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1 enobarbital, oltipraz, and, in particular, 3-methylcholanthrene.
2 h different doses of the chemical carcinogen methylcholanthrene.
3 ducing CYP1A1 mRNA were benzo[e]pyrene and 3-methylcholanthrene.
4 hylchrysene, 11,12-dihydroxy-11,12-dihydro-3-methylcholanthrene, 1,2-dihydroxy-1,2-dihydro-6-methylch
5 ss to oltipraz (2- to 5-fold increase) and 3-methylcholanthrene (10- to 30-fold increase).
6 l (2 mmol/L), oltipraz (50 micromol/L), or 3-methylcholanthrene (2.5 micromol/L) revealed UGT1A1-indu
7                            Advanced 10-day 3-methylcholanthrene 205 intracranial tumors could be cure
8                    For treatment of 10-day 3-methylcholanthrene 205 pulmonary metastases, systemic tr
9 tumors (B16), but not gp100-negative tumors (methylcholanthrene 205), implanted on opposing flanks of
10 y we confirmed that rejection of established methylcholanthrene-205 (MCA-205) pulmonary metastases di
11                          Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flox)
12 ed to determine whether tumor induction by 3-methylcholanthrene (3-MC), a carcinogenic hydrocarbon, c
13 ced lung tumors following exposure to BaP, 3-methylcholanthrene (3-MC), and urethane.
14 ue-Dawley rats were injected with PB, PCN, 3-methylcholanthrene (3-MC), or vehicle for 4 days.
15  exposure of liver slices to the model POP 3-methylcholanthrene (3-MC; 25 muM) at levels of hydrostat
16                                            3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor
17 he aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigrator
18 ydrocarbon environmental toxicants such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-diox
19 sed by pretreatment with the CYP1A inducer 3-methylcholanthrene and decreased by coincubation with th
20 ignated AHR repressor (AHRR) is induced by 3-methylcholanthrene and represses the transcriptional act
21  stimulators, such as beta-naphthoflavone, 3-methylcholanthrene, and tBHQ, significantly upregulated
22   Polycyclic aromatic hydrocarbons such as 3-methylcholanthrene are toxic to rat epidermal cells in l
23 Cs with 0.3 or 3 microM hydrogen peroxide, 3-methylcholanthrene, benzo[a]pyrene-7,8-diol, 3-hydroxy b
24     Lung tumorigenesis was induced using a 3-methylcholanthrene/butylated hydroxytoluene (BHT; 3,5-di
25 r embryo fibroblasts with a single dose of 3-methylcholanthrene caused the activation of the transfor
26 s of CHE cells transformed by benz[a]pyrene, methylcholanthrene, dimethylbenzanthracene, and colcemid
27                                 Treatment of methylcholanthrene-induced (Meth A) ascites tumors with
28                            When murine MC38 (methylcholanthrene-induced adenocarcinoma 38) cells were
29 de-specific CTL that reacted against several methylcholanthrene-induced BALB/c sarcomas, including CM
30                             Incubations of 3-methylcholanthrene-induced colon slices dosed with 50 mi
31                                              Methylcholanthrene-induced fibrosarcoma (Meth-A) cells w
32 cination with hsp110 or grp170 purified from methylcholanthrene-induced fibrosarcoma caused complete
33 udies were carried out with locally advanced methylcholanthrene-induced fibrosarcoma grown in BALB/c
34 or perfusion studies, using locally advanced methylcholanthrene-induced fibrosarcoma grown in BALB/c
35                                     The s.c. methylcholanthrene-induced fibrosarcoma leg tumors were
36 ones, generated from mice immunized with the methylcholanthrene-induced fibrosarcoma Meth A (H-2(d)),
37 ogenesis was also observed in the nonrelated methylcholanthrene-induced fibrosarcoma model.
38                        Our recent studies in methylcholanthrene-induced fibrosarcomas have indicated
39                We subjected a heterozygous 3-methylcholanthrene-induced murine sarcoma cell line to C
40 e established solid tumor (20 mm), MCA207, a methylcholanthrene-induced murine sarcoma.
