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1 evelopment of cancer using a two-stage [7,12-dimethylbenz(a)-anthracene plus 12-O-tetradecanoylphorbo
2 ion, epidermal proliferation induced by 7,12-dimethylbenz(a)-anthracene/12-O-tetradecanoylphorbol-13-
5 the T cell-mediated immune response to 7,12-dimethylbenz(a)anthracene (DMBA) and benzo(a)pyrene in C
6 apillomas in SENCAR mice initiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with 12-O-
7 en K5-PKCalpha mice were initiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with a low
9 perties of complete carcinogens such as 7,12-dimethylbenz(a)anthracene (DMBA) are well known but not
10 mice treated with the initiating agent 7,12-dimethylbenz(a)anthracene (DMBA) developed more papillom
11 and CYP1A1 expression and metabolism of 7,12-dimethylbenz(a)anthracene (DMBA) have been characterized
12 ainst mammary carcinogenesis induced by 7,12-dimethylbenz(a)anthracene (DMBA) in female Sprague Dawle
13 rats with the prototypic xenobiotic PAH 7,12-dimethylbenz(a)anthracene (DMBA) induces mammary tumors
14 mice that were subjected to a two-stage 7,12-dimethylbenz(a)anthracene (DMBA) initiation, 12-O-tetrad
15 n of NQO2-deficient mice was exposed to 7,12-dimethylbenz(a)anthracene (DMBA) or benzo(a)pyrene alone
16 implantation of the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) or transgenic expressio
17 ly lower dose (2 to 5 mug per ovary) of 7,12-dimethylbenz(a)anthracene (DMBA) was applied to the one
20 he metabolism of the mammary carcinogen 7,12-dimethylbenz(a)anthracene (DMBA), as assessed by increas
24 d by polyaromatic hydrocarbons, such as 7,12-dimethylbenz(a)anthracene (DMBA), often harbor an H-ras
26 her AP-1 signaling is also required for 7,12-dimethylbenz(a)anthracene (DMBA)-initiated/OA-promoted s
27 esistant to skin tumor formation by the 7,12-dimethylbenz(a)anthracene (DMBA)-initiation and 12-O-tet
31 nt progression and metastatic spread of 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl-phor
33 e of Hpa-Tg mice to a classical two-stage 12-dimethylbenz(a)anthracene (DMBA)/12-o-tetradecanoylphorb
34 inogenesis [methylcholanthrene (MCA) or 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorb
36 compared with wild type (WT) mice in a 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorb
38 ith the polycyclic aromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA; rel-3983D cells) or DMS
39 e with respect to their sensitivity to 7, 12-dimethylbenz(a)anthracene /12-Otetradecanoylphorbol-13-a
40 ed with exposure to TPA and the mutagen 7,12-dimethylbenz(a)anthracene accelerated SCC development wi
42 o multistage skin carcinogenesis, using 7,12-dimethylbenz(a)anthracene as carcinogen and 12-O-tetrade
43 two-stage carcinogenesis regimen using 7,12-dimethylbenz(a)anthracene as initiator and TPA as promot
44 tage skin carcinogenesis protocol using 7,12-dimethylbenz(a)anthracene as the initiator and 12-O-tetr
45 ic mice treated with the chemical carcinogen dimethylbenz(a)anthracene developed tumors with much sho
46 d non-Tg mice by topical application of 7,12-dimethylbenz(a)anthracene did not reveal significant dif
47 type mice using a single application of 7,12-dimethylbenz(a)anthracene followed by repetitive applica
48 from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly higher mam
49 preneoplastic ductal lesions induced by 7,12-dimethylbenz(a)anthracene in these mammary glands (IC50
50 uamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetradecan
51 uamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetradecan
53 are caused by exposure to topical carcinogen dimethylbenz(a)anthracene or benzo(a)pyrene (BP) followe
54 to each other [in both methylnitrosourea and dimethylbenz(a)anthracene rat mammary tumor models].
55 at3 prior to skin tumor initiation with 7,12-dimethylbenz(a)anthracene significantly increased the nu
57 reover, mouse mammary tumors induced by 7,12-dimethylbenz(a)anthracene treatment displayed increased
58 on of preneoplastic lesions (induced by 7,12-dimethylbenz(a)anthracene) and PR expression (with or wi
59 tiated by the ras-activating carcinogen 7,12-dimethylbenz(a)anthracene, Bin1 loss strongly accentuate
61 carcinogens indicated that NMU, but not 7,12-dimethylbenz(a)anthracene, initiated the loss of this st
62 ice ("UV resistant") and when the hapten was dimethylbenz(a)anthracene, thus indicating that the gene
63 protein showed increased sensitivity to 7,12-dimethylbenz(a)anthracene- and benzo(a)pyrene-induced sk
64 served even though the levels of stable 7,12-dimethylbenz(a)anthracene-DNA adducts were increased abo
65 sulfone also inhibited the formation of 7,12-dimethylbenz(a)anthracene-induced hyperplastic alveolar
66 ls were highly susceptible to progestin/7,12-dimethylbenz(a)anthracene-induced mammary carcinogenesis
67 homa development and the development of 7,12-dimethylbenz(a)anthracene-induced mammary gland tumors.
