ライフサイエンスコーパス: carcinogenicity

1 a carcinogenicity predictor, InCa (Index of Carcinogenicity).

2 tic mechanisms may contribute to FA-mediated carcinogenicity.

3 rch for reliable parameters expressing their carcinogenicity.

4 ancer risk associated with estrogen-mediated carcinogenicity.

5 factor in protection against benzo(a)pyrene carcinogenicity.

6 ancer risk associated with estrogen-mediated carcinogenicity.

7 provides a basis for their mutagenicity and carcinogenicity.

8 nce of a Cr(III)-dependent pathway in Cr(VI) carcinogenicity.

9 ect DNA damage may also be involved in their carcinogenicity.

10 telomere length and the different stages of carcinogenicity.

11 g agent ezetimibe corroborates its potential carcinogenicity.

12 t role in chemical metabolism, toxicity, and carcinogenicity.

13 role for mutagenicity in TCE-induced kidney carcinogenicity.

14 aromatic amines, which may account for their carcinogenicity.

15 e-centric predictors of chronic toxicity and carcinogenicity.

16 underlying formaldehyde-induced toxicity and carcinogenicity.

17 as banned in children's sleepwear because of carcinogenicity.

18 l effects contribute to Acr mutagenicity and carcinogenicity.

19 us (HPV) types differ profoundly in cervical carcinogenicity.

20 dentify the genetic basis for HPV16's unique carcinogenicity.

21 n of signatures that predict mutagenicity or carcinogenicity.

22 ivity of NQO2-/- mice skin to benzo(a)pyrene carcinogenicity.

23 the liver is an organ susceptible to tobacco carcinogenicity.

24 ating evidence in the determination of human carcinogenicity.

25 ein may predispose human populations to lead carcinogenicity.

26 ossible effects of PKCI on susceptibility to carcinogenicity.

27 udy tobacco use as a model for environmental carcinogenicity.

28 c data hold promise for predicting long-term carcinogenicity and also for its ability to extrapolate

29 +)Fbxw7(DeltaG) mice may be used for testing carcinogenicity and drug screening.

30 hundreds of chemical compounds with varying carcinogenicity and genotoxicity.

31 DNA damage is a source of carcinogenicity and is also the source of the cytotoxici

32 gment-based approaches for the prediction of carcinogenicity and mutagenicity in methods described in

33 -dG lesion and contribute to the much higher carcinogenicity and mutagenicity of (+)-BPDE-2 compared

34 ity of PAH o-quinones may play a role in the carcinogenicity and mutagenicity of the parent hydrocarb

35 raise concerns for health effects including carcinogenicity and neurotoxicity.

36 Key issues related to the carcinogenicity and noncancer health hazards of biphenyl

37 he importance of metabolic activation in HCA carcinogenicity and the finding that several HCAs are ro

38 eoplastic cell line previously developed for carcinogenicity and tumor promotion studies.

39 xpression that may have implications for the carcinogenicity and/or therapeutic activity of the drug.

40 cal effects, such as toxicity, mutagenicity, carcinogenicity, and endocrine disrupter activity, are g

41 into 17 groups, based on exposure potential, carcinogenicity, and structural similarity.

42 , but the molecular mechanisms underlying AA carcinogenicity are unclear.

43 challenges in the development of alternative carcinogenicity assays is the prediction of non-genotoxi

44 Little is known about the potential carcinogenicity associated with routine application of d

45 nic in humans based primarily on evidence of carcinogenicity at two sites (liver and lung) in male an

46 ws the range of uncertainty on potential TFE carcinogenicity but cannot conclusively confirm or refut

47 aimed to resolve the issue of azathioprine's carcinogenicity by conducting a systematic review of the

48 high grade or worse, consistent with strong carcinogenicity, compared with 10.7% in women infected w

49 Quantitative carcinogenicity data are less strongly correlated with l

50 We tabulated rodent carcinogenicity data from the 1994 PDR for all drugs lis

51 Dismissing animal carcinogenicity findings would lead to human cancer case

52 eriments may underestimate the potential for carcinogenicity for compounds that follow this pattern.

