ライフサイエンスコーパス: diethylnitrosamine

1 the development of liver cancer mediated by diethylnitrosamine.

2 mor development in 100% of mice treated with diethylnitrosamine.

3 n response to the genotoxic hepatocarcinogen diethylnitrosamine.

4 th a single dose of the genotoxic carcinogen diethylnitrosamine.

5 treatment with the potent hepatocarcinogen N-diethylnitrosamine.

6 oplastic livers in C3H/HeJ mice treated with diethylnitrosamine.

7 arded progression of liver tumors induced by diethylnitrosamine.

8 B6 and B6BRF1 x B6BRF1 (F2) animals with N,N-diethylnitrosamine (0.1 micromol/g of body weight) and e

9 iliary system after institution in rats of a diethylnitrosamine, 2-acetylaminofluorene, partial hepat

10 largely protected from tumor formation in a diethylnitrosamine/3,3',5,5'-tetrachloro-1,4-bis(pyridyl

11 d fewer liver tumors after administration of diethylnitrosamine and carbon tetrachloride than control

12 liver tumorigenesis after administration of diethylnitrosamine and carbon tetrachloride.

13 After a single injection with diethylnitrosamine and subsequent treatment with phenoba

14 eras were treated at 12 days of age with N,N-diethylnitrosamine, and individual tumors were dissected

15 nics, and wild type received an injection of diethylnitrosamine at 15 days of age.

16 .001), and, after exposure to the carcinogen diethylnitrosamine, Cx32-deficient mice exhibited a high

17 nd HCC in mice treated with a combination of diethylnitrosamine (DEN) and CCl4, along with either LPS

18 ion after a single injection of 10 micro g/g diethylnitrosamine (DEN) and continued administration of

19 le mice were exposed to the liver carcinogen diethylnitrosamine (DEN) and fed diets with well-defined

20 TKO) and wild-type (WT) mice were exposed to diethylnitrosamine (DEN) and induction of HCC was monito

21 granatum peel and seed oil extracts against diethylnitrosamine (DEN) and phenobarbital (PB) induced

22 the FVBxC57Bl/6 background were treated with diethylnitrosamine (DEN) and sacrificed at 32 weeks old.

23 treated with or without the tumor initiator diethylnitrosamine (DEN) at 5 weeks of age and then oral

24 Using the diethylnitrosamine (DEN) HCC carcinogenesis model, we fu

25 Diethylnitrosamine (DEN) injection induce DSBs along wit

26 Rats were initiated with diethylnitrosamine (DEN) or vehicle at 70 days of age.

27 Liver carcinogenesis induced by diethylnitrosamine (DEN) produced large carcinomas in al

28 Using the procarcinogen diethylnitrosamine (DEN) to initiate tumorigenesis in mi

29 origenesis induced by the genotoxic chemical diethylnitrosamine (DEN), a hepatic carcinogen that is n

30 However, intraperitoneal delivery of diethylnitrosamine (DEN), a known carcinogen, induced HC

31 induced by repeated, low-dose injections of diethylnitrosamine (DEN), a mouse model induced by carbo

32 We treated AAV-TBG-Cre; Rosa(YFP) mice with diethylnitrosamine (DEN), followed by multiple injection

33 Six months after a single injection of diethylnitrosamine (DEN), SV1 hepatocyte transgenic mice

34 luding N,N-dimethylnitrosamine (DMN) and N,N-diethylnitrosamine (DEN), to alkyl diazohydroxides (whic

35 e lacking TGR5 were much more susceptible to diethylnitrosamine (DEN)-induced acute liver injury and

36 ic reduction in hepatocytes protects against diethylnitrosamine (DEN)-induced HCC.

37 -specific deletion of c-Fos protects against diethylnitrosamine (DEN)-induced HCCs, whereas liver-spe

38 kbeta(Deltahep) mice are hypersusceptible to diethylnitrosamine (DEN)-induced hepatocarcinogenesis.

39 s of ERRalpha accelerates the development of diethylnitrosamine (DEN)-induced hepatocellular carcinom

40 3-dependent and -independent apoptosis, in a diethylnitrosamine (DEN)-induced liver carcinogenesis mo

41 In this study, the diethylnitrosamine (DEN)-induced liver tumor model and t

42 in human hepatocellular carcinoma (HCC) and diethylnitrosamine (DEN)-induced mouse hepatocarcinogene

43 In the diethylnitrosamine (DEN)-induced mouse hepatocarcinogene

44 We show that diethylnitrosamine (DEN)-induced murine HCC is attenuate

45 3), and nitric oxide (NO) in spontaneous and diethylnitrosamine (DEN)-initiated and/or phenobarbital

46 Examination of liver cancer in diethylnitrosamine (DEN)-treated CUGBP1-S302A mice showe

47 multiplicity induced by the hepatocarcinogen diethylnitrosamine (DEN).

48 ce treated with the known hepatic carcinogen diethylnitrosamine (DEN).

49 nockout (LKO) mice with the hepatocarcinogen diethylnitrosamine (DEN).

50 d hepatocellular carcinogenesis triggered by diethylnitrosamine (DEN).

51 is seen in mice given a chemical carcinogen, diethylnitrosamine (DEN).

52 ermates were exposed to the hepatocarcinogen diethylnitrosamine (DEN).

53 tocarcinogenesis initiated by the carcinogen diethylnitrosamine (DEN).

54 d increase in hepatocarcinogenesis caused by diethylnitrosamine (DEN).

55 the mice with the hepatocellular carcinogen diethylnitrosamine (DEN).