68 dose of both drugs required to inhibit 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth i
69 ase, we generated cell line models from 7,12-dimethylbenz(a)anthracene-induced murine primary OSCC ca
73 rior to that of each TPA application to 7,12-dimethylbenz(a)anthracene-initiated SENCAR mice resulted
74 I or mezerein in stage II tumor promotion in dimethylbenz(a)anthracene-initiated SENCAR mouse skin re
75 amous cell carcinoma (mSCC) elicited by 7,12-dimethylbenz(a)anthracene-initiation and 12-O-tetradecan
76 he stratified squamous epithelia of the 7,12-dimethylbenz(a)anthracene-treated hamster cheek pouch mo
85 ly with data obtained using the classic 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
86 -/-) mice were also more susceptible to 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
87 k2 in skin neoplasia using the two-step 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
88 d a marked resistance to development of 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
89 on was either induced by application of 7,12-Dimethylbenz(a)anthracene/12-O-Tetradecanoylphorbol-13-a
90 neoplastic lesions that arise following 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
91 g p38delta knockout mice to a two-stage 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
92 of 59) that developed following UVB or 7,12-dimethylbenz(a)anthracene/phorbol 12-myristate 13-acetat
94 emopreventive activity in the two-stage 7,12-dimethylbenz(a)anthracene/TPA skin carcinogenesis model
95 74% of the BK5.IGF-1 mice treated with 7,12-dimethylbenz[a]anthracene (20 microg/day) developed mamm
96 n of a carcinogen and a tumor promoter (7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylp
97 ncreased survival following exposure to 7,12-dimethylbenz[a]anthracene (DMBA) and enhanced proliferat
98 carcinogenic response to initiation by 7,12-dimethylbenz[a]anthracene (DMBA) followed by promotion w
99 are prevalent, potent carcinogens, and 7,12-dimethylbenz[a]anthracene (DMBA) is a model PAH widely u
100 The polycyclic aromatic hydrocarbon 7,12-dimethylbenz[a]anthracene (DMBA) is a potent carcinogen
102 Treatment with the tumor initiator 7,12-dimethylbenz[a]anthracene (DMBA) resulted in a significa
103 marrow stromal cells and the model PAH 7,12-dimethylbenz[a]anthracene (DMBA) results in pre-B cell a
104 with the MMP-9 reporter transgene with 7, 12-dimethylbenz[a]anthracene (DMBA) treatment followed by p
105 5 min before application of 100 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) twice a week for 4 week
107 y, exposure of BU-11/BMS2 cocultures to 7,12-dimethylbenz[a]anthracene (DMBA), a prototypic PAH, down
109 he proximate carcinogenic metabolite of 7,12-dimethylbenz[a]anthracene (DMBA), a widely studied exper
110 ce treated with the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA), AIB1 deficiency protec
111 he K-region of benz[a]-anthracene (BA), 7,12-dimethylbenz[a]anthracene (DMBA), chrysene (CR), benzo[a
112 10(-8) M) of the prototypic AhR ligand, 7,12-dimethylbenz[a]anthracene (DMBA), induce preB cell apopt
113 er exposure to the chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), to which mice carrying
114 to a desensitization to tumor initiator 7,12-dimethylbenz[a]anthracene (DMBA)-induced apoptosis both
115 Previous studies have reported that 7,12-dimethylbenz[a]anthracene (DMBA)-induced bone marrow tox
116 y label-free dark-field microscopy of a 7,12-Dimethylbenz[a]anthracene (DMBA)-induced hamster cheek p
117 Using a well-established mouse model of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcino
118 he chemopreventive effect of SP against 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat breast carc
119 /fl) mice were completely refractory to 7,12 dimethylbenz[a]anthracene (DMBA)-induced skin tumorigene
129 ne derivatives of benzo[a]pyrene (BPQ), 7,12-dimethylbenz[a]anthracene (DMBAQ), and benz[a]anthracene
130 stage skin carcinogenesis protocol with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-
131 two-stage initiation and promotion with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-
132 effects, BaP and other PAHs, including 7,12-dimethylbenz[a]anthracene and 2,3,7,8-tetrachlorodibenzo
134 ihydroxy-8,9-dihydrobenzo[a]anthracene, 7,12-dimethylbenz[a]anthracene and its cis-5,6-dihydrodiol, 5
