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1 the biosynthesis of aflatoxin B(1), a potent environmental carcinogen.
2 s, the relevant cell type for this important environmental carcinogen.
3 raviolet radiation (UVR), the most prevalent environmental carcinogen.
4 ion of the skin from sunlight, an ubiquitous environmental carcinogen.
5 icity of several chemotherapeutic agents and environmental carcinogens.
6 nce reduce the impact of future exposures to environmental carcinogens.
7 aromatic hydrocarbons (PAHs) are ubiquitous environmental carcinogens.
8 patocellular carcinoma following exposure to environmental carcinogens.
9 fragile site, FRA3B, that is susceptible to environmental carcinogens.
10 on fragile site and is highly susceptible to environmental carcinogens.
11 bladder, and showed that it is the target of environmental carcinogens.
12 of multiple primary tumors, when exposed to environmental carcinogens.
13 vivo cooperation between HBx expression and environmental carcinogens.
14 ancer as it is for other neoplasms caused by environmental carcinogens.
15 in patients exposed to ionizing radiation or environmental carcinogens.
16 cularly in tumors resulting from exposure to environmental carcinogens.
17 in other tissues associated with exposure to environmental carcinogens.
18 ify cancer risk associated with exposures to environmental carcinogens.
19 ssment of individual susceptibility to these environmental carcinogens.
20 tary constituents, pharmaceutical drugs, and environmental carcinogens.
21 of the more susceptible groups from risks of environmental carcinogens.
22 or individual variation in susceptibility to environmental carcinogens.
23 er smoked and in rodents exposed to specific environmental carcinogens.
24 ing neoplasia and increase susceptibility to environmental carcinogens.
25 involved in processing DNA damage induced by environmental carcinogens.
27 The aryl hydrocarbon receptor (AhR) is an environmental carcinogen-activated transcription factor
29 PksA, which initiates biosynthesis of the environmental carcinogen aflatoxin B1, is one of the mul
30 ts but complex exposure to other therapeutic/environmental carcinogens also leads to the frequent occ
31 e tumors, particularly those associated with environmental carcinogens, alterations in the FHIT gene
32 Radiation exposure is an important form of environmental carcinogen and has been associated with in
33 of cancer is influenced both by exposure to environmental carcinogens and by the host genetic backgr
34 enine adducts (epsilonA) are formed by known environmental carcinogens and found to be removed by hum
35 his enzyme in the activation of a variety of environmental carcinogens and mutagens in Salmonella typ
36 GST) genes are involved in the metabolism of environmental carcinogens and of some classes of chemoth
37 e-3-thione (D3T) enhance the detoxication of environmental carcinogens and protect against neoplasia.
39 at the FHIT gene is a preferential target of environmental carcinogens and that FHIT inactivation pla
40 ytotoxic O6-alkylguanine lesions produced by environmental carcinogens and the chemotherapeutic nitro
41 ine the sensitivity of PMS2 knockout mice to environmental carcinogens and the protective effect of O
42 produced by endogenous cellular metabolites, environmental carcinogens, and chemotherapeutic alkylati
43 yze the metabolism of endogenous substrates, environmental carcinogens, and clinically important exog
44 osure constitutes one of the most widespread environmental carcinogens, and is associated with increa
46 , which mediates malignant transformation by environmental carcinogens, are highly elevated and appea
49 nvestigated the mechanisms through which the environmental carcinogen benzo[a]pyrene (B[a]P) lowered
50 ]P-N(2)-dG (G*) DNA adduct, derived from the environmental carcinogen benzo[a]pyrene (B[a]P): 5'-C-C-
51 A convenient new synthesis of the ubiquitous environmental carcinogen benzo[a]pyrene (BaP) is describ
55 anine with anti-B[a]PDE (a metabolite of the environmental carcinogen benzo[a]pyrene) at CpG mutation
56 etrahydrobenzo[a]pyrene (a metabolite of the environmental carcinogen benzo[a]pyrene), to the exocycl
58 ce of physiological factors combined with an environmental carcinogen can lead to transformation of n
59 Here we show that nickel, a nonmutagenic environmental carcinogen, disrupted H3K9me2 domains, res
62 These findings support the hypothesis that environmental carcinogen exposure, in addition to cigare
64 in cellular responses to the endogenous and environmental carcinogen formaldehyde (FA) that binds to
68 2), such that CYP2S1 oxidized many important environmental carcinogens, including benzo[a]pyrene, 9,1
69 tigating mutagenesis induced by a variety of environmental carcinogens, including sunlight ultraviole
71 that chlorogenic acid could protect against environmental carcinogen-induced carcinogenesis and sugg
72 own about the alteration and role of MEG3 in environmental carcinogen-induced lung tumorigenesis.
73 establish their links to tissues of origin, environmental/carcinogen influences, and DNA repair defe
74 our knowledge about how this most ubiquitous environmental carcinogen interacts with the largest orga
76 c estrogen metabolites and the activation of environmental carcinogens is cytochrome P450 1B1 (CYP1B1
77 y activated benzo[a]pyrene (BP), a prominent environmental carcinogen, is the 10S (+)-trans-anti-[BP]
78 epeated exposures to UV radiation (UVR), the environmental carcinogen linked to the development of hu
79 s that genetically determined sensitivity to environmental carcinogens may play a role in the pathoge
80 though arsenic is one of the most widespread environmental carcinogens, methods of remediation are st
81 bined with non-carcinogenic low doses of the environmental carcinogen, N-nitrosomethylbenzylamine (NM
82 o the best of our knowledge, discovered that environmental carcinogen nickel exposure led to MEG3 dow
84 gle and combined exposures to two ubiquitous environmental carcinogens, polycyclic aromatic hydrocarb
85 hemical lesions to DNA that are derived from environmental carcinogens present in tobacco smoke, auto
87 yclic aromatic hydrocarbons (PAHs) are major environmental carcinogens produced in the combustion of
88 n the world, and UV radiation is the primary environmental carcinogen responsible for its development
89 ike those derived from a number of activated environmental carcinogens such as polycyclic aromatic hy
90 trated by molecular epidemiologic studies of environmental carcinogens such as polycyclic aromatic hy
94 Benzo[a]pyrene (B[a]P) is a well-studied environmental carcinogen that when activated can react w
98 ontributions of other genetic alterations or environmental carcinogens to lung tumor development.
99 pathways, ranging from the detoxification of environmental carcinogens to steroid hormone metabolism,
100 that CYP2S1 contributes to the metabolism of environmental carcinogens via an NADPH independent activ
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