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1 ns when mouse mammary glands were exposed to 7,12-dimethylbenz(a)anthracene.
2 g a single dose of Ras-activating carcinogen 7,12-dimethylbenz(a)anthracene.
3 E and a single application of the carcinogen 7,12-dimethylbenz(a)anthracene.
6 ll mice with respect to their sensitivity to 7, 12-dimethylbenz(a)anthracene /12-Otetradecanoylphorbo
7 tivation, epidermal proliferation induced by 7,12-dimethylbenz(a)-anthracene/12-O-tetradecanoylphorbo
8 btb4(-/-) mice were also more susceptible to 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol
9 nd Mek2 in skin neoplasia using the two-step 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol
10 ibited a marked resistance to development of 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol
11 n preneoplastic lesions that arise following 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol
12 rmation was either induced by application of 7,12-Dimethylbenz(a)anthracene/12-O-Tetradecanoylphorbol
13 ecting p38delta knockout mice to a two-stage 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol
14 sharply with data obtained using the classic 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol
16 Ras(Q61L))-driven papilloma formation in the 7,12-Dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol
17 irst time that RhoA is a tumor suppressor in 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol
18 nduced from a two-stage carcinogen bioassay (7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol
19 , and 74% of the BK5.IGF-1 mice treated with 7,12-dimethylbenz[a]anthracene (20 microg/day) developed
20 [a]anthracene-3(S),4(S)-dihydrodiol, and (-)-7,12-dimethylbenz[a]anthracene-3(R),4(R)-dihydrodiol.
21 ost potent proximate carcinogens known (e.g. 7,12-dimethylbenz[a]anthracene-3,4-diol (DMBA-3,4-diol)
22 itiating activity of (+/-)syn- and (+/-)anti-7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide (syn
24 as oxidized by AKR1C4 to the highly reactive 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione
25 benzo[a]pyrene-7,8-dione (BP-7,8-dione), and 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione
26 ombined with exposure to TPA and the mutagen 7,12-dimethylbenz(a)anthracene accelerated SCC developme
30 two-stage skin carcinogenesis protocol with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylpho
31 e or two-stage initiation and promotion with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylpho
32 genic effects, BaP and other PAHs, including 7,12-dimethylbenz[a]anthracene and 2,3,7,8-tetrachlorodi
33 r to those of the potent mammary carcinogens 7,12-dimethylbenz[a]anthracene and dibenzo[a,l]pyrene.
34 8,9-dihydroxy-8,9-dihydrobenzo[a]anthracene, 7,12-dimethylbenz[a]anthracene and its cis-5,6-dihydrodi
35 ance to chemical carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene and promoted by phorbol 1
36 ontrols were initiated with 25 micrograms of 7,12-dimethylbenz[a]anthracene and promoted weekly with
38 rmation of preneoplastic lesions (induced by 7,12-dimethylbenz(a)anthracene) and PR expression (with
39 hydrofluoranthene, 3,4-dihydroxy-3,4-dihydro-7,12-dimethylbenz[a]anthracene, and 6-nitrochrysene to a
40 NQO1 protein showed increased sensitivity to 7,12-dimethylbenz(a)anthracene- and benzo(a)pyrene-induc
41 ice to multistage skin carcinogenesis, using 7,12-dimethylbenz(a)anthracene as carcinogen and 12-O-te
42 y the two-stage carcinogenesis regimen using 7,12-dimethylbenz(a)anthracene as initiator and TPA as p
43 two-stage skin carcinogenesis protocol using 7,12-dimethylbenz(a)anthracene as the initiator and 12-O
44 benzo[a]pyrene, 9,10-dihydro-benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene, benzo[a]pyrene-7,8-dihyd
45 e initiated by the ras-activating carcinogen 7,12-dimethylbenz(a)anthracene, Bin1 loss strongly accen
47 in and non-Tg mice by topical application of 7,12-dimethylbenz(a)anthracene did not reveal significan
48 mice with the MMP-9 reporter transgene with 7, 12-dimethylbenz[a]anthracene (DMBA) treatment followe
49 ta(fl/fl) mice were completely refractory to 7,12 dimethylbenz[a]anthracene (DMBA)-induced skin tumor
51 its mammary tumor-resistant phenotype after 7,12-dimethylbenz(a)anthracene (DMBA) administration.
