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1 raviolet radiation (UVR), the most prevalent environmental carcinogen.
2 the biosynthesis of aflatoxin B(1), a potent environmental carcinogen.
3 s, the relevant cell type for this important environmental carcinogen.
4 ion of the skin from sunlight, an ubiquitous environmental carcinogen.
5 ing neoplasia and increase susceptibility to environmental carcinogens.
6 involved in processing DNA damage induced by environmental carcinogens.
7 ines tested, to magnitudes that exceed known environmental carcinogens.
8 itrosamines (TONO) is critical for assessing environmental carcinogens.
9 in patients exposed to ionizing radiation or environmental carcinogens.
10 icity of several chemotherapeutic agents and environmental carcinogens.
11  stem cells exposed to 79 known or suspected environmental carcinogens.
12 nce reduce the impact of future exposures to environmental carcinogens.
13  aromatic hydrocarbons (PAHs) are ubiquitous environmental carcinogens.
14 patocellular carcinoma following exposure to environmental carcinogens.
15  fragile site, FRA3B, that is susceptible to environmental carcinogens.
16 on fragile site and is highly susceptible to environmental carcinogens.
17 bladder, and showed that it is the target of environmental carcinogens.
18  of multiple primary tumors, when exposed to environmental carcinogens.
19  vivo cooperation between HBx expression and environmental carcinogens.
20 ancer as it is for other neoplasms caused by environmental carcinogens.
21 cularly in tumors resulting from exposure to environmental carcinogens.
22 in other tissues associated with exposure to environmental carcinogens.
23 ify cancer risk associated with exposures to environmental carcinogens.
24 ssment of individual susceptibility to these environmental carcinogens.
25 tary constituents, pharmaceutical drugs, and environmental carcinogens.
26 of the more susceptible groups from risks of environmental carcinogens.
27 or individual variation in susceptibility to environmental carcinogens.
28 er smoked and in rodents exposed to specific environmental carcinogens.
29         Here, we report that exposure to the environmental carcinogen (7R,8S)-dihydroxy-(9S,10R)-epox
30    The aryl hydrocarbon receptor (AhR) is an environmental carcinogen-activated transcription factor
31               The biosynthesis of the potent environmental carcinogen aflatoxin B1 involves ca. 15 st
32    PksA, which initiates biosynthesis of the environmental carcinogen aflatoxin B1, is one of the mul
33 ts but complex exposure to other therapeutic/environmental carcinogens also leads to the frequent occ
34 e tumors, particularly those associated with environmental carcinogens, alterations in the FHIT gene
35   Radiation exposure is an important form of environmental carcinogen and has been associated with in
36  of cancer is influenced both by exposure to environmental carcinogens and by the host genetic backgr
37 enine adducts (epsilonA) are formed by known environmental carcinogens and found to be removed by hum
38 his enzyme in the activation of a variety of environmental carcinogens and mutagens in Salmonella typ
39 GST) genes are involved in the metabolism of environmental carcinogens and of some classes of chemoth
40 e-3-thione (D3T) enhance the detoxication of environmental carcinogens and protect against neoplasia.
41 lved in the activation and detoxification of environmental carcinogens and teratogens.
42 at the FHIT gene is a preferential target of environmental carcinogens and that FHIT inactivation pla
43 ytotoxic O6-alkylguanine lesions produced by environmental carcinogens and the chemotherapeutic nitro
44 ine the sensitivity of PMS2 knockout mice to environmental carcinogens and the protective effect of O
45 produced by endogenous cellular metabolites, environmental carcinogens, and chemotherapeutic alkylati
46 yze the metabolism of endogenous substrates, environmental carcinogens, and clinically important exog
47 osure constitutes one of the most widespread environmental carcinogens, and is associated with increa
48 -specific effects of endogenous mutagens and environmental carcinogens, and pathobiology of early-sta
49           It is also generally believed that environmental carcinogens are responsible for the initia
50       Collectively, our findings reveal that environmental carcinogens are the link between HBV and H
51 , which mediates malignant transformation by environmental carcinogens, are highly elevated and appea
52                          Arsenicals are both environmental carcinogens as well as therapeutic agents
53                                          The environmental carcinogen benzo(a)pyrene-7,8-diol-9,10-ep
54 nvestigated the mechanisms through which the environmental carcinogen benzo[a]pyrene (B[a]P) lowered
55 ]P-N(2)-dG (G*) DNA adduct, derived from the environmental carcinogen benzo[a]pyrene (B[a]P): 5'-C-C-
56 A convenient new synthesis of the ubiquitous environmental carcinogen benzo[a]pyrene (BaP) is describ
57                                   The potent environmental carcinogen benzo[a]pyrene (BaP), following
58                                          The environmental carcinogen benzo[a]pyrene (BP) is metaboli
59                                          The environmental carcinogen benzo[a]pyrene is metabolically
60 anine with anti-B[a]PDE (a metabolite of the environmental carcinogen benzo[a]pyrene) at CpG mutation
61 etrahydrobenzo[a]pyrene (a metabolite of the environmental carcinogen benzo[a]pyrene), to the exocycl
62 an P53 gene is a mutational hot spot for the environmental carcinogen benzo[a]pyrene.
