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1 pression was restored after treatment with a demethylating agent.
2 lines was reactivated after treatment with a demethylating agent.
3 R amplicons of the region, and exposure to a demethylating agent.
4 ll line MDA-MB-231, which was treated with a demethylating agent.
5 ous p16ink4a in response to treatment with a demethylating agent.
6 xpression, which could be reactivated with a demethylating agent.
7 rtunity for treatment of SONFH patients with demethylating agents.
8 2'-deoxy-5-azacytidine (DAC, decitabine) as demethylating agents.
9 and changes that occur after treatment with demethylating agents.
10 its expression is restored by treatment with demethylating agents.
11 gene, Ogg1, could be reversed by the use of demethylating agents.
12 RMS biopsies and could be reactivated by DNA-demethylating agents.
13 erapeutic options such as Syk inhibitors and demethylating agents.
14 al specimens and functionally verified using demethylating agents.
17 omoters of these genes; furthermore, the DNA demethylating agent 5 aza-2'deoxycytidine (5-Aza-dC) ant
19 emonstrated recently that treatment with the demethylating agent 5'-aza-2'-deoxycytidine (5-Aza-dC) s
21 noma cells MAP2 expression is induced by the demethylating agent 5-aza-2'-cytidine, and MAP2 promoter
24 Treatment of LNCaP(CS) and PC-3 with the demethylating agent 5-aza-2'-deoxycytidine (5-AZAdC) rea
25 Ns might be silenced by methylation, the DNA demethylating agent 5-aza-2'-deoxycytidine (5-AZAdC) was
26 c cancer cell lines after treatment with the demethylating agent 5-aza-2'-deoxycytidine (5Aza-dC) and
29 he HER4-negative BT20 cell line with the DNA demethylating agent 5-aza-2'-deoxycytidine (DAC)-enhance
33 apitulated or enhanced by treatment with the demethylating agent 5-aza-2'-deoxycytidine as well as by
34 wild-type female mice with low doses of the demethylating agent 5-aza-2'-deoxycytidine decreased the
36 CRBP1 mRNA, and in vitro treatment with the demethylating agent 5-aza-2'-deoxycytidine reactivated C
37 th loss of expression and treatment with the demethylating agent 5-aza-2'-deoxycytidine reactivated S
39 ermore, treatment of melanoma cells with the demethylating agent 5-aza-2'-deoxycytidine reinduces Rap
42 and UM-UC13), and exposure to the chromatin demethylating agent 5-aza-2'-deoxycytidine restored HSPA
49 owever, demethylation at SIE-1, induced by a demethylating agent 5-aza-2'-deoxycytidine, reactivated
50 cription of PLCepsilon1a and PLCepsilon1b by demethylating agent 5-aza-2'-deoxycytidine, suggesting e
65 arcinogen-transformed HBECs treated with the demethylating agent 5-aza-2'deoxycytidine revealed miR-1
67 Ha, CaSki, and HeLa cells and treatment with demethylating agent 5-aza-2-deoxycytidine restored DOC2B
69 recapitulated by a co-treatment with the DNA-demethylating agent 5-Aza-C and retinoic acid across var
70 treatment of humanized NSG mice with the DNA-demethylating agent 5-aza-cytidine distinctly enhanced t
72 Treatment of CypA-KD P19 cells with the DNA demethylating agent 5-aza-dC reversed the silencing of P
74 In response to the chemotherapeutic and DNA-demethylating agent 5-aza-deoxycytidine (5-aza-dC), tran
76 om MCF-7 and HepG2 cells, treatment with the demethylating agent 5-azacytidine (10 microM for 6 days)
78 Treatment of COX-2-methylated cells with the demethylating agent 5-azacytidine had a modest effect on
79 broblasts to nanomolar concentrations of the demethylating agent 5-azacytidine increased basal expres
80 urthermore, in each case, treatment with the demethylating agent 5-azacytidine induced expression of
81 that co-culturing HCT-116 cells with the DNA demethylating agent 5-azacytidine reverses promoter meth
86 an inactive human X chromosome with the DNA demethylating agent 5-azadeoxycytidine (5aCdr), and we t
87 ion of the silenced allele by either the DNA demethylating agent 5-azadeoxycytidine or the SIRT1 inhi
92 MOR expression could also be induced by a demethylating agent (5'-aza-2'-deoxycytidine) or histone
94 ported by inducing p16 expression with a DNA demethylating agent (5-aza-2'-deoxycytidine) in a melano
95 ng growth factor beta (TGF-beta) cytokine, a demethylating agent (5-azacytidine), B cell receptor eng
96 ment of ER-negative breast cancer cells with demethylating agents [5-aza-2'-deoxycytidine (5-aza-dC)]
99 and two human fibroblast cell strains to the demethylating agent, 5-aza-2'-deoxycytidine (5-Aza-CdR),
103 he CHS response in mice treated with the DNA demethylating agent, 5-aza-2'-deoxycytidine, after UVB e
106 astric cancer cell lines, treatment with the demethylating agent, 5-aza-2'-deoxycytidine, resulted in
107 l expressed CDX1 mRNA; when treated with the demethylating agent, 5-aza-2'-deoxycytidine, these five
108 -dependent manner following treatment with a demethylating agent, 5-aza-2'-deoxycytidine, was shown.