135 to chemical carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene and promoted by phorbol 12-myr
136 ls were initiated with 25 micrograms of 7,12-dimethylbenz[a]anthracene and promoted weekly with 5 mic
139 ranscription induced by the aryl hydrocarbon dimethylbenz[a]anthracene in human mammary carcinoma MCF
140 ted the bone marrow ablative effects of 7,12-dimethylbenz[a]anthracene in vivo, demonstrating drug ab
141 d in FVB mice by a two-stage regimen of 7,12-dimethylbenz[a]anthracene initiation followed by repetit
142 magnitude of mammary tumor inhibition in the dimethylbenz[a]anthracene model as that produced by 1 mo
144 nsgenic mice with an initiating dose of 7,12-dimethylbenz[a]anthracene only led to the formation of a
145 tic level when exposed to a carcinogen (7,12-dimethylbenz[a]anthracene), which subsequently seem to b
146 Tumors were elicited by the initiation (7,12-dimethylbenz[a]anthracene, 100 nmol)-promotion (TPA, 5 n
147 When challenged with the carcinogen 7,12-dimethylbenz[a]anthracene, all mice, regardless of genot
148 fluoranthene, 3,4-dihydroxy-3,4-dihydro-7,12-dimethylbenz[a]anthracene, and 6-nitrochrysene to apprec
149 [a]pyrene, 9,10-dihydro-benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene, benzo[a]pyrene-7,8-dihydrodio
150 resistant to another aryl hydrocarbon (AH), dimethylbenz[a]anthracene, but not to pleiotropic drugs
151 o carcinogen-induced tumor development (7,12-dimethylbenz[a]anthracene, DMBA), and find these mice to
152 AF1 gene were treated once with 25 nmol 7,12-dimethylbenz[a]anthracene, followed by 5 microg of TPA t
153 applied following tumor initiation with 7,12-dimethylbenz[a]anthracene, the papilloma and carcinoma r
154 ollowing initiation with the carcinogen 7,12-dimethylbenz[a]anthracene, the transgenic group showed a
156 otent proximate carcinogens known (e.g. 7,12-dimethylbenz[a]anthracene-3,4-diol (DMBA-3,4-diol) and b
157 ing activity of (+/-)syn- and (+/-)anti-7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide (syn- and
159 [a]pyrene-7,8-dione (BP-7,8-dione), and 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione) pot
160 idized by AKR1C4 to the highly reactive 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione), wh
161 inbred strain, resistant to developing 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis
162 increased susceptibility of -/- mice to 7,12-dimethylbenz[a]anthracene-induced skin carcinogenesis an
164 and carcinogenesis protocols, including 7,12-dimethylbenz[a]anthracene-initiation/12-O-tetradecanoylp
166 fold) in the epidermal keratinocytes of 7,12-dimethylbenz[a]anthracene-treated C/EBPbeta-null mice co
167 n in control, dysplasia, and cancerous 7, 12-dimethylbenz[a]anthracene-treated hamster cheek pouch mu
168 VP-16-induced melanomas in the skin of 7,12-dimethylbenz[a]anthracene-treated mice is found to be si
169 Also, skin carcinogen challenge by 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoyl-phorbol-13-
170 time that RhoA is a tumor suppressor in 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol 13-a
171 61L))-driven papilloma formation in the 7,12-Dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
172 d from a two-stage carcinogen bioassay (7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
173 two-stage skin carcinogenesis protocol [7,12-dimethylbenz[a]anthracene/phorbol 12-tetradecanoate 13-a
174 hanges of MnSOD transcription using the 7,12-dimethylbenz(alpha)anthracene (DMBA)/12-O-tetradecanoylp
175 two-stage chemical carcinogenesis protocol (dimethylbenz[alpha]anthracene (DMBA) initiation with 12-
176 moid cells to chemicals/drugs including 7,12-dimethylbenz[alpha]anthracene (mutagen) and camptothecin
177 alGDS-related (Rgr) oncogene in a DMBA (7,12-dimethylbenz[alpha]anthracene)-induced rabbit squamous c
178 mice and wild-type (WT) mice in a DMBA (7,12-dimethylbenz[alpha]anthracene)/TPA (12-O-tetradecanoylph
181 skin tumors arising from treatment with 7,12-dimethylbenz[alpha]anthracene/12-o-tetradecanoylphorbol-
182 nalyzed effects of the skin cancer initiator dimethylbenz-anthracene and/or the tumor promoter 12-O-t
183 ramagnetic resonance experiments with [(15)N-dimethylbenz-imidazole]adenosylcobalamin demonstrate bas
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