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1 treatment with the potent hepatocarcinogen N-diethylnitrosamine.
2 oplastic livers in C3H/HeJ mice treated with diethylnitrosamine.
3 arded progression of liver tumors induced by diethylnitrosamine.
4 ellular carcinoma model induced by genotoxin diethylnitrosamine.
5 tochthonous HCCs induced in rats with use of diethylnitrosamine.
6 C double transgenic mice and mice exposed to diethylnitrosamine.
7 eated with vehicle, carbon tetrachloride, or diethylnitrosamine.
8  the development of liver cancer mediated by diethylnitrosamine.
9 mor development in 100% of mice treated with diethylnitrosamine.
10 n response to the genotoxic hepatocarcinogen diethylnitrosamine.
11 th a single dose of the genotoxic carcinogen diethylnitrosamine.
12 B6 and B6BRF1 x B6BRF1 (F2) animals with N,N-diethylnitrosamine (0.1 micromol/g of body weight) and e
13 iliary system after institution in rats of a diethylnitrosamine, 2-acetylaminofluorene, partial hepat
14  largely protected from tumor formation in a diethylnitrosamine/3,3',5,5'-tetrachloro-1,4-bis(pyridyl
15                         Mice were then given diethylnitrosamine and carbon tetrachloride (CCl(4)) to
16 d fewer liver tumors after administration of diethylnitrosamine and carbon tetrachloride than control
17  liver tumorigenesis after administration of diethylnitrosamine and carbon tetrachloride.
18 y fewer liver tumors after administration of diethylnitrosamine and CCl(4) compared with control mice
19                After a single injection with diethylnitrosamine and subsequent treatment with phenoba
20 eras were treated at 12 days of age with N,N-diethylnitrosamine, and individual tumors were dissected
21  of liver cancer, in which mice treated with diethylnitrosamine at 15 days develop liver tumors by 6
22 nics, and wild type received an injection of diethylnitrosamine at 15 days of age.
23 .001), and, after exposure to the carcinogen diethylnitrosamine, Cx32-deficient mice exhibited a high
24  In mice receiving a high-fat diet (HFD) and diethylnitrosamine (DEN) administration, E2f1 and E2f2 e
25 nd HCC in mice treated with a combination of diethylnitrosamine (DEN) and CCl4, along with either LPS
26 ion after a single injection of 10 micro g/g diethylnitrosamine (DEN) and continued administration of
27 le mice were exposed to the liver carcinogen diethylnitrosamine (DEN) and fed diets with well-defined
28 TKO) and wild-type (WT) mice were exposed to diethylnitrosamine (DEN) and induction of HCC was monito
29  granatum peel and seed oil extracts against diethylnitrosamine (DEN) and phenobarbital (PB) induced
30 the FVBxC57Bl/6 background were treated with diethylnitrosamine (DEN) and sacrificed at 32 weeks old.
31  treated with or without the tumor initiator diethylnitrosamine (DEN) at 5 weeks of age and then oral
32 7BL/6J mice were given a single injection of diethylnitrosamine (DEN) followed by weekly doses of car
33                                    Using the diethylnitrosamine (DEN) HCC carcinogenesis model, we fu
34                                              Diethylnitrosamine (DEN) injection induce DSBs along wit
35 y(2)r (-/-) knockout mice by intraperitoneal diethylnitrosamine (DEN) injection.
