in clinical use, was p

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

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

234 um-breeding lines were treated with 5-methyl-azacytidine to test the feasibility of generating source

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

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

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

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

239 5'-azacytidine treatment additionally regulated BMPER expre

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

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

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

243 lation state of its proximal enhancer, and 5-azacytidine treatment increased IGFBP2 expression.

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

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

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

247 2-Deoxy-5-azacytidine treatment of cell lines with aberrant methyl

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

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

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

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

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

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

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

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

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

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

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

259 5-Azacytidine treatments also resulted in stabilization of

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

261 methylation in human and mouse cells, and 5-azacytidine triggered DNA demethylation is more pronounc

262 metabolite decitabine triphosphate, but not azacytidine triphosphate, functions as activator and sub

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

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

265 5-Azacytidine was first synthesized almost 40 years ago.

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

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

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

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

270 2 after the treatment of HCT116 cells with 5-azacytidine, which resulted in differential expression o