ライフサイエンスコーパス: DMBA

1 DMBA alone resulted in low frequency of tumor developmen

2 DMBA implantation to the rat pancreas induces ductal ade

3 DMBA induced characteristic stages of neoplasia at the i

4 DMBA induces characteristic stages of neoplasia in the e

5 DMBA treatment induces an activating mutation in the Har

6 DMBA- or UVB-induced tumors in the VDR-null mice also ov

7 DMBA-DE is known to bind to DNA leading to strand breaks

8 DMBA-induced mutagenesis was additionally combined with

9 DMBA/TPA treatment of Hras(G12V) knock-in mice induced a

10 DMBA/TPA-treated TRAIL-R-deficient mice showed neither a

11 ary isografts; (3) multiple pregnancies; (4) DMBA alone; and (5) DMBA+pituitary isografts.

12 ultiple pregnancies; (4) DMBA alone; and (5) DMBA+pituitary isografts.

13 ified the RalGDS-related (Rgr) oncogene in a DMBA (7,12-dimethylbenz[alpha]anthracene)-induced rabbit

14 genic (TG) mice and wild-type (WT) mice in a DMBA (7,12-dimethylbenz[alpha]anthracene)/TPA (12-O-tetr

15 ncidence and multiplicity of papillomas in a DMBA/TPA multi-stage skin carcinogenesis model.

16 DMBA and that the ultimate death signal is a DMBA metabolite generated by the stromal cells and trans

17 ine IL-1alpha antibody (Ab) nearly abolished DMBA-induced IL-1alpha mRNA (P = 0.0001) in skin and sub

18 LCs rapidly internalize and accumulate DMBA as numerous membrane-independent cytoplasmic foci.

19 )anthracene/phorbol 12-myristate 13-acetate (DMBA/PMA) treatment developed in sites of preexisting hy

20 racene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA) model of skin carcinogenesis.

21 racene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA) skin carcinogenesis model.

22 racene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA)-induced skin carcinogenesis.

23 racene /12-Otetradecanoylphorbol-13-acetate (DMBA/TPA)-induced skin carcinogenesis.

24 racene/phorbol 12-tetradecanoate 13-acetate (DMBA/TPA)], K14.ATF2(f/f) mice showed significant increa

25 Thus, Sdc1-/- mice administered DMBA during juvenile development are resistant not only

26 gene could be detected as early as 1 d after DMBA application.

27 wild-type and TNF-alpha(-/-) epidermis after DMBA treatment, suggesting that TNF-alpha was not involv

28 Mutation frequency after DMBA treatment was threefold higher in Gadd45a-null live

29 rrantly accumulated DNA damage markers after DMBA treatment.

30 f spleen cells in WT and AhR-null mice after DMBA treatment, but not in CYP1B1-null or mEH-null mice.

31 bers of apoptotic cells in the KO mice after DMBA/TPA treatment.

32 r(1987)), and ATR levels were observed after DMBA treatment in WT, p53-null, and AhR-null mice but no

33 Again, DMBA/PMA-induced tumor formation was less (71% versus 89

34 sults demonstrate that NQO2 protects against DMBA- and benzo(a)pyrene-induced skin carcinogenesis and

35 in vivo chemopreventive effect of SP against DMBA-induced breast carcinogenesis in rat, supporting it

36 on of TGF-beta signaling through Smad2/3 and DMBA treatment.

37 Therefore, lack of basal and DMBA-induced Gadd45a may result in enhanced tumorigenesi

38 By contrast, BP and DMBA each suppressed tumor multiplicity in the absence o

39 H-ras mutations at codon 61 in the DMBA and DMBA/TPA models, respectively, as well as a significant

40 ate proximal to oncogenic Hras mutation, and DMBA-treated LC-deficient skin contained significantly f

41 Tgfbr1 cKO mice 4 weeks after tamoxifen and DMBA treatment.

42 Tumors and 7 x TPA-treated and DMBA-TPA-treated (6 weeks) skins from EP2 TG mice produc

43 excision repair, which repairs both UV- and DMBA-induced DNA lesions, was substantially reduced in G

44 notype after 7,12-dimethylbenz(a)anthracene (DMBA) administration.

45 response to 7,12-dimethylbenz(a)anthracene (DMBA) and benzo(a)pyrene in C3H/HeN mice and resulted in

46 itiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with a low dose of TPA, 58% of K5-PKC

47 itiated with 7,12-dimethylbenz(a)anthracene (DMBA) applied on to the dorsal skin followed by twice we

48 gens such as 7,12-dimethylbenz(a)anthracene (DMBA) are well known but not the mechanism of DMBA-media

49 iating agent 7,12-dimethylbenz(a)anthracene (DMBA) developed more papillomas than like-treated nontra

50 s induced by 7,12-dimethylbenz(a)anthracene (DMBA) in female Sprague Dawley rats.

51 nobiotic PAH 7,12-dimethylbenz(a)anthracene (DMBA) induces mammary tumors with an invasive phenotype.

52 a two-stage 7,12-dimethylbenz(a)anthracene (DMBA) initiation, 12-O-tetradecanoylphorbol-13-acetate (

53 s exposed to 7,12-dimethylbenz(a)anthracene (DMBA) or benzo(a)pyrene alone (complete carcinogen) or w

54 l carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) or transgenic expression of mutant Kras.

55 er ovary) of 7,12-dimethylbenz(a)anthracene (DMBA) was applied to the one ovary to maximally preserve

56 duction with 7,12-dimethylbenz(a)anthracene (DMBA), 45% of Tgfbr1 conditional knockout (cKO) mice (n

57 7,12-Dimethylbenz(a)anthracene (DMBA), but not benzo(a)pyrene (BP), depletes BM hematopo

58 at mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), cisplatin and etoposide induce nuclear DNA leakag

59 ith 200 nmol 7,12-dimethylbenz(a)anthracene (DMBA), mice were promoted with 12-O-tetradecanoylphorbol

60 ons, such as 7,12-dimethylbenz(a)anthracene (DMBA), often harbor an H-ras point mutation, suggesting

61 rats with 7, 12-dimethyl benz(a)anthracene (DMBA)-induced breast cancer decreased tumor volume signi

62 required for 7,12-dimethylbenz(a)anthracene (DMBA)-initiated/OA-promoted skin tumorigenesis.

63 ation by the 7,12-dimethylbenz(a)anthracene (DMBA)-initiation and 12-O-tetradecanoylphorbol-13-acetat

64 hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA).

65 l carcinogen 7,12-dimethylbenz(a)anthracene (DMBA).

66 th the carcinogen dimethylbenz(a)anthracene (DMBA).

67 ic spread of 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induce

68 he two-stage 7,12-dimethylbenz(a)anthracene (DMBA)/12-o-tetradecanoylphorbol-13-acetate (TPA) model o

69 ene (MCA) or 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) models]

70 ponse to the 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) mouse s

71 ical two-stage 12-dimethylbenz(a)anthracene (DMBA)/12-o-tetradecanoylphorbol-13-acetate (TPA) protoco

72 T) mice in a 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) two-sta

73 resistant to 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced

74 Two-stage [7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)] skin c

75 hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA; rel-3983D cells) or DMSO vehicle (rel-3983V cells)

76 or promoter (7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA), re

77 nogens 9,10-di-methyl-1,2-benz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA).

78 exposure to 7,12-dimