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1 rofen, and to a control group receiving only dimethylbenz(a)anthracene.
2 a single application of the carcinogen 7,12-dimethylbenz(a)anthracene.
3 en mouse mammary glands were exposed to 7,12-dimethylbenz(a)anthracene.
4 ingle dose of Ras-activating carcinogen 7,12-dimethylbenz(a)anthracene.
5 ubstitute for the initiation step induced by dimethylbenz(a)anthracene.
6 ed skin tumor incidence after treatment with dimethylbenz(a)anthracene.
8 Tumors were elicited by the initiation (7,12-dimethylbenz[a]anthracene, 100 nmol)-promotion (TPA, 5 n
9 e with respect to their sensitivity to 7, 12-dimethylbenz(a)anthracene /12-Otetradecanoylphorbol-13-a
10 ion, epidermal proliferation induced by 7,12-dimethylbenz(a)-anthracene/12-O-tetradecanoylphorbol-13-
11 ly with data obtained using the classic 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
12 on was either induced by application of 7,12-Dimethylbenz(a)anthracene/12-O-Tetradecanoylphorbol-13-a
13 k2 in skin neoplasia using the two-step 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
14 d a marked resistance to development of 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
15 neoplastic lesions that arise following 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
16 g p38delta knockout mice to a two-stage 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
17 -/-) mice were also more susceptible to 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
19 time that RhoA is a tumor suppressor in 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol 13-a
20 tes keratinocyte differentiation in the 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
21 61L))-driven papilloma formation in the 7,12-Dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
22 d from a two-stage carcinogen bioassay (7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
23 74% of the BK5.IGF-1 mice treated with 7,12-dimethylbenz[a]anthracene (20 microg/day) developed mamm
25 otent proximate carcinogens known (e.g. 7,12-dimethylbenz[a]anthracene-3,4-diol (DMBA-3,4-diol) and b
26 ing activity of (+/-)syn- and (+/-)anti-7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide (syn- and
28 [a]pyrene-7,8-dione (BP-7,8-dione), and 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione) pot
29 idized by AKR1C4 to the highly reactive 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione), wh
30 ed with exposure to TPA and the mutagen 7,12-dimethylbenz(a)anthracene accelerated SCC development wi
31 When challenged with the carcinogen 7,12-dimethylbenz[a]anthracene, all mice, regardless of genot
33 stage skin carcinogenesis protocol with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-
34 two-stage initiation and promotion with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-
35 effects, BaP and other PAHs, including 7,12-dimethylbenz[a]anthracene and 2,3,7,8-tetrachlorodibenzo
37 ihydroxy-8,9-dihydrobenzo[a]anthracene, 7,12-dimethylbenz[a]anthracene and its cis-5,6-dihydrodiol, 5
38 to chemical carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene and promoted by phorbol 12-myr
39 ls were initiated with 25 micrograms of 7,12-dimethylbenz[a]anthracene and promoted weekly with 5 mic
42 on of preneoplastic lesions (induced by 7,12-dimethylbenz(a)anthracene) and PR expression (with or wi
43 fluoranthene, 3,4-dihydroxy-3,4-dihydro-7,12-dimethylbenz[a]anthracene, and 6-nitrochrysene to apprec
44 protein showed increased sensitivity to 7,12-dimethylbenz(a)anthracene- and benzo(a)pyrene-induced sk
45 o multistage skin carcinogenesis, using 7,12-dimethylbenz(a)anthracene as carcinogen and 12-O-tetrade
46 two-stage carcinogenesis regimen using 7,12-dimethylbenz(a)anthracene as initiator and TPA as promot
47 tage skin carcinogenesis protocol using 7,12-dimethylbenz(a)anthracene as the initiator and 12-O-tetr
48 [a]pyrene, 9,10-dihydro-benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene, benzo[a]pyrene-7,8-dihydrodio
49 tiated by the ras-activating carcinogen 7,12-dimethylbenz(a)anthracene, Bin1 loss strongly accentuate
50 resistant to another aryl hydrocarbon (AH), dimethylbenz[a]anthracene, but not to pleiotropic drugs
51 duced cSCC, where a subclinical dose of 7,12-dimethylbenz[a]anthracene causes oncogenic mutations in
53 by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key f
54 ic mice treated with the chemical carcinogen dimethylbenz(a)anthracene developed tumors with much sho
55 d non-Tg mice by topical application of 7,12-dimethylbenz(a)anthracene did not reveal significant dif
57 the T cell-mediated immune response to 7,12-dimethylbenz(a)anthracene (DMBA) and benzo(a)pyrene in C
58 apillomas in SENCAR mice initiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with 12-O-
59 en K5-PKCalpha mice were initiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with a low
61 perties of complete carcinogens such as 7,12-dimethylbenz(a)anthracene (DMBA) are well known but not
62 mice treated with the initiating agent 7,12-dimethylbenz(a)anthracene (DMBA) developed more papillom
63 and CYP1A1 expression and metabolism of 7,12-dimethylbenz(a)anthracene (DMBA) have been characterized