53 correlation between DNA adduct formation and carcinogenicity for these compounds.

54 However, the underlying mechanism of carcinogenicity for UVA is not fully delineated.

55 The parent PAHs represent a range of carcinogenicity from inactive to highly potent.

56 chemicals with similar functions and similar carcinogenicity/genotoxicity profiles.

57 rouping chemicals with similar functions and carcinogenicity/genotoxicity profiles.

58 antiepileptic drugs appear to be safe, as no carcinogenicity has been demonstrated either during regu

59 dies suggest that it may be clastogenic, its carcinogenicity has not been demonstrated in rodents.

60 a role for genotoxicity in biphenyl-induced carcinogenicity has not been established.

61 involved in TiO(2)-induced genotoxicity and carcinogenicity have not been clearly defined and are po

62 Carcinogenicity in humans and rodents is generally consi

63 or biphenyl provides suggestive evidence for carcinogenicity in humans, based on increased incidences

64 ed mechanism underlying arsenic toxicity and carcinogenicity in humans.

65 ays involved in arsenic-induced toxicity and carcinogenicity in humans.

66 nt hepatic tumor promoter, with inconclusive carcinogenicity in humans.

67 ndrial processes involved in arsenic-induced carcinogenicity in humans.

68 occupationally exposed to BD and its potent carcinogenicity in laboratory mice.

69 osure to UVR is a contributing factor to its carcinogenicity in mice, and possibly in humans.

70 This carcinogenicity in rats has been linked to the formation

71 get site for chemically-induced toxicity and carcinogenicity in rodents.

72 ve been previously implicated as a source of carcinogenicity in tobacco and cigarette smoke.

73 eas of biomedicine, concerns regarding their carcinogenicity, inefficient dispersion in aqueous solut

74 BaP carcinogenicity is believed to occur mainly through its

75 both antiepileptic drugs, evidence for human carcinogenicity is not consistent and both are considere

76 The underlying mechanism of action for UVB carcinogenicity is well defined; however, the mechanisti

77 A pragmatic threshold for carcinogenicity may therefore exist for such genotoxins.

78 st that LOH contributes significantly to the carcinogenicity of a variety of mutagens and raises the

79 that could explain an important step in the carcinogenicity of aflatoxin B1.

80 dG adducts, which may be responsible for the carcinogenicity of alcoholic beverage consumption.

81 However, little is known about the carcinogenicity of arsenic at levels commonly observed i

82 best places in the world to investigate the carcinogenicity of arsenic.

83 Thus, the carcinogenicity of arsenite can be explained at least in

84 The mechanism responsible for the carcinogenicity of asbestos is not known.

85 anism-based biomarker for rapid screening of carcinogenicity of CNTs and related nanomaterials for th

86 the antidiabetic activity of Cr(III) and the carcinogenicity of Cr(VI) compounds arise from similar m

87 The carcinogenicity of Cr(VI) is related to its solubility,

88 The potential carcinogenicity of crystalline silica to humans remains

89 lusively at extrahepatic sites, mediates the carcinogenicity of DMBA.

90 ation of MCF-10F cells in vitro confirms the carcinogenicity of E2, supporting the concept that this

91 cer cases as the only means of demonstrating carcinogenicity of environmental agents.

92 ant role with regard to the genotoxicity and carcinogenicity of formaldehyde.