52 on in the T cell-mediated immune response to 7,12-dimethylbenz(a)anthracene (DMBA) and benzo(a)pyrene
53 ous papillomas in SENCAR mice initiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with
54 e, when K5-PKCalpha mice were initiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with
56 g properties of complete carcinogens such as 7,12-dimethylbenz(a)anthracene (DMBA) are well known but
57 K14E5 mice treated with the initiating agent 7,12-dimethylbenz(a)anthracene (DMBA) developed more pap
58 P1B1 and CYP1A1 expression and metabolism of 7,12-dimethylbenz(a)anthracene (DMBA) have been characte
59 it against mammary carcinogenesis induced by 7,12-dimethylbenz(a)anthracene (DMBA) in female Sprague
60 male rats with the prototypic xenobiotic PAH 7,12-dimethylbenz(a)anthracene (DMBA) induces mammary tu
61 /HeN mice that were subjected to a two-stage 7,12-dimethylbenz(a)anthracene (DMBA) initiation, 12-O-t
62 l skin of NQO2-deficient mice was exposed to 7,12-dimethylbenz(a)anthracene (DMBA) or benzo(a)pyrene
63 upon implantation of the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) or transgenic expr
64 icantly lower dose (2 to 5 mug per ovary) of 7,12-dimethylbenz(a)anthracene (DMBA) was applied to the
66 in the metabolism of the mammary carcinogen 7,12-dimethylbenz(a)anthracene (DMBA), as assessed by in
70 oduced by polyaromatic hydrocarbons, such as 7,12-dimethylbenz(a)anthracene (DMBA), often harbor an H
72 whether AP-1 signaling is also required for 7,12-dimethylbenz(a)anthracene (DMBA)-initiated/OA-promo
73 are resistant to skin tumor formation by the 7,12-dimethylbenz(a)anthracene (DMBA)-initiation and 12-
77 carcinogenesis [methylcholanthrene (MCA) or 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl
79 lignant progression and metastatic spread of 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl
80 dence compared with wild type (WT) mice in a 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl
82 ure with the polycyclic aromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA; rel-3983D cells) o
83 cation of a carcinogen and a tumor promoter (7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradeca
84 wed increased survival following exposure to 7,12-dimethylbenz[a]anthracene (DMBA) and enhanced proli
85 anced carcinogenic response to initiation by 7,12-dimethylbenz[a]anthracene (DMBA) followed by promot
86 PAHs) are prevalent, potent carcinogens, and 7,12-dimethylbenz[a]anthracene (DMBA) is a model PAH wid
90 bone marrow stromal cells and the model PAH 7,12-dimethylbenz[a]anthracene (DMBA) results in pre-B c
91 ice 15 min before application of 100 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) twice a week for 4
93 ilarly, exposure of BU-11/BMS2 cocultures to 7,12-dimethylbenz[a]anthracene (DMBA), a prototypic PAH,
95 uce the proximate carcinogenic metabolite of 7,12-dimethylbenz[a]anthracene (DMBA), a widely studied
96 In mice treated with the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA), AIB1 deficiency p
97 at the K-region of benz[a]-anthracene (BA), 7,12-dimethylbenz[a]anthracene (DMBA), chrysene (CR), be
98 or = 10(-8) M) of the prototypic AhR ligand, 7,12-dimethylbenz[a]anthracene (DMBA), induce preB cell
99 d after exposure to the chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), to which mice car
100 led to a desensitization to tumor initiator 7,12-dimethylbenz[a]anthracene (DMBA)-induced apoptosis
102 ion by label-free dark-field microscopy of a 7,12-Dimethylbenz[a]anthracene (DMBA)-induced hamster ch
103 Using a well-established mouse model of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary ca
104 ted the chemopreventive effect of SP against 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat breast
113 ice to carcinogen-induced tumor development (7,12-dimethylbenz[a]anthracene, DMBA), and find these mi
114 quinone derivatives of benzo[a]pyrene (BPQ), 7,12-dimethylbenz[a]anthracene (DMBAQ), and benz[a]anthr
115 as observed even though the levels of stable 7,12-dimethylbenz(a)anthracene-DNA adducts were increase
116 wild-type mice using a single application of 7,12-dimethylbenz(a)anthracene followed by repetitive ap
117 p21WAF1 gene were treated once with 25 nmol 7,12-dimethylbenz[a]anthracene, followed by 5 microg of
118 chow from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly highe
119 dent preneoplastic ductal lesions induced by 7,12-dimethylbenz(a)anthracene in these mammary glands (
120 nhibited the bone marrow ablative effects of 7,12-dimethylbenz[a]anthracene in vivo, demonstrating dr
121 ndac sulfone also inhibited the formation of 7,12-dimethylbenz(a)anthracene-induced hyperplastic alve
122 animals were highly susceptible to progestin/7,12-dimethylbenz(a)anthracene-induced mammary carcinoge
123 lymphoma development and the development of 7,12-dimethylbenz(a)anthracene-induced mammary gland tum
124 ctive dose of both drugs required to inhibit 7,12-dimethylbenz(a)anthracene-induced mammary tumor gro
125 disease, we generated cell line models from 7,12-dimethylbenz(a)anthracene-induced murine primary OS
126 owth and are prone to spontaneous tumors and 7,12-dimethylbenz(a)anthracene-induced skin tumors.