112 l re-expression of ER was achieved using the demethylating agent, 5-azacytidine, and the HDAC inhibit
115 d when these cells were treated with the DNA demethylating agents, 5-azacytidine or 2-deoxy-5-azacyti
116 f the offspring because treatment with a DNA-demethylating agent alleviated exacerbation of allergic
118 Pure GuaUre-dR was found to be an effective demethylating agent and was able to induce 5azaC-dR type
119 ad- lines or hybrids by treatment with a DNA demethylating agent and/or a histone deacetylase inhibit
121 tionale for sequential administration of DNA demethylating agents and HDAC inhibitors in cancer patie
122 derstanding the anti-tumor mechanisms of DNA-demethylating agents and highlight the MDA5/MAVS/IRF7 pa
123 eactivation of tumor suppressor genes by DNA-demethylating agents and histone deacetylase (HDAC) inhi
124 n cancer cells, but not normal cells, by DNA-demethylating agents and histone deacetylase inhibitors
125 if so, novel therapeutic strategies such as demethylating agents and probiotic adjuncts, particularl
126 garding the advantage of aerosol delivery of demethylating agents and the concept of priming tumors f
128 nografts were treated with decitabine, a DNA demethylating agent, and cytarabine, a frontline cytotox
132 ntial use of Ras and Jak/Stat inhibitors and demethylating agents as therapeutic modality for human l
133 ol on Ddo expression, treatment with the DNA-demethylating agent, azacitidine, causes increased mRNA
136 lenic marginal zone lymphoma cell lines to a demethylating agent caused partial reversion of the High
138 Treatment of the K562 leukemia cells with demethylating agent combined with all-trans-retinoic aci
139 2 was achieved by treatment with 5-aza-dC, a demethylating agent, concomitant with the release of MBD
140 ound that the endothelial cells treated with demethylating agents could significantly increase the ex
141 Treatment of tumor-bearing mice with the demethylating agent DAC at a nontoxic dose induces MLH1
142 st (VDA) nor an HDAC inhibitor (HDACI) nor a demethylating agent (DAC) individually could optimally u
146 treatment of a heterozygous cell line with a demethylating agent further increased the allelic expres
149 version of an adult cell by exposing it to a demethylating agent immediately followed by differentiat
150 malignancy and a basis for potential use of demethylating agents in conjunction with TSH-promoted ra
151 inding warrants strong consideration for DNA demethylating agents in future clinical trials for child
152 view, we discuss the clinical development of demethylating agents in hematology, with a focus on azac
154 leukemic LGL survival, and suggest a role of demethylating agents in the treatment of this disorder.
156 5), that express little ER-beta mRNA, with a demethylating agent increased levels of receptor express
158 hepatoma bearing rats with 5-azacytidine, a demethylating agent, induced basal as well as heavy meta
159 ed with 5-aza-2'-deoxycytidine (5-aza-dC), a demethylating agent, induced p16 expression, inhibited c
161 ncer cell lines to 5-aza-2' deoxycytidine, a demethylating agent, induces the reexpression of AR RNA
162 hether a histone deacetylase inhibitor and a demethylating agent influence CCR7 and CXCR4 expression
163 Treatment of NES1-nonexpressing cells with a demethylating agent led to reexpression of NES1, suggest
164 ulmonary carcinogenesis and suggest that DNA demethylating agents may be useful for activating miR-48
165 our results demonstrate that treatment with demethylating agents may engender the reexpression and f
166 n and systemic treatment with 5-Aza or other demethylating agents may have significant therapeutic be
169 gene expression is induced by treatment with demethylating agents, may identify novel genes with tumo
170 st importantly, treatment of AI cells with a demethylating agent or histone deacetylase inhibitors re
172 Treatment of IDH mutant gliomaspheres with a demethylating agent partially restores insulator functio
173 with loss of expression and treatment with a demethylating agent-reactivated RASSF1A gene expression.
174 Ku-80 cells with 5-azacytidine, a potent DNA demethylating agent, rendered MT-I gene inducible by hea
176 addition, treatment of these leukemias with demethylating agents restored the C/EBPalpha-C/EBPgamma
177 sion; (2) treatment of L/L cell lines with a demethylating agent resulted in re-expression of SHP1 pr
178 o a combination of hypoxia, TGF-beta1, and a demethylating agent results in NK cells that express kil
180 eactivation by 5-aza-2'-deoxycytidine, a DNA demethylating agent, show that DNA methylation occurring
183 ls caution against the indiscriminate use of demethylating agents, such as 5-aza-2'-deoxycytidine (5-
184 at were upregulated after treatment with DNA demethylating agents, such as Azacytidine and several na
185 ild-type fibroblasts were treated with a DNA-demethylating agent, suggesting that genomic hypomethyla
186 cytosine analog 5-azacytidine (5-AzaC) is a demethylating agent that is also known to induce mutagen
187 zone lymphoma and optimize therapy by using demethylating agents to reverse the high-methylation phe
188 mmary, a histone deacetylase inhibitor and a demethylating agent up-regulated CCR7 and CXCR4 expressi
189 ne deacetylase inhibitor entinostat with the demethylating agent vidaza profoundly affected growth of
190 breast cancer CLCA2-negative cell lines with demethylating agents was able to restore CLCA2 expressio
191 cell lines and inducing resensitizaton with demethylating agents, we aimed to identify consistent me
193 egulated in glioma cell lines treated with a demethylating agent, whereas the expression level of the
194 in mouse and hP4 in human) responded to DNA demethylating agents, whereas the expression of IGF-II f
196 Rb cells and suggest that the combination of demethylating agents with DR-activating modalities, such
197 significantly abated by Zebularine, a potent demethylating agent, with a consequent increase in the h
198 and Jak/Stat inhibitors as well as with the demethylating agent zebularine induced a strong apoptoti
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