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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 that these mice were also resistant to 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorb
37 compared with wild type (WT) mice in a 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorb
39 ith the polycyclic aromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA; rel-3983D cells) or DMS
40 e with respect to their sensitivity to 7, 12-dimethylbenz(a)anthracene /12-Otetradecanoylphorbol-13-a
41 ed with exposure to TPA and the mutagen 7,12-dimethylbenz(a)anthracene accelerated SCC development wi
43 o multistage skin carcinogenesis, using 7,12-dimethylbenz(a)anthracene as carcinogen and 12-O-tetrade
44 two-stage carcinogenesis regimen using 7,12-dimethylbenz(a)anthracene as initiator and TPA as promot
45 tage skin carcinogenesis protocol using 7,12-dimethylbenz(a)anthracene as the initiator and 12-O-tetr
46 ic mice treated with the chemical carcinogen dimethylbenz(a)anthracene developed tumors with much sho
47 d non-Tg mice by topical application of 7,12-dimethylbenz(a)anthracene did not reveal significant dif
48 type mice using a single application of 7,12-dimethylbenz(a)anthracene followed by repetitive applica
49 from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly higher mam
50 preneoplastic ductal lesions induced by 7,12-dimethylbenz(a)anthracene in these mammary glands (IC50
51 uamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetradecan
52 uamous cell carcinoma (SCC) elicited by 7,12-dimethylbenz(a)anthracene initiation and 12-O-tetradecan
54 are caused by exposure to topical carcinogen dimethylbenz(a)anthracene or benzo(a)pyrene (BP) followe
55 to each other [in both methylnitrosourea and dimethylbenz(a)anthracene rat mammary tumor models].
56 at3 prior to skin tumor initiation with 7,12-dimethylbenz(a)anthracene significantly increased the nu
58 reover, mouse mammary tumors induced by 7,12-dimethylbenz(a)anthracene treatment displayed increased
59 on of preneoplastic lesions (induced by 7,12-dimethylbenz(a)anthracene) and PR expression (with or wi
60 tiated by the ras-activating carcinogen 7,12-dimethylbenz(a)anthracene, Bin1 loss strongly accentuate
62 carcinogens indicated that NMU, but not 7,12-dimethylbenz(a)anthracene, initiated the loss of this st
63 ice ("UV resistant") and when the hapten was dimethylbenz(a)anthracene, thus indicating that the gene
64 protein showed increased sensitivity to 7,12-dimethylbenz(a)anthracene- and benzo(a)pyrene-induced sk
65 served even though the levels of stable 7,12-dimethylbenz(a)anthracene-DNA adducts were increased abo
66 sulfone also inhibited the formation of 7,12-dimethylbenz(a)anthracene-induced hyperplastic alveolar
67 ls were highly susceptible to progestin/7,12-dimethylbenz(a)anthracene-induced mammary carcinogenesis
68 homa development and the development of 7,12-dimethylbenz(a)anthracene-induced mammary gland tumors.
69 dose of both drugs required to inhibit 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth i
70 ase, we generated cell line models from 7,12-dimethylbenz(a)anthracene-induced murine primary OSCC ca
74 rior to that of each TPA application to 7,12-dimethylbenz(a)anthracene-initiated SENCAR mice resulted
75 I or mezerein in stage II tumor promotion in dimethylbenz(a)anthracene-initiated SENCAR mouse skin re
76 amous cell carcinoma (mSCC) elicited by 7,12-dimethylbenz(a)anthracene-initiation and 12-O-tetradecan
77 he stratified squamous epithelia of the 7,12-dimethylbenz(a)anthracene-treated hamster cheek pouch mo
86 -/-) mice were also more susceptible to 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
87 ly with data obtained using the classic 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
88 on was either induced by application of 7,12-Dimethylbenz(a)anthracene/12-O-Tetradecanoylphorbol-13-a
89 k2 in skin neoplasia using the two-step 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
90 d a marked resistance to development of 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
91 neoplastic lesions that arise following 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
92 g p38delta knockout mice to a two-stage 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-a
93 of 59) that developed following UVB or 7,12-dimethylbenz(a)anthracene/phorbol 12-myristate 13-acetat
95 emopreventive activity in the two-stage 7,12-dimethylbenz(a)anthracene/TPA skin carcinogenesis model
96 74% of the BK5.IGF-1 mice treated with 7,12-dimethylbenz[a]anthracene (20 microg/day) developed mamm
97 by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key f
98 n of a carcinogen and a tumor promoter (7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylp
99 ncreased survival following exposure to 7,12-dimethylbenz[a]anthracene (DMBA) and enhanced proliferat
100 2(-/-) mice were treated with the carcinogen dimethylbenz[a]anthracene (DMBA) and maintained on HFD.