64 ainst mammary carcinogenesis induced by 7,12-dimethylbenz(a)anthracene (DMBA) in female Sprague Dawle
65 rats with the prototypic xenobiotic PAH 7,12-dimethylbenz(a)anthracene (DMBA) induces mammary tumors
66 mice that were subjected to a two-stage 7,12-dimethylbenz(a)anthracene (DMBA) initiation, 12-O-tetrad
67 n of NQO2-deficient mice was exposed to 7,12-dimethylbenz(a)anthracene (DMBA) or benzo(a)pyrene alone
68 implantation of the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) or transgenic expressio
69 ly lower dose (2 to 5 mug per ovary) of 7,12-dimethylbenz(a)anthracene (DMBA) was applied to the one
72 he metabolism of the mammary carcinogen 7,12-dimethylbenz(a)anthracene (DMBA), as assessed by increas
76 d by polyaromatic hydrocarbons, such as 7,12-dimethylbenz(a)anthracene (DMBA), often harbor an H-ras
78 her AP-1 signaling is also required for 7,12-dimethylbenz(a)anthracene (DMBA)-initiated/OA-promoted s
79 esistant to skin tumor formation by the 7,12-dimethylbenz(a)anthracene (DMBA)-initiation and 12-O-tet
83 nt progression and metastatic spread of 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl-phor
85 e of Hpa-Tg mice to a classical two-stage 12-dimethylbenz(a)anthracene (DMBA)/12-o-tetradecanoylphorb
86 inogenesis [methylcholanthrene (MCA) or 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorb
88 that these mice were also resistant to 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorb
89 compared with wild type (WT) mice in a 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorb
91 ith the polycyclic aromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA; rel-3983D cells) or DMS
92 n of a carcinogen and a tumor promoter (7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylp
93 ncreased survival following exposure to 7,12-dimethylbenz[a]anthracene (DMBA) and enhanced proliferat
94 2(-/-) mice were treated with the carcinogen dimethylbenz[a]anthracene (DMBA) and maintained on HFD.
96 carcinogenic response to initiation by 7,12-dimethylbenz[a]anthracene (DMBA) followed by promotion w
97 are prevalent, potent carcinogens, and 7,12-dimethylbenz[a]anthracene (DMBA) is a model PAH widely u
100 Treatment with the tumor initiator 7,12-dimethylbenz[a]anthracene (DMBA) resulted in a significa
101 marrow stromal cells and the model PAH 7,12-dimethylbenz[a]anthracene (DMBA) results in pre-B cell a
102 offspring were administered 3 doses of 7,12-dimethylbenz[a]anthracene (DMBA) to initiate mammary can
103 with the MMP-9 reporter transgene with 7, 12-dimethylbenz[a]anthracene (DMBA) treatment followed by p
104 5 min before application of 100 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) twice a week for 4 week
106 y, exposure of BU-11/BMS2 cocultures to 7,12-dimethylbenz[a]anthracene (DMBA), a prototypic PAH, down
108 he proximate carcinogenic metabolite of 7,12-dimethylbenz[a]anthracene (DMBA), a widely studied exper
109 ce treated with the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA), AIB1 deficiency protec
110 he K-region of benz[a]-anthracene (BA), 7,12-dimethylbenz[a]anthracene (DMBA), chrysene (CR), benzo[a
111 10(-8) M) of the prototypic AhR ligand, 7,12-dimethylbenz[a]anthracene (DMBA), induce preB cell apopt
112 er exposure to the chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), to which mice carrying
113 to a desensitization to tumor initiator 7,12-dimethylbenz[a]anthracene (DMBA)-induced apoptosis both
114 Previous studies have reported that 7,12-dimethylbenz[a]anthracene (DMBA)-induced bone marrow tox
115 y label-free dark-field microscopy of a 7,12-Dimethylbenz[a]anthracene (DMBA)-induced hamster cheek p
116 Using a well-established mouse model of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcino
117 he chemopreventive effect of SP against 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat breast carc
118 /fl) mice were completely refractory to 7,12 dimethylbenz[a]anthracene (DMBA)-induced skin tumorigene
128 o carcinogen-induced tumor development (7,12-dimethylbenz[a]anthracene, DMBA), and find these mice to
129 ne derivatives of benzo[a]pyrene (BPQ), 7,12-dimethylbenz[a]anthracene (DMBAQ), and benz[a]anthracene
130 served even though the levels of stable 7,12-dimethylbenz(a)anthracene-DNA adducts were increased abo
131 type mice using a single application of 7,12-dimethylbenz(a)anthracene followed by repetitive applica
132 AF1 gene were treated once with 25 nmol 7,12-dimethylbenz[a]anthracene, followed by 5 microg of TPA t
133 from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly higher mam
134 preneoplastic ductal lesions induced by 7,12-dimethylbenz(a)anthracene in these mammary glands (IC50
135 ranscription induced by the aryl hydrocarbon dimethylbenz[a]anthracene in human mammary carcinoma MCF
136 ted the bone marrow ablative effects of 7,12-dimethylbenz[a]anthracene in vivo, demonstrating drug ab
137 sulfone also inhibited the formation of 7,12-dimethylbenz(a)anthracene-induced hyperplastic alveolar
138 ls were highly susceptible to progestin/7,12-dimethylbenz(a)anthracene-induced mammary carcinogenesis
139 homa development and the development of 7,12-dimethylbenz(a)anthracene-induced mammary gland tumors.