63 ce of physiological factors combined with an environmental carcinogen can lead to transformation of n
64 sure to various alkylating agents, including environmental carcinogens, cancer chemotherapeutics, and
65             DNA alkylation damage induced by environmental carcinogens, chemotherapy drugs, or endoge
66     Here we show that nickel, a nonmutagenic environmental carcinogen, disrupted H3K9me2 domains, res
67                       If the hypothesis that environmental carcinogen exposure contributes to human b
68                                              Environmental carcinogen exposure is requisite for the d
69   These findings support the hypothesis that environmental carcinogen exposure, in addition to cigare
70 emain resistant to the disease despite heavy environmental carcinogen exposure.
71        UVR is known to be the most important environmental carcinogen for cutaneous melanoma.
72  in cellular responses to the endogenous and environmental carcinogen formaldehyde (FA) that binds to
73                      The mutagenic effect of environmental carcinogens has been well documented in an
74              Prevention of tumors induced by environmental carcinogens has not been achieved.
75                             Even though many environmental carcinogens have been identified, studying
76     Also, polycyclic aromatic amines, potent environmental carcinogens, have been implicated in produ
77  as evidence supporting a causative role for environmental carcinogens in certain tumor types.
78 2), such that CYP2S1 oxidized many important environmental carcinogens, including benzo[a]pyrene, 9,1
79 tigating mutagenesis induced by a variety of environmental carcinogens, including sunlight ultraviole
80                                      Indeed, environmental carcinogens increase the frequency of HR,
81  that chlorogenic acid could protect against environmental carcinogen-induced carcinogenesis and sugg
82 own about the alteration and role of MEG3 in environmental carcinogen-induced lung tumorigenesis.
83  establish their links to tissues of origin, environmental/carcinogen influences, and DNA repair defe
84 our knowledge about how this most ubiquitous environmental carcinogen interacts with the largest orga
85 he few tumor types for which the predominant environmental carcinogen is known.
86 c estrogen metabolites and the activation of environmental carcinogens is cytochrome P450 1B1 (CYP1B1
87 y activated benzo[a]pyrene (BP), a prominent environmental carcinogen, is the 10S (+)-trans-anti-[BP]
88 n younger females and over-representation of environmental carcinogen-like mutational signatures in o
89 epeated exposures to UV radiation (UVR), the environmental carcinogen linked to the development of hu
90 s that genetically determined sensitivity to environmental carcinogens may play a role in the pathoge
91 though arsenic is one of the most widespread environmental carcinogens, methods of remediation are st
92 bined with non-carcinogenic low doses of the environmental carcinogen, N-nitrosomethylbenzylamine (NM
93 o the best of our knowledge, discovered that environmental carcinogen nickel exposure led to MEG3 dow
94                       Chromium (VI), a major environmental carcinogen, not only failed to activate th
95 carcinoma (HNSCC) arises through exposure to environmental carcinogens or malignant transformation by
96 eaction site in DNA for numerous dietary and environmental carcinogens or their electrophilic metabol
97 lterations that may be inherited, induced by environmental carcinogens, or caused due to random repli
98 gle and combined exposures to two ubiquitous environmental carcinogens, polycyclic aromatic hydrocarb
99 hemical lesions to DNA that are derived from environmental carcinogens present in tobacco smoke, auto
100                     Aflatoxin B1 is a potent environmental carcinogen produced by certain strains of
101 yclic aromatic hydrocarbons (PAHs) are major environmental carcinogens produced in the combustion of
102                                        Toxic environmental carcinogens promote cancer via genotoxic a
103 n the world, and UV radiation is the primary environmental carcinogen responsible for its development
104 ike those derived from a number of activated environmental carcinogens such as polycyclic aromatic hy
105 trated by molecular epidemiologic studies of environmental carcinogens such as polycyclic aromatic hy
106 mammalian genome, including those induced by environmental carcinogens such as UV radiation, and anti
107                      Arsenic is an important environmental carcinogen that affects millions of people
108    Hexavalent chromium (Cr(VI)) is a class I environmental carcinogen that induces lung epithelial ce
109           Benzo[a]pyrene (B[a]P) is a potent environmental carcinogen that is metabolized into diol e
110       Benzo[a]pyrene (B[a]P) is a widespread environmental carcinogen that must be activated by cellu
111     Benzo[a]pyrene (B[a]P) is a well-studied environmental carcinogen that when activated can react w
112            Methylating agents are widespread environmental carcinogens that generate a broad spectrum
113                                     PAHs are environmental carcinogens that, upon metabolic activatio
114 structurally diverse chemicals, ranging from environmental carcinogens to dietary metabolites.
115 ontributions of other genetic alterations or environmental carcinogens to lung tumor development.
116 pathways, ranging from the detoxification of environmental carcinogens to steroid hormone metabolism,
117                                          The environmental carcinogen urethane exhibits a profound sp
118 that CYP2S1 contributes to the metabolism of environmental carcinogens via an NADPH independent activ
119                   Benzo[a]pyrene is a potent environmental carcinogen, which can be metabolized in ce

 
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