102 carcinogenic response to initiation by 7,12-dimethylbenz[a]anthracene (DMBA) followed by promotion w
103 are prevalent, potent carcinogens, and 7,12-dimethylbenz[a]anthracene (DMBA) is a model PAH widely u
104 The polycyclic aromatic hydrocarbon 7,12-dimethylbenz[a]anthracene (DMBA) is a potent carcinogen
106 Treatment with the tumor initiator 7,12-dimethylbenz[a]anthracene (DMBA) resulted in a significa
107 marrow stromal cells and the model PAH 7,12-dimethylbenz[a]anthracene (DMBA) results in pre-B cell a
108 offspring were administered 3 doses of 7,12-dimethylbenz[a]anthracene (DMBA) to initiate mammary can
109 with the MMP-9 reporter transgene with 7, 12-dimethylbenz[a]anthracene (DMBA) treatment followed by p
110 5 min before application of 100 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) twice a week for 4 week
112 y, exposure of BU-11/BMS2 cocultures to 7,12-dimethylbenz[a]anthracene (DMBA), a prototypic PAH, down
114 he proximate carcinogenic metabolite of 7,12-dimethylbenz[a]anthracene (DMBA), a widely studied exper
115 ce treated with the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA), AIB1 deficiency protec
116 he K-region of benz[a]-anthracene (BA), 7,12-dimethylbenz[a]anthracene (DMBA), chrysene (CR), benzo[a
117 10(-8) M) of the prototypic AhR ligand, 7,12-dimethylbenz[a]anthracene (DMBA), induce preB cell apopt
118 er exposure to the chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), to which mice carrying
119 to a desensitization to tumor initiator 7,12-dimethylbenz[a]anthracene (DMBA)-induced apoptosis both
120 Previous studies have reported that 7,12-dimethylbenz[a]anthracene (DMBA)-induced bone marrow tox
121 y label-free dark-field microscopy of a 7,12-Dimethylbenz[a]anthracene (DMBA)-induced hamster cheek p
122 Using a well-established mouse model of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcino
123 he chemopreventive effect of SP against 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat breast carc
124 /fl) mice were completely refractory to 7,12 dimethylbenz[a]anthracene (DMBA)-induced skin tumorigene
134 ne derivatives of benzo[a]pyrene (BPQ), 7,12-dimethylbenz[a]anthracene (DMBAQ), and benz[a]anthracene
135 two-stage initiation and promotion with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-
136 stage skin carcinogenesis protocol with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-
137 effects, BaP and other PAHs, including 7,12-dimethylbenz[a]anthracene and 2,3,7,8-tetrachlorodibenzo
139 ihydroxy-8,9-dihydrobenzo[a]anthracene, 7,12-dimethylbenz[a]anthracene and its cis-5,6-dihydrodiol, 5
140 to chemical carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene and promoted by phorbol 12-myr
141 ls were initiated with 25 micrograms of 7,12-dimethylbenz[a]anthracene and promoted weekly with 5 mic
144 duced cSCC, where a subclinical dose of 7,12-dimethylbenz[a]anthracene causes oncogenic mutations in
145 ranscription induced by the aryl hydrocarbon dimethylbenz[a]anthracene in human mammary carcinoma MCF
146 ted the bone marrow ablative effects of 7,12-dimethylbenz[a]anthracene in vivo, demonstrating drug ab
147 d in FVB mice by a two-stage regimen of 7,12-dimethylbenz[a]anthracene initiation followed by repetit
148 magnitude of mammary tumor inhibition in the dimethylbenz[a]anthracene model as that produced by 1 mo
150 nsgenic mice with an initiating dose of 7,12-dimethylbenz[a]anthracene only led to the formation of a
151 y did not affect the cancer response to 7,12-dimethylbenz[a]anthracene treatment alone but reduced th
152 tic level when exposed to a carcinogen (7,12-dimethylbenz[a]anthracene), which subsequently seem to b
