ライフサイエンスコーパス: chemical carcinogen

1 de (FA) is an environmental and occupational chemical carcinogen.

2 human prostate epithelial cells exposed to a chemical carcinogen.

3 susceptibility to HNSCC when treated with a chemical carcinogen.

4 HMEC lines immortalized after exposure to a chemical carcinogen.

5 6 Dna became tumorigenic after exposure to a chemical carcinogen.

6 when challenged with gamma-irradiation or a chemical carcinogen.

7 nt in carcinogenesis induced by radiation or chemical carcinogens.

8 epresent a preferential target for exogenous chemical carcinogens.

9 largely because of their ability to activate chemical carcinogens.

10 Chk1 in the mouse skin on tumors induced by chemical carcinogens.

11 fter induction of oval cell proliferation by chemical carcinogens.

12 e-dependent susceptibility and resistance to chemical carcinogens.

13 lipid oxidation products and also from some chemical carcinogens.

14 ding of the Tg.AC's discriminate response to chemical carcinogens.

15 the joint effects of viruses and hepatotoxic chemical carcinogens.

16 on of benign skin tumors in conjunction with chemical carcinogens.

17 zation of a Th1/Th2 inflammatory response to chemical carcinogens.

18 y an important role in the detoxification of chemical carcinogens.

19 , breast, colon, and skin cancers induced by chemical carcinogens.

20 types of DNA adducts formed by UV light and chemical carcinogens.

21 C57BL/6 background, noted for resistance to chemical carcinogens.

22 atoxin, alcohol consumption, and exposure to chemical carcinogens.

23 l death in response to DNA damage induced by chemical carcinogens.

24 ding irradiation, inflammatory cytokines and chemical carcinogens.

25 the polycylic aromatic hydrocarbon class of chemical carcinogens.

26 lar stimulants including cytotoxic drugs and chemical carcinogens.

27 well as in colonic tumors of rats induced by chemical carcinogens.

28 esponsible for the induction of mdr1b by the chemical carcinogen 2-AAF.

29 nitrenium ion 12 derived from the well-known chemical carcinogen 4-aminobiphenyl.

30 was also performed after treatment with the chemical carcinogen, 4-nitroquinoline-1-oxide (4-NQO).

31 arked sensitivity of Lkb1 mutant mice to the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA

32 reatic acinar cells upon implantation of the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA

33 In mice treated with the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA

34 nd, surprisingly, was much stronger than the chemical carcinogen 7,12-dimethylbenzanthracene.

35 ary carcinogenesis induced by oncogenes or a chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMB

36 ling were not observed after exposure to the chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMB

37 a direct etiological link between a defined chemical carcinogen and human cancer.

38 seful information about the bioactivation of chemical carcinogens and can be used to investigate the

39 ation of chronic inflammation in response to chemical carcinogens and environmental stresses, includi

40 DNA damage from exposure to environmental chemical carcinogens and failure of repair systems to el

41 c DNA adducts are formed from metabolites of chemical carcinogens and have also been detected as endo

42 immune response also occurs with UV-mimetic chemical carcinogens and in a manner that is independent

43 oplastic Syrian hamster cells transformed by chemical carcinogens and oncogenic viruses, the localiza

44 philes formed during metabolic activation of chemical carcinogens and reactive oxygen species generat

45 dder cancer risk factor and a rich source of chemical carcinogens and reactive oxygen species that ca

46 nt mouse skin carcinogenesis induced by both chemical carcinogens and UV exposure.

47 patic P450s in determining susceptibility to chemical carcinogens and validates the search for associ

48 ous melanoma was produced without the use of chemical carcinogens and without resulting in other skin

49 ro exposure of finite lifespan 184 HMEC to a chemical carcinogen, and both are clonally derived.

50 inal tumor formation after administration of chemical carcinogens, and in Apc(min/+) mice.

51 been known to remove DNA lesions induced by chemical carcinogens, and the molecular mechanism has be

52 Rats treated with chemical carcinogen are similarly protected by a previou

53 however, preexisting oncogenic mutations or chemical carcinogens are required to initiate tumorigene

54 tumorigenesis of FVB/N mice treated with the chemical carcinogen azoxymethane and subsequently expose

55 MEC immortalized by a variety of agents (the chemical carcinogen benzo(a)pyrene, oncogenes c-myc and

56 /-) and wild-type mice were treated with two chemical carcinogens, benzo(a)pyrene and urethane, to in

57 significantly more tumors in response to the chemical carcinogen diethyl nitrosamine (DEN) than wild-

58 lar gender disparity is seen in mice given a chemical carcinogen, diethylnitrosamine (DEN).

59 The treatment of these mice with the chemical carcinogen, diethylnitrosamine, results in a si

60 i) no treatment; (ii) one treatment with the chemical carcinogen dimethyl-(a)benzanthracene; (iii) ul

61 evelopment, transgenic mice treated with the chemical carcinogen dimethylbenz(a)anthracene developed

62 ant, as they have been shown to operate upon chemical carcinogen DNA damage at levels to which humans

63 HMECs immortalized after chemical carcinogen exposure initially expressed little

64 ults provide a transcriptional signature for chemical carcinogen exposure; in addition, they suggest

65 nduced by the environmental and occupational chemical carcinogen FA.

66 The influence of chemical carcinogen, hormonal stimulation, and chronic d

67 bility to develop lung carcinomas induced by chemical carcinogens in Mmp1a(-/-) mice.

68 gest that most, if not all, target cells for chemical carcinogens in the skin reside in hair follicle

69 ne has high efficacy in protecting them from chemical carcinogen induced mammary cancers.

70 The chemical carcinogen-induced H-Ras mutations were detecte

71 n in epithelial cells and sensitizes mice to chemical carcinogen-induced intestinal and skin tumorige

72 tential modulator of tumor susceptibility in chemical carcinogen-induced lung tumorigenesis.

73 gen/progesterone)-induced protection against chemical carcinogen-induced mammary carcinogenesis in an

74 ion of IKKalpha in the epidermis antagonized chemical carcinogen-induced mitogenic and angiogenic act

75 Furthermore, in a chemical carcinogen-induced skin carcinogenesis setting,

76 he susceptibility of Ikkalpha hemizygotes to chemical carcinogen-induced skin carcinogenesis.

77 astly, HDAC6-null mice are more resistant to chemical carcinogen-induced skin tumors.

78 application of the lunasin peptide inhibits chemical carcinogen-induced transformation of murine fib

79 A review of the results of X-ray and chemical carcinogen induction of transformation of mouse

80 of tumor development after challenge with a chemical carcinogen methylcholanthrene (MCA) or inoculat

81 when challenged with different doses of the chemical carcinogen methylcholanthrene.

82 ts with TEL2-expressing bone marrow with the chemical carcinogen N-ethyl-N-nitrosourea (ENU) resulted

83 noncancerous breast tissue, treated with the chemical carcinogen N-ethyl-N-nitrosourea, and continuou

84 helial cells after multiple exposures to the chemical carcinogen N-nitroso-N-methylurea.

85 CI+/+ and PKCI-/- mice were treated with the chemical carcinogen N-nitrosomethylbenzylamine (NMBA) by

86 that were transformed either by exposure to chemical carcinogen or stable transfection of activated

87 in these animals in the absence of any known chemical carcinogen or ultraviolet radiation.

88 Recently, we have found that bulky chemical carcinogens preferentially form DNA adducts at

89 on of the susceptibility of mammary gland to chemical carcinogens remains uncharacterized.

90 ent of p18 null and heterozygous mice with a chemical carcinogen resulted in tumor development at an

91 Treatment of these mice with chemical carcinogens resulted in enhanced tumorigenesis

92 he hypothesis that cell-mediated immunity to chemical carcinogens serves to protect individuals by re

93 Chemical carcinogens such as benzo[a]pyrene (BaP) and 2-

94 data are consistent with the hypothesis that chemical carcinogens such as BP in cigarette smoke cause

95 rious environmental cues, including those to chemical carcinogens, such as 2,3,7,8-tetrachlorodibenzo

96 efficiently recognized DNA damage induced by chemical carcinogens, suggesting a direct participation

97 rowth factors and may be a rare example of a chemical carcinogen that acts as a co-promoter.

98 Benzo[a]pyrene (BP) is a representative chemical carcinogen that can be metabolically converted

99 is well known as an important environmental chemical carcinogen that preferentially modifies DNA in

100 N-Acetyl-2-aminofluorene (AAF) is a chemical carcinogen that reacts with guanines at the C8

101 cted in an attempt to document the fact that chemical carcinogens that are thought to induce producti

102 ells underwent apoptosis upon treatment with chemical carcinogens, the apoptotic response is dependen

103 lial proliferation and, in the presence of a chemical carcinogen, they increase dramatically the anim

104 samino)-1-(3-pyridyl)-1-butanone (NNK), is a chemical carcinogen thought to be involved in the initia

105 ed cell line, 6A/SB1, which was derived from chemical carcinogen transformed MSU-1.1 cells, we identi

106 denal anastomosis (EGDA) without concomitant chemical carcinogen treatment leads to gastroesophageal

107 and p21(Cip1)-null mice were exposed to the chemical carcinogen, urethane.

108 expression of mdr gene by anticancer drugs, chemical carcinogens, UV light, and other DNA-damaging a

109 transcriptionally silent until activated by chemical carcinogens, UV light, or full-thickness woundi

110 echanisms after exposure of human cells to a chemical carcinogen, we generated a plasmid expressing R

111 highly sensitive to the cytotoxic effects of chemical carcinogens, while cells defective in either hu

112 moves DNA damages induced by a wide range of chemical carcinogens with variable efficiencies.