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1 human prostate epithelial cells exposed to a chemical carcinogen.
2  susceptibility to HNSCC when treated with a chemical carcinogen.
3  HMEC lines immortalized after exposure to a chemical carcinogen.
4 de (FA) is an environmental and occupational chemical carcinogen.
5 6 Dna became tumorigenic after exposure to a chemical carcinogen.
6  when challenged with gamma-irradiation or a chemical carcinogen.
7 ce of DNA damage to the epithelium by UVR or chemical carcinogens.
8 lar stimulants including cytotoxic drugs and chemical carcinogens.
9 well as in colonic tumors of rats induced by chemical carcinogens.
10 nt in carcinogenesis induced by radiation or chemical carcinogens.
11 epresent a preferential target for exogenous chemical carcinogens.
12 largely because of their ability to activate chemical carcinogens.
13 fter induction of oval cell proliferation by chemical carcinogens.
14 zation of a Th1/Th2 inflammatory response to chemical carcinogens.
15  Chk1 in the mouse skin on tumors induced by chemical carcinogens.
16 s various DNA lesions caused by UV light and chemical carcinogens.
17  research and identifying potential drug and chemical carcinogens.
18 e-dependent susceptibility and resistance to chemical carcinogens.
19  lipid oxidation products and also from some chemical carcinogens.
20 ding of the Tg.AC's discriminate response to chemical carcinogens.
21 the joint effects of viruses and hepatotoxic chemical carcinogens.
22 on of benign skin tumors in conjunction with chemical carcinogens.
23 y an important role in the detoxification of chemical carcinogens.
24 , breast, colon, and skin cancers induced by chemical carcinogens.
25  types of DNA adducts formed by UV light and chemical carcinogens.
26  C57BL/6 background, noted for resistance to chemical carcinogens.
27 atoxin, alcohol consumption, and exposure to chemical carcinogens.
28 l death in response to DNA damage induced by chemical carcinogens.
29 ding irradiation, inflammatory cytokines and chemical carcinogens.
30  the polycylic aromatic hydrocarbon class of chemical carcinogens.
31 esponsible for the induction of mdr1b by the chemical carcinogen 2-AAF.
32 nitrenium ion 12 derived from the well-known chemical carcinogen 4-aminobiphenyl.
33  was also performed after treatment with the chemical carcinogen, 4-nitroquinoline-1-oxide (4-NQO).
34 reatic acinar cells upon implantation of the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA
35 arked sensitivity of Lkb1 mutant mice to the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA
36                     In mice treated with the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA
37 nd, surprisingly, was much stronger than the chemical carcinogen 7,12-dimethylbenzanthracene.
38 ary carcinogenesis induced by oncogenes or a chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMB
39 ling were not observed after exposure to the chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMB
40  a direct etiological link between a defined chemical carcinogen and human cancer.
41 seful information about the bioactivation of chemical carcinogens and can be used to investigate the
42 ation of chronic inflammation in response to chemical carcinogens and environmental stresses, includi
43    DNA damage from exposure to environmental chemical carcinogens and failure of repair systems to el
44 c DNA adducts are formed from metabolites of chemical carcinogens and have also been detected as endo
45 on during cellular transformation induced by chemical carcinogens and identified a subset of cell tra
46  immune response also occurs with UV-mimetic chemical carcinogens and in a manner that is independent
47 oplastic Syrian hamster cells transformed by chemical carcinogens and oncogenic viruses, the localiza
48 philes formed during metabolic activation of chemical carcinogens and reactive oxygen species generat
49 dder cancer risk factor and a rich source of chemical carcinogens and reactive oxygen species that ca
50 nt mouse skin carcinogenesis induced by both chemical carcinogens and UV exposure.
51 patic P450s in determining susceptibility to chemical carcinogens and validates the search for associ
52 ous melanoma was produced without the use of chemical carcinogens and without resulting in other skin
53 ro exposure of finite lifespan 184 HMEC to a chemical carcinogen, and both are clonally derived.
54 inal tumor formation after administration of chemical carcinogens, and in Apc(min/+) mice.
55  been known to remove DNA lesions induced by chemical carcinogens, and the molecular mechanism has be
56                            Rats treated with chemical carcinogen are similarly protected by a previou
57  however, preexisting oncogenic mutations or chemical carcinogens are required to initiate tumorigene
58 tumorigenesis of FVB/N mice treated with the chemical carcinogen azoxymethane and subsequently expose
59 MEC immortalized by a variety of agents (the chemical carcinogen benzo(a)pyrene, oncogenes c-myc and
60 /-) and wild-type mice were treated with two chemical carcinogens, benzo(a)pyrene and urethane, to in
61 significantly more tumors in response to the chemical carcinogen diethyl nitrosamine (DEN) than wild-
62                                          The chemical carcinogen diethylnitrosamine (DEN) is often us
63 lar gender disparity is seen in mice given a chemical carcinogen, diethylnitrosamine (DEN).
64         The treatment of these mice with the chemical carcinogen, diethylnitrosamine, results in a si
65 i) no treatment; (ii) one treatment with the chemical carcinogen dimethyl-(a)benzanthracene; (iii) ul
66 evelopment, transgenic mice treated with the chemical carcinogen dimethylbenz(a)anthracene developed
67  and HCC development after administration of chemical carcinogens (dimethylbenzanthrazene).