140 dose of both drugs required to inhibit 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth i
141 ase, we generated cell line models from 7,12-dimethylbenz(a)anthracene-induced murine primary OSCC ca
143 inbred strain, resistant to developing 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis
144 laced adjacent to mammary tissue in the 7,12-dimethylbenz[a]anthracene-induced rat breast cancer mode
145 increased susceptibility of -/- mice to 7,12-dimethylbenz[a]anthracene-induced skin carcinogenesis an
146 carcinogens indicated that NMU, but not 7,12-dimethylbenz(a)anthracene, initiated the loss of this st
149 rior to that of each TPA application to 7,12-dimethylbenz(a)anthracene-initiated SENCAR mice resulted
150 I or mezerein in stage II tumor promotion in dimethylbenz(a)anthracene-initiated SENCAR mouse skin re
152 uamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetradecan
153 uamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetradecan
155 d in FVB mice by a two-stage regimen of 7,12-dimethylbenz[a]anthracene initiation followed by repetit
156 amous cell carcinoma (mSCC) elicited by 7,12-dimethylbenz(a)anthracene-initiation and 12-O-tetradecan
157 and carcinogenesis protocols, including 7,12-dimethylbenz[a]anthracene-initiation/12-O-tetradecanoylp
158 magnitude of mammary tumor inhibition in the dimethylbenz[a]anthracene model as that produced by 1 mo
160 nsgenic mice with an initiating dose of 7,12-dimethylbenz[a]anthracene only led to the formation of a
161 are caused by exposure to topical carcinogen dimethylbenz(a)anthracene or benzo(a)pyrene (BP) followe
162 of 59) that developed following UVB or 7,12-dimethylbenz(a)anthracene/phorbol 12-myristate 13-acetat
163 two-stage skin carcinogenesis protocol [7,12-dimethylbenz[a]anthracene/phorbol 12-tetradecanoate 13-a
164 evelopment of cancer using a two-stage [7,12-dimethylbenz(a)-anthracene plus 12-O-tetradecanoylphorbo
165 to each other [in both methylnitrosourea and dimethylbenz(a)anthracene rat mammary tumor models].
166 at3 prior to skin tumor initiation with 7,12-dimethylbenz(a)anthracene significantly increased the nu
168 applied following tumor initiation with 7,12-dimethylbenz[a]anthracene, the papilloma and carcinoma r
169 ollowing initiation with the carcinogen 7,12-dimethylbenz[a]anthracene, the transgenic group showed a
170 ice ("UV resistant") and when the hapten was dimethylbenz(a)anthracene, thus indicating that the gene
172 emopreventive activity in the two-stage 7,12-dimethylbenz(a)anthracene/TPA skin carcinogenesis model
173 he stratified squamous epithelia of the 7,12-dimethylbenz(a)anthracene-treated hamster cheek pouch mo
176 fold) in the epidermal keratinocytes of 7,12-dimethylbenz[a]anthracene-treated C/EBPbeta-null mice co
177 n in control, dysplasia, and cancerous 7, 12-dimethylbenz[a]anthracene-treated hamster cheek pouch mu
178 VP-16-induced melanomas in the skin of 7,12-dimethylbenz[a]anthracene-treated mice is found to be si
180 reover, mouse mammary tumors induced by 7,12-dimethylbenz(a)anthracene treatment displayed increased
181 y did not affect the cancer response to 7,12-dimethylbenz[a]anthracene treatment alone but reduced th
182 tic level when exposed to a carcinogen (7,12-dimethylbenz[a]anthracene), which subsequently seem to b