127 (WKy) inbred strain, resistant to developing 7,12-dimethylbenz[a]anthracene-induced mammary carcinoge
128 the increased susceptibility of -/- mice to 7,12-dimethylbenz[a]anthracene-induced skin carcinogenes
129 e to carcinogens indicated that NMU, but not 7,12-dimethylbenz(a)anthracene, initiated the loss of th
130 ficant protection against tumor promotion in 7,12-dimethylbenz(a)anthracene-initiated mouse skin.
131 2-O-tetradecanolyphorbol-13-acetate (TPA) in 7,12-dimethylbenz(a)anthracene-initiated mouse skin.
132 min prior to that of each TPA application to 7,12-dimethylbenz(a)anthracene-initiated SENCAR mice res
133 2-O-tetradecanolyphorbol-13-acetate (TPA) in 7,12-dimethylbenz[a]anthracene-initiated mouse skin.
134 nd squamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetra
135 nt squamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetra
137 nduced in FVB mice by a two-stage regimen of 7,12-dimethylbenz[a]anthracene initiation followed by re
138 c squamous cell carcinoma (mSCC) elicited by 7,12-dimethylbenz(a)anthracene-initiation and 12-O-tetra
139 gens and carcinogenesis protocols, including 7,12-dimethylbenz[a]anthracene-initiation/12-O-tetradeca
140 1 transgenic mice with an initiating dose of 7,12-dimethylbenz[a]anthracene only led to the formation
141 s (57 of 59) that developed following UVB or 7,12-dimethylbenz(a)anthracene/phorbol 12-myristate 13-a
142 to a two-stage skin carcinogenesis protocol [7,12-dimethylbenz[a]anthracene/phorbol 12-tetradecanoate
143 the development of cancer using a two-stage [7,12-dimethylbenz(a)-anthracene plus 12-O-tetradecanoylp
144 of Stat3 prior to skin tumor initiation with 7,12-dimethylbenz(a)anthracene significantly increased t
146 was applied following tumor initiation with 7,12-dimethylbenz[a]anthracene, the papilloma and carcin
147 er, following initiation with the carcinogen 7,12-dimethylbenz[a]anthracene, the transgenic group sho
149 or chemopreventive activity in the two-stage 7,12-dimethylbenz(a)anthracene/TPA skin carcinogenesis m
150 ression in control, dysplasia, and cancerous 7, 12-dimethylbenz[a]anthracene-treated hamster cheek po
151 in the stratified squamous epithelia of the 7,12-dimethylbenz(a)anthracene-treated hamster cheek pou
153 (17-fold) in the epidermal keratinocytes of 7,12-dimethylbenz[a]anthracene-treated C/EBPbeta-null mi
154 ce of VP-16-induced melanomas in the skin of 7,12-dimethylbenz[a]anthracene-treated mice is found to
155 Moreover, mouse mammary tumors induced by 7,12-dimethylbenz(a)anthracene treatment displayed incre
156 somatic level when exposed to a carcinogen (7,12-dimethylbenz[a]anthracene), which subsequently seem
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