ライフサイエンスコーパス: 5-aza-CdR

1 how that short oligonucleotides containing a 5-aza-CdR can also inhibit DNA methylation in cancer cel

2 e p16 promoter CpG island in T24 cells after 5-aza-CdR treatment cannot be halted by subsequent conti

3 The induction of p53 protein after 5-aza-CdR treatment did not correlate with an increase i

4 Although 5-aza-CdR increased miR-370 expression by 2.1-fold in ma

5 Although 5-aza-CdR is an extremely potent inhibitor of DNA methyl

6 valent bond formation between the enzyme and 5-aza-CdR-incorporated DNA is not essential for enzyme d

7 ced the level of Dnmt1 in both untreated and 5-aza-CdR-treated cells.

8 reased the basal level of DNMT1 that blocked 5-aza-CdR-induced degradation.

9 This revised model for gene activation by 5-aza-CdR has important implications for the use of DNA

10 is latter requirement for gene activation by 5-aza-CdR is probably mediated by sequence-specific tran

11 miR-370, and its expression was decreased by 5-aza-CdR in cholangiocarcinoma cells.

12 evel of Dnmt1 and blocked its degradation by 5-aza-CdR.

13 ion (<0.4-fold) and upregulated (>2-fold) by 5-aza-CdR.

14 the limited number of human genes induced by 5-aza-CdR treatment.

15 ogic inhibitors abolishes TRAIL induction by 5-aza-CdR.

16 Induction of TRAIL by 5-aza-CdR correlated with inactivation of Akt.

17 r results suggest that induction of TRAIL by 5-aza-CdR is critical for enhancing chemosensitivity of

18 In contrast, 5-aza-CdR treatment induced the expression of cancer-tes

19 y small interference RNA silencing decreased 5-aza-CdR-mediated Adriamycin-induced caspase activation

20 ransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) and the histone deacetylase inhibitor 4-pheny

21 ransferase inhibitor 5-Aza-2'-deoxycytidine (5-aza-CdR) induced higher levels of mRNA expression and

22 1 and UACC 1179 with 5-aza-2'-deoxycytidine (5-aza-CdR) induced transcriptional reactivation of both

23 ransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) inhibits DNA methyltransferase activity and s

24 thylation inhibitor, 5-aza-2'-deoxycytidine (5-aza-CdR) resulted in increased Syk mRNA expression.

25 ch were treated with 5-aza-2'-deoxycytidine (5-aza-CdR) to yield clones which expressed human IGF2 an

26 5-Aza-2'-deoxycytidine (5-aza-CdR), an inhibitor of DNA methylation, increases T

27 Decitabine, or 5-aza-2'-deoxycytidine (5-aza-CdR), is a well-characterized drug that is now Foo

28 w doses of the DNMTi 5-aza-2'-deoxycytidine (5-aza-CdR), there is a synergistic inhibition of cancer-

29 ethylation inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

30 methylase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

31 ransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

32 ion of HbF levels by 5-aza-2'-deoxycytidine (5-aza-CdR, decitabine) could serve as an alternate mode

33 he nucleoside analog 5-aza-2'-deoxycytidine (5-aza-CdR, decitabine) is a potent inhibitor of DNA meth

34 are highly sensitive to 5-aza-deoxycytidine (5-aza-CdR) compared with somatic solid tumor cells.

35 5-Azacytidine- and 5-aza-deoxycytidine (5-aza-CdR)-mediated reactivation of tumor suppressor gen

36 yltransferase inhibitor 5-aza-deoxycytidine (5-aza-CdR).

37 5-Aza-2'-deoxycytidine [5-aza-CdR (decitabine)], a potent inhibitor of DNA methy

38 retain an exquisite sensitivity to low-dose 5-aza-CdR treatment, and pretreatment of 5-aza-CdR resen

39 sensitizes TGCT-derived EC cells to low-dose 5-aza-CdR treatment.

40 of the gene expression changes that followed 5-aza-CdR treatment were conserved in tumor and normal c

41 ional, complimentary mechanism of action for 5-aza-CdR in the reactivation of epigenetically silenced

42 tidine in DNA) to serine (CS) did not impede 5-aza-CdR-induced degradation.

43 Moreover, 5-aza-CdR treatment also resulted in global decreases in

44 Notably, 5-aza-CdR hypersensitivity is associated with markedly a

45 urvival with low nanomolar concentrations of 5-aza-CdR is associated with ATM activation, H2AX phosph

46 The efficacy of 5-aza-CdR may be related to the induction of methylation

47 ose 5-aza-CdR treatment, and pretreatment of 5-aza-CdR resensitizes these cells to cisplatin-mediated

48 it works via a mechanism similar to that of 5-aza-CdR after incorporation of its aza-moiety into DNA

49 to the clinical efficacy and/or toxicity of 5-aza-CdR.

50 /- 1.61% to 2.6% +/- 2.15% on HU, whereas on 5-aza-CdR HbF increased to 12.70% +/- 1.81%.

51 Notably, we found that 5-aza-CdR treatment induced a limited number of genes (m

52 Here, we test the hypothesis that 5-aza-CdR treatment is perceived as DNA damage, as asses

53 tance to 5-aza-CdR, strongly indicating that 5-aza-CdR sensitivity is mechanistically linked to high

54 s of MAGE-1 gene regulation, we propose that 5-aza-CdR-mediated gene activation has two distinct requ

55 It is relevant that 5-aza-CdR has shown the greatest promise in clinical tri

56 Here, we show that 5-aza-CdR induces tumor necrosis factor-related apoptosi

57 The 5-aza-CdR-induced degradation, which occurs in the nucle

58 sential for nuclear localization and for the 5-aza-CdR-mediated degradation of Dnmt1.

59 Therefore 5-aza-CdR could be effective in increasing HbF in patien

60 els following transient exposure of cells to 5-aza-CdR, whereas Dnmt1 by itself could not.

61 C cells results in substantial resistance to 5-aza-CdR, strongly indicating that 5-aza-CdR sensitivit

62 on of Dnmt1 but did not confer resistance to 5-aza-CdR-induced degradation.

63 linked to the ability of cells to respond to 5-aza-CdR.

64 arrest and cytotoxicity; 2) the response to 5-aza-CdR treatment includes the induction and activatio

65 pressing wild-type p53 are more sensitive to 5-aza-CdR mediated growth arrest and cytotoxicity; 2) th

66 mutant of Dnmt3a or Dnmt3b was sensitive to 5-aza-CdR-mediated degradation.

67 gene is resilenced with kinetics similar to 5-aza-CdR only-treated cells, which is also marked by a

68 Cdh1 was significantly dephosphorylated upon 5-aza-CdR treatment, suggesting its involvement in initi

69 tivated only the mitochondrial pathway while 5-aza-CdR failed to activate either.

70 mbined treatment of breast cancer cells with 5-aza-CdR and Adriamycin significantly increases apoptot

71 Pretreatment of LNCaP cells with 5-aza-CdR partially restores TCDD-inducible DRE occupanc

72 ncer cells at concentrations comparable with 5-aza-CdR.

73 d in a dose-escalating phase I/II study with 5-aza-CdR at doses ranging from 0.15 to 0.30 mg/kg given

74 myotonic dystrophy patients, treatment with 5-aza-CdR strongly destabilized repeat tracts in the DMP