56 ated with a single dose (200 mg/kg, i.p.) of diethylnitrosamine (DEN).

57 e lambda transgene with the hepatocarcinogen diethylnitrosamine (DEN).

58 Diethylnitrosamine (DEN)/carbon tetrachloride (CCl4) ext

59 resistant to developing HCC in response to a Diethylnitrosamine (DEN)/Phenobarbital (PB) liver tumor-

60 1B in the hepatocytes of mice treated with a diethylnitrosamine (DEN)/phenobarbital tumor induction p

61 given 2 weekly intraperitoneal injections of diethylnitrosamine (DEN); 2 weeks later, some mice also

62 With N-nitrosodiethylamine [N,N-diethylnitrosamine (DEN)], the intrinsic KIE was slightl

63 e model, consisting of the administration of diethylnitrosamine followed by a brief exposure to 2-ace

64 We found that diethylnitrosamine increases the levels of CUGBP1 and ac

65 TRAIL-R also suppressed diethylnitrosamine-induced (DEN-induced) hepatocarcinoge

66 PC-specific knockout of Ripk1 showed reduced diethylnitrosamine-induced (DEN-induced) liver tumorigen

67 transplanted (1 x 10(6) cells) in mice with diethylnitrosamine-induced cirrhosis at week 6.

68 Deletion of Gab2 dramatically suppressed diethylnitrosamine-induced HCC in mice.

69 imited to different types of spontaneous and diethylnitrosamine-induced hepatic tumors.

70 instability such that both the incidence of diethylnitrosamine-induced hepatocarcinogenesis and mali

71 of TGF-beta1 on both naturally occurring and diethylnitrosamine-induced hepatocarcinogenesis using si

72 kt1(-/-) nor Akt2(-/-) mice are resistant to diethylnitrosamine-induced hepatocarcinogenesis, and Akt

73 sed in Foxa1- and Foxa2-deficient mice after diethylnitrosamine-induced hepatocarcinogenesis.

74 umors, IL-22TG mice were more susceptible to diethylnitrosamine-induced liver cancer.

75 We report that Bcl-2 expression inhibited diethylnitrosamine-induced liver carcinogenesis and coun

76 Similarly, diethylnitrosamine-induced liver carcinogenesis is reduc

77 Thirty rats with varying levels of diethylnitrosamine-induced liver fibrosis were imaged be

78 letion of Ncoa2/Src-2 in mice predisposes to diethylnitrosamine-induced liver tumorigenesis.

79 uman hepatocellular carcinomas (HCCs) and in diethylnitrosamine-induced liver tumors in mice, which i

80 in HCCs from Myc Tgfa transgenic mice and in diethylnitrosamine-induced mouse HCCs were most similar

81 s immediately become elevated in response to diethylnitrosamine-induced or genome instability-driven

82 imental mouse model of hepatocarcinogenesis (diethylnitrosamine-induced), tumors showed increased act

83 expressed allele of the M6p/Igf2r in 40% of diethylnitrosamine-initiated rat liver tumors.

84 Moreover, diethylnitrosamine-initiated tumors in the c-myc/TGF-bet

85 oderma pigmentosum group A knockout mice and diethylnitrosamine-injected mice, both prone to HCC deve

86 effectively inhibited HCC development in the diethylnitrosamine-injected mice.

87 ncidence of large and multifocal tumors with diethylnitrosamine injection compared to wild-type mice.

88 f basophilic foci, and by 10-12 months after diethylnitrosamine injection, tumors had developed in Mg

89 Female rats were administered 10 mg diethylnitrosamine/kg at 5 days of age.

90 ministration of hepatocarcinogenic compound, diethylnitrosamine, led to persistent DNA damage and sus

91 The IPP group was initiated with diethylnitrosamine, maintained on phenobarbital for 6 mo

92 Tg), we assessed the effects of SULF1 on the diethylnitrosamine model of liver carcinogenesis.

93 in liver tumor development using a neonatal diethylnitrosamine model.

94 Administration of diethylnitrosamine, phenobarbital, or 2-amino-3,8-diethy

95 However, treatment of these mice with diethylnitrosamine/phenobarbital (DEN/PB), which induces

96 In this study, we used diethylnitrosamine/phenobarbital treatment to induce hep

97 With diethylnitrosamine, RB deletion resulted in inappropriat

98 leted at the Tg737 locus with the carcinogen diethylnitrosamine resulted in an increase in preneoplas

99 of these mice with the chemical carcinogen, diethylnitrosamine, results in a significantly enhanced

100 However, when one line was treated with diethylnitrosamine, the occurrence of precancerous lesio

101 re significantly less proliferating cells in diethylnitrosamine-treated bid-null livers.

102 However, in diethylnitrosamine-treated mice, the chronic FGFR1 activ

103 s lesions was enhanced compared with that in diethylnitrosamine-treated nontransgenic controls.

104 lar carcinomas (HCC) from Ras-gal-transduced diethylnitrosamine-treated rats were analyzed for liver

105 or hepatocellular carcinoma was observed in diethylnitrosamine-treated wild-type (WT) livers at 4 or

106 Postnatal diethylnitrosamine treatment induced HCC within 8 months

107 B-dependent cell cycle entry, occurring with diethylnitrosamine treatment, was independent of cyclin

108 Spontaneous and carcinogen-induced (diethylnitrosamine) tumorigenesis were studied in mice w

109 Hepatocytes from Ras-gal-transduced diethylnitrosamine-untreated livers and hepatocellular c

110 Diethylnitrosamine was administrated to 15-day-old wild-

111 iethylamide results in the formation of free diethylnitrosamine, whereas the reaction with azide resu