36                      The chemical carcinogen diethylnitrosamine (DEN) is often used to induce HCC in
37                     Rats were initiated with diethylnitrosamine (DEN) or vehicle at 70 days of age.
38            Twenty-two rats were administered diethylnitrosamine (DEN) orally for 12 weeks to induce h
39              Liver carcinogenesis induced by diethylnitrosamine (DEN) produced large carcinomas in al
40                   Using the hepatocarcinogen diethylnitrosamine (DEN) to induce HCC in the rat, we co
41  (Cxcr6(eGfp/eGfp)) were given injections of diethylnitrosamine (DEN) to induce liver cancer and alph
42                      Using the procarcinogen diethylnitrosamine (DEN) to initiate tumorigenesis in mi
43 ific knockout (LKO) mice in combination with diethylnitrosamine (DEN) treatment, we demonstrated that
44 origenesis induced by the genotoxic chemical diethylnitrosamine (DEN), a hepatic carcinogen that is n
45         However, intraperitoneal delivery of diethylnitrosamine (DEN), a known carcinogen, induced HC
46  induced by repeated, low-dose injections of diethylnitrosamine (DEN), a mouse model induced by carbo
47 ittermates were injected with the carcinogen diethylnitrosamine (DEN), followed by chronic ethanol fe
48  We treated AAV-TBG-Cre; Rosa(YFP) mice with diethylnitrosamine (DEN), followed by multiple injection
49       Six months after a single injection of diethylnitrosamine (DEN), SV1 hepatocyte transgenic mice
50 luding N,N-dimethylnitrosamine (DMN) and N,N-diethylnitrosamine (DEN), to alkyl diazohydroxides (whic
51 e lacking TGR5 were much more susceptible to diethylnitrosamine (DEN)-induced acute liver injury and
52                Deletion of Cnpy2 obliterates diethylnitrosamine (DEN)-induced HCC in mice.
53 ic reduction in hepatocytes protects against diethylnitrosamine (DEN)-induced HCC.
54 -specific deletion of c-Fos protects against diethylnitrosamine (DEN)-induced HCCs, whereas liver-spe
55 kbeta(Deltahep) mice are hypersusceptible to diethylnitrosamine (DEN)-induced hepatocarcinogenesis.
56  are found to be the main cellular origin of diethylnitrosamine (DEN)-induced hepatocellular carcinom
57 s of ERRalpha accelerates the development of diethylnitrosamine (DEN)-induced hepatocellular carcinom
58 er-specific deletion of Asb3 gene suppressed diethylnitrosamine (DEN)-induced liver cancer developmen
59 luding TrxR1/Gsr-null, were susceptible to N-diethylnitrosamine (DEN)-induced liver cancer, indicatin
60 3-dependent and -independent apoptosis, in a diethylnitrosamine (DEN)-induced liver carcinogenesis mo
61                           In this study, the diethylnitrosamine (DEN)-induced liver tumor model and t
62  in human hepatocellular carcinoma (HCC) and diethylnitrosamine (DEN)-induced mouse hepatocarcinogene
63                                       In the diethylnitrosamine (DEN)-induced mouse hepatocarcinogene
64                                 We show that diethylnitrosamine (DEN)-induced murine HCC is attenuate
65 ealthy and liver tumor models, especially in diethylnitrosamine (DEN)-induced tumors and HepG2-transp
66 3), and nitric oxide (NO) in spontaneous and diethylnitrosamine (DEN)-initiated and/or phenobarbital
67               Examination of liver cancer in diethylnitrosamine (DEN)-treated CUGBP1-S302A mice showe
68 ated with a single dose (200 mg/kg, i.p.) of diethylnitrosamine (DEN).
69 e lambda transgene with the hepatocarcinogen diethylnitrosamine (DEN).
70 hepatocarcinogenicity had been induced using diethylnitrosamine (DEN).
71 nd cancer propensity caused by a carcinogen, diethylnitrosamine (DEN).
72  the mice with the hepatocellular carcinogen diethylnitrosamine (DEN).
73 multiplicity induced by the hepatocarcinogen diethylnitrosamine (DEN).
74 ce treated with the known hepatic carcinogen diethylnitrosamine (DEN).
75 nockout (LKO) mice with the hepatocarcinogen diethylnitrosamine (DEN).
76 d hepatocellular carcinogenesis triggered by diethylnitrosamine (DEN).
77 ng mouse models of HCC induced by carcinogen diethylnitrosamine (DEN).
78 is seen in mice given a chemical carcinogen, diethylnitrosamine (DEN).
79 ermates were exposed to the hepatocarcinogen diethylnitrosamine (DEN).
80 tocarcinogenesis initiated by the carcinogen diethylnitrosamine (DEN).
81 d increase in hepatocarcinogenesis caused by diethylnitrosamine (DEN).
82                                              Diethylnitrosamine (DEN)/carbon tetrachloride (CCl4) ext
83 resistant to developing HCC in response to a Diethylnitrosamine (DEN)/Phenobarbital (PB) liver tumor-
84 1B in the hepatocytes of mice treated with a diethylnitrosamine (DEN)/phenobarbital tumor induction p
85 given 2 weekly intraperitoneal injections of diethylnitrosamine (DEN); 2 weeks later, some mice also
86              With N-nitrosodiethylamine [N,N-diethylnitrosamine (DEN)], the intrinsic KIE was slightl
87  diet (ChD-HFD) or an HFD after injection of diethylnitrosamine (DEN-HFD) to induce metabolic dysfunc
88            In pre-clinical models, including diethylnitrosamine- (DEN-) induced hepatocellular carcin
89 e model, consisting of the administration of diethylnitrosamine followed by a brief exposure to 2-ace
90 nts, in vivo hepatocarcinogenesis induced by diethylnitrosamine in Nox4 -deficient mice, and analyses
91                                We found that diethylnitrosamine increases the levels of CUGBP1 and ac
92                      TRAIL-R also suppressed diethylnitrosamine-induced (DEN-induced) hepatocarcinoge
93 PC-specific knockout of Ripk1 showed reduced diethylnitrosamine-induced (DEN-induced) liver tumorigen
94  transplanted (1 x 10(6) cells) in mice with diethylnitrosamine-induced cirrhosis at week 6.
95 five annexins during hepatocarcinogenesis by diethylnitrosamine-induced cirrhosis-HCC.
96  DDX17 deficiency was also demonstrated in a diethylnitrosamine-induced DDX17(HKO) mouse model.
97 by LRPPRC depletion synergistically enhances diethylnitrosamine-induced DNA damage, genome instabilit
98     Deletion of Gab2 dramatically suppressed diethylnitrosamine-induced HCC in mice.
99 e efficiency of PD-1 antibody treatment in a diethylnitrosamine-induced HCC mouse model, suggesting t
100                                    Using the diethylnitrosamine-induced HCC mouse model, we analyzed
101 this model, Sulf2 overexpression potentiated diethylnitrosamine-induced HCC.
102 imited to different types of spontaneous and diethylnitrosamine-induced hepatic tumors.
103  instability such that both the incidence of diethylnitrosamine-induced hepatocarcinogenesis and mali
104 of TGF-beta1 on both naturally occurring and diethylnitrosamine-induced hepatocarcinogenesis using si
105 kt1(-/-) nor Akt2(-/-) mice are resistant to diethylnitrosamine-induced hepatocarcinogenesis, and Akt
106 sed in Foxa1- and Foxa2-deficient mice after diethylnitrosamine-induced hepatocarcinogenesis.
107            ROCK1nc mice also developed fewer diethylnitrosamine-induced hepatocellular carcinoma (HCC
108 umors, IL-22TG mice were more susceptible to diethylnitrosamine-induced liver cancer.
109    We report that Bcl-2 expression inhibited diethylnitrosamine-induced liver carcinogenesis and coun
110                                   Similarly, diethylnitrosamine-induced liver carcinogenesis is reduc
111           Thirty rats with varying levels of diethylnitrosamine-induced liver fibrosis were imaged be
112 letion of Ncoa2/Src-2 in mice predisposes to diethylnitrosamine-induced liver tumorigenesis.
113 uman hepatocellular carcinomas (HCCs) and in diethylnitrosamine-induced liver tumors in mice, which i
114 on, DNA integrity, and cell proliferation in diethylnitrosamine-induced liver tumors.
115                                            A diethylnitrosamine-induced model of hepatocellular carci
116 in HCCs from Myc Tgfa transgenic mice and in diethylnitrosamine-induced mouse HCCs were most similar
117 s immediately become elevated in response to diethylnitrosamine-induced or genome instability-driven
118 imental mouse model of hepatocarcinogenesis (diethylnitrosamine-induced), tumors showed increased act
119  expressed allele of the M6p/Igf2r in 40% of diethylnitrosamine-initiated rat liver tumors.
120                                    Moreover, diethylnitrosamine-initiated tumors in the c-myc/TGF-bet
121                                Additionally, diethylnitrosamine-injected and fibrogenic diet-fed Tm6
122 oderma pigmentosum group A knockout mice and diethylnitrosamine-injected mice, both prone to HCC deve
123 effectively inhibited HCC development in the diethylnitrosamine-injected mice.
124 ncidence of large and multifocal tumors with diethylnitrosamine injection compared to wild-type mice.
125 zotocin (NASH/STAM) and high-fat fed or with diethylnitrosamine injection plus fibrogenic diet feedin
126 f basophilic foci, and by 10-12 months after diethylnitrosamine injection, tumors had developed in Mg
127 han wild-type (WT) controls 30 weeks after N-diethylnitrosamine injury.
128          Female rats were administered 10 mg diethylnitrosamine/kg at 5 days of age.
129 ministration of hepatocarcinogenic compound, diethylnitrosamine, led to persistent DNA damage and sus
130             The IPP group was initiated with diethylnitrosamine, maintained on phenobarbital for 6 mo
131 Tg), we assessed the effects of SULF1 on the diethylnitrosamine model of liver carcinogenesis.
132  in liver tumor development using a neonatal diethylnitrosamine model.
133                            Administration of diethylnitrosamine, phenobarbital, or 2-amino-3,8-diethy
134        However, treatment of these mice with diethylnitrosamine/phenobarbital (DEN/PB), which induces
135                       In this study, we used diethylnitrosamine/phenobarbital treatment to induce hep
136                                         With diethylnitrosamine, RB deletion resulted in inappropriat
137 leted at the Tg737 locus with the carcinogen diethylnitrosamine resulted in an increase in preneoplas
138  of these mice with the chemical carcinogen, diethylnitrosamine, results in a significantly enhanced
139 th the liver-selective apoptotic stimulus of diethylnitrosamine, ROCK1nc mice had more profound liver
140      However, when one line was treated with diethylnitrosamine, the occurrence of precancerous lesio
141 re significantly less proliferating cells in diethylnitrosamine-treated bid-null livers.
142  burden compared with flox controls, whereas diethylnitrosamine-treated Fabp1/Mttp DKO mice exhibited
143 mor foci number surrounding the CL region in diethylnitrosamine-treated liver.
144                                  However, in diethylnitrosamine-treated mice, the chronic FGFR1 activ
145                                              Diethylnitrosamine-treated Mttp-LKO mice exhibited steat
146 s lesions was enhanced compared with that in diethylnitrosamine-treated nontransgenic controls.
147 lar carcinomas (HCC) from Ras-gal-transduced diethylnitrosamine-treated rats were analyzed for liver
148  or hepatocellular carcinoma was observed in diethylnitrosamine-treated wild-type (WT) livers at 4 or
149                                    Postnatal diethylnitrosamine treatment induced HCC within 8 months
150 B-dependent cell cycle entry, occurring with diethylnitrosamine treatment, was independent of cyclin
151 nked with the development of HCC cells after diethylnitrosamine treatment.
152          Spontaneous and carcinogen-induced (diethylnitrosamine) tumorigenesis were studied in mice w
153          Hepatocytes from Ras-gal-transduced diethylnitrosamine-untreated livers and hepatocellular c
154                                              Diethylnitrosamine was administrated to 15-day-old wild-
155 iethylamide results in the formation of free diethylnitrosamine, whereas the reaction with azide resu
156 e) and male C57Bl/6 mice given injections of diethylnitrosamine, which each develop HCCs.

 
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