93 ic variation in xenobiotic metabolism in the carcinogenicity of hair dye use needs to be confirmed in

94 Our findings do not indicate that the carcinogenicity of high sun exposure can be counteracted

95 ole of this phenomenon in the regulation and carcinogenicity of HPV-16, 115 clinical samples were stu

96 Evidence of carcinogenicity of lipid-lowering drugs from clinical tr

97 Because the carcinogenicity of N-nitrosamines depends on formation o

98 ferase (MGMT) is a major defense against the carcinogenicity of N-nitroso compounds and other alkylat

99 The potential carcinogenicity of naphthalene (NA), a ubiquitous enviro

100 The carcinogenicity of nickel compounds has been well docume

101 volved in the essentiality, toxicity, and/or carcinogenicity of nickel compounds, a mRNA differential

102 Given the carcinogenicity of NNN and the frequent use of nicotine

103 nism for the genotoxicity, mutagenicity, and carcinogenicity of PAHs.

104 d with log(k(az)/k(s)), so prediction of the carcinogenicity of PhIP and other HCAs or AAs based prim

105 lon, yet the role of colon metabolism on the carcinogenicity of PhIP is not clearly understood.

106 g steroid hormones and may contribute to the carcinogenicity of polycyclic aromatic hydrocarbons (PAH

107 (CYP) enzymes are involved in activating the carcinogenicity of polycyclic aromatic hydrocarbons (PAH

108 One potential mechanism for the carcinogenicity of PPs is epigenetic modulation of growt

109 Shortcomings are length of protocol and carcinogenicity of retrorsine.

110 The genotoxicity and carcinogenicity of tamoxifen have been attributed to met

111 The carcinogenicity of tamoxifen is ascribed to its genotoxi

112 A MEDLINE search on the carcinogenicity of tamoxifen was conducted and the liter

113 gues that may provide an explanation for the carcinogenicity of the altered insulin protein?

114 The carcinogenicity of the more abundant UVA (320-400 nm) is

115 rpretation of mechanisms contributing to the carcinogenicity of these helminth infections, including

116 rpretation of mechanisms contributing to the carcinogenicity of these helminth infections, including

117 A strong correlation between the carcinogenicity of these isomers and methyl substitution

118 by ER would help in better understanding the carcinogenicity of these steroidogenic compounds and ass

119 of the clinical efficacy and, possibly, the carcinogenicity of these widely used chemotherapeutic ag

120 ta-estradiol (E2) has been implicated in the carcinogenicity of this hormone.

121 ullin (ADM) significantly contributes to the carcinogenicity of tobacco-activated AHR.

122 n a long-term rodent bioassay evaluating the carcinogenicity of triethanolamine, there was equivocal

123 ch as arachidonic acid, and to the toxicity, carcinogenicity, or teratogenicity of foreign compounds,

124 lay between all pathway responses leading to carcinogenicity predictions.

125 and interface properties we have developed a carcinogenicity predictor, InCa (Index of Carcinogenicit

126 nce of these two adduct groups for tamoxifen carcinogenicity remains to be established.

127 ver 8000 studies including all available NTP carcinogenicity, short-term toxicity and genetic toxicit

128 also reviewed methods and interpretation of carcinogenicity studies in rodents and results of clinic

129 ghtly worsens sputum cytology, and in animal carcinogenicity studies, in which beta-carotene has esta

130 A formaldehyde carcinogenicity study was conducted in which a major end

131 of 51 liver tissue samples from the original carcinogenicity study was conducted to determine the inc

132 estyle exposure that causes cancer, exerting carcinogenicity through >60 chemicals that bind and muta

133 The role of CYP1B1 in estradiol carcinogenicity thus depends on the identity of this sin

134 ly popular theory ascribes UVA (>320-400 nm) carcinogenicity to the ability of this wavelength to tri

135 to its widespread occurrence, toxicity, and carcinogenicity-to bioconcentrate in periphyton and thus

136 Transplacental inorganic arsenic carcinogenicity, together with postnatal exposure to die

137 of considerable interest because of its high carcinogenicity, was identified and quantified in the fo

138 hanism by which folate deficiency influences carcinogenicity, we have analyzed the effect of folate d

139 TLE protocol suggest minimal genotoxicity or carcinogenicity with long-term hydroxyurea exposure.

140 Nickel compounds have demonstrated carcinogenicity without any associated mutagenesis, sugg