153 Tumors were elicited by the initiation (7,12-dimethylbenz[a]anthracene, 100 nmol)-promotion (TPA, 5 n
154 When challenged with the carcinogen 7,12-dimethylbenz[a]anthracene, all mice, regardless of genot
155 fluoranthene, 3,4-dihydroxy-3,4-dihydro-7,12-dimethylbenz[a]anthracene, and 6-nitrochrysene to apprec
156 [a]pyrene, 9,10-dihydro-benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene, benzo[a]pyrene-7,8-dihydrodio
157 resistant to another aryl hydrocarbon (AH), dimethylbenz[a]anthracene, but not to pleiotropic drugs
158 o carcinogen-induced tumor development (7,12-dimethylbenz[a]anthracene, DMBA), and find these mice to
159 AF1 gene were treated once with 25 nmol 7,12-dimethylbenz[a]anthracene, followed by 5 microg of TPA t
160 applied following tumor initiation with 7,12-dimethylbenz[a]anthracene, the papilloma and carcinoma r
161 ollowing initiation with the carcinogen 7,12-dimethylbenz[a]anthracene, the transgenic group showed a
163 otent proximate carcinogens known (e.g. 7,12-dimethylbenz[a]anthracene-3,4-diol (DMBA-3,4-diol) and b
164 ing activity of (+/-)syn- and (+/-)anti-7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide (syn- and
166 [a]pyrene-7,8-dione (BP-7,8-dione), and 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione) pot
167 idized by AKR1C4 to the highly reactive 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione), wh
168 inbred strain, resistant to developing 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis
169 laced adjacent to mammary tissue in the 7,12-dimethylbenz[a]anthracene-induced rat breast cancer mode
170 increased susceptibility of -/- mice to 7,12-dimethylbenz[a]anthracene-induced skin carcinogenesis an
172 and carcinogenesis protocols, including 7,12-dimethylbenz[a]anthracene-initiation/12-O-tetradecanoylp
174 fold) in the epidermal keratinocytes of 7,12-dimethylbenz[a]anthracene-treated C/EBPbeta-null mice co
175 n in control, dysplasia, and cancerous 7, 12-dimethylbenz[a]anthracene-treated hamster cheek pouch mu
176 VP-16-induced melanomas in the skin of 7,12-dimethylbenz[a]anthracene-treated mice is found to be si
177 Also, skin carcinogen challenge by 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoyl-phorbol-13-
178 time that RhoA is a tumor suppressor in 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol 13-a
179 tes keratinocyte differentiation in the 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
180 d from a two-stage carcinogen bioassay (7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
181 61L))-driven papilloma formation in the 7,12-Dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-a
182 two-stage skin carcinogenesis protocol [7,12-dimethylbenz[a]anthracene/phorbol 12-tetradecanoate 13-a
183 hanges of MnSOD transcription using the 7,12-dimethylbenz(alpha)anthracene (DMBA)/12-O-tetradecanoylp
184 two-stage chemical carcinogenesis protocol (dimethylbenz[alpha]anthracene (DMBA) initiation with 12-
185 moid cells to chemicals/drugs including 7,12-dimethylbenz[alpha]anthracene (mutagen) and camptothecin
186 alGDS-related (Rgr) oncogene in a DMBA (7,12-dimethylbenz[alpha]anthracene)-induced rabbit squamous c
187 mice and wild-type (WT) mice in a DMBA (7,12-dimethylbenz[alpha]anthracene)/TPA (12-O-tetradecanoylph
188 origenesis is initiated by a carcinogen 7,12-dimethylbenz[alpha]anthracene, and then promoted by 12-O
191 skin tumors arising from treatment with 7,12-dimethylbenz[alpha]anthracene/12-o-tetradecanoylphorbol-
192 nalyzed effects of the skin cancer initiator dimethylbenz-anthracene and/or the tumor promoter 12-O-t
193 ramagnetic resonance experiments with [(15)N-dimethylbenz-imidazole]adenosylcobalamin demonstrate bas