68 ant, as they have been shown to operate upon chemical carcinogen DNA damage at levels to which humans
69 y carcinogenesis were generated by combining chemical carcinogen exposure [using 7,12-dimethylbenzant
70                     HMECs immortalized after chemical carcinogen exposure initially expressed little
71 ults provide a transcriptional signature for chemical carcinogen exposure; in addition, they suggest
72 nduced by the environmental and occupational chemical carcinogen FA.
73                             The influence of chemical carcinogen, hormonal stimulation, and chronic d
74 ldehyde is an environmental and occupational chemical carcinogen implicated in the damage of proteins
75 bility to develop lung carcinomas induced by chemical carcinogens in Mmp1a(-/-) mice.
76 m(6)A-CDCP1 axis has synergistic effect with chemical carcinogens in promoting malignant transformati
77 gest that most, if not all, target cells for chemical carcinogens in the skin reside in hair follicle
78 ne has high efficacy in protecting them from chemical carcinogen induced mammary cancers.
79                                          The chemical carcinogen-induced H-Ras mutations were detecte
80 n in epithelial cells and sensitizes mice to chemical carcinogen-induced intestinal and skin tumorige
81 tential modulator of tumor susceptibility in chemical carcinogen-induced lung tumorigenesis.
82 gen/progesterone)-induced protection against chemical carcinogen-induced mammary carcinogenesis in an
83 ion of IKKalpha in the epidermis antagonized chemical carcinogen-induced mitogenic and angiogenic act
84                            Furthermore, in a chemical carcinogen-induced skin carcinogenesis setting,
85 he susceptibility of Ikkalpha hemizygotes to chemical carcinogen-induced skin carcinogenesis.
86 astly, HDAC6-null mice are more resistant to chemical carcinogen-induced skin tumors.
87  application of the lunasin peptide inhibits chemical carcinogen-induced transformation of murine fib
88         A review of the results of X-ray and chemical carcinogen induction of transformation of mouse
89  of tumor development after challenge with a chemical carcinogen methylcholanthrene (MCA) or inoculat
90  when challenged with different doses of the chemical carcinogen methylcholanthrene.
91 ts with TEL2-expressing bone marrow with the chemical carcinogen N-ethyl-N-nitrosourea (ENU) resulted
92 noncancerous breast tissue, treated with the chemical carcinogen N-ethyl-N-nitrosourea, and continuou
93 helial cells after multiple exposures to the chemical carcinogen N-nitroso-N-methylurea.
94 CI+/+ and PKCI-/- mice were treated with the chemical carcinogen N-nitrosomethylbenzylamine (NMBA) by
95                         In mice exposed to a chemical carcinogen, obesity-related immune dysfunction
96  that were transformed either by exposure to chemical carcinogen or stable transfection of activated
97 in these animals in the absence of any known chemical carcinogen or ultraviolet radiation.
98           Recently, we have found that bulky chemical carcinogens preferentially form DNA adducts at
99 on of the susceptibility of mammary gland to chemical carcinogens remains uncharacterized.
100 ent of p18 null and heterozygous mice with a chemical carcinogen resulted in tumor development at an
101                 Treatment of these mice with chemical carcinogens resulted in enhanced tumorigenesis
102 he hypothesis that cell-mediated immunity to chemical carcinogens serves to protect individuals by re
103                                              Chemical carcinogens such as benzo[a]pyrene (BaP) and 2-
104 data are consistent with the hypothesis that chemical carcinogens such as BP in cigarette smoke cause
105 rious environmental cues, including those to chemical carcinogens, such as 2,3,7,8-tetrachlorodibenzo
106 efficiently recognized DNA damage induced by chemical carcinogens, suggesting a direct participation
107 rowth factors and may be a rare example of a chemical carcinogen that acts as a co-promoter.
108      Benzo[a]pyrene (BP) is a representative chemical carcinogen that can be metabolically converted
109  is well known as an important environmental chemical carcinogen that preferentially modifies DNA in
110          N-Acetyl-2-aminofluorene (AAF) is a chemical carcinogen that reacts with guanines at the C8
111 cted in an attempt to document the fact that chemical carcinogens that are thought to induce producti
112 ells underwent apoptosis upon treatment with chemical carcinogens, the apoptotic response is dependen
113 lial proliferation and, in the presence of a chemical carcinogen, they increase dramatically the anim
114 samino)-1-(3-pyridyl)-1-butanone (NNK), is a chemical carcinogen thought to be involved in the initia
115 V alters the chronic inflammation induced by chemical carcinogens to promote liver carcinogenesis.
116 ed cell line, 6A/SB1, which was derived from chemical carcinogen transformed MSU-1.1 cells, we identi
117 denal anastomosis (EGDA) without concomitant chemical carcinogen treatment leads to gastroesophageal
118  and p21(Cip1)-null mice were exposed to the chemical carcinogen, urethane.
119  expression of mdr gene by anticancer drugs, chemical carcinogens, UV light, and other DNA-damaging a
120  transcriptionally silent until activated by chemical carcinogens, UV light, or full-thickness woundi
121 echanisms after exposure of human cells to a chemical carcinogen, we generated a plasmid expressing R
122 highly sensitive to the cytotoxic effects of chemical carcinogens, while cells defective in either hu
123  the impact of chronic low-level exposure to chemical carcinogens with different modes of action on t
124 moves DNA damages induced by a wide range of chemical carcinogens with variable efficiencies.

 
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