41 ze expressed mutations in highly immunogenic methylcholanthrene-induced sarcomas derived from immunod
42 mpared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-ty
43 igens expressed by cell lines derived from 3-methylcholanthrene-induced sarcomas of (C57BL/6J X SPRET
44 n-specific CD8(+) T cells in mice bearing T3 methylcholanthrene-induced sarcomas that are susceptible
45 ed in significantly increased incidence of 3-methylcholanthrene-induced spontaneous sarcoma developme
46    The QT35 cell line was established from a methylcholanthrene-induced tumor in Japanese quail (Cotu
47 ive analysis of the antitumor response to 3'-methylcholanthrene-induced tumors, which either grow pro
48 rmone (insulin and glucagon) and chemical (3-methylcholanthrene) induction agents in a microfluidic d
49                                We inoculated methylcholanthrene (MCA) 205 in the flanks of normal mic
50  In mice with 10-day established pulmonary 3-methylcholanthrene (MCA) 205 metastases, accumulation of
51 njection of ethyl carbamate (urethane), or 3-methylcholanthrene (MCA) and butylated hydroxytoluene (B
52 a low dose (10 microg/g of body weight) of 3-methylcholanthrene (MCA) develop no lung tumors unless t
53    The effects of conditioned media from the methylcholanthrene (MCA) fibrosarcoma on hepatocyte albu
54  protocols for chemical skin carcinogenesis [methylcholanthrene (MCA) or 7,12-dimethylbenz(a)anthrace
55 t after challenge with a chemical carcinogen methylcholanthrene (MCA) or inoculation with the melanom
56  or IFN-alpha reduce expression of H60 on 3'-methylcholanthrene (MCA) sarcomas from 129/Sv mice.
57 an hamster embryo fibroblasts initiated by 3-methylcholanthrene (MCA), and was shown to be a single c
58                       Using the carcinogen 3-methylcholanthrene (MCA), we demonstrate with Fourier tr
59 reatment of mice challenged with a syngeneic methylcholanthrene (MCA)-induced fibrosarcoma would augm
60 3 deficiency suppressed the development of 3-methylcholanthrene (MCA)-induced fibrosarcomas through a
61 e equilibrium phase during immune control of methylcholanthrene (MCA)-induced or p53 mutant cancers a
62 aneous and experimental tumor metastases and methylcholanthrene (MCA)-induced sarcomas in mice defici
63 or prone when challenged with the carcinogen methylcholanthrene (MCA).
64 ere induced in Rosa26-Foxm1 mice using the 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT)
65 in 1 week of treatment with the carcinogen 3-methylcholanthrene (MCA; 10 microg/g body weight), lung
66 e reduced the effects of both oltipraz and 3-methylcholanthrene on the P1 reporter.
67        Comparative effects of oltipraz and 3-methylcholanthrene on transfected cytochrome P4501A1 rep
68                             Treatment with 3-methylcholanthrene or oltipraz had no effect compared wi
69                                Clofibrate, 3-methylcholanthrene, or beta-naphthoflavone treatment of
70     Previously, we reported the absence of 3-methylcholanthrene- or oltipraz-responsive elements in t
71 ll as other known P450 inducers, including 3-methylcholanthrene, pregnenolone-16alpha-carbonitrile, a
72 on of AhR agonists beta-naphthoflavone and 3-methylcholanthrene, respectively, into partial agonists/
73 ferase activities expressed from basal and 3-methylcholanthrene-responsive UGT1A7 gene reporter const
74 a cell lines compared with that in edited 3'-methylcholanthrene sarcoma cell lines (i.e., some unedit
75  more heterogeneous in groups of unedited 3'-methylcholanthrene sarcoma cell lines compared with that
76 , hamsters, and mice by carcinogenic agents (methylcholanthrene, thioacetamide), oncogenic viruses (S
77               Using tumor cells derived from methylcholanthrene-treated IFN-gamma-insensitive mice, w
78  by TCDD but not by beta-naphthoflavone or 3-methylcholanthrene was significantly diminished.
79 as a reference for radiation effects, and 20-methylcholanthrene was used as a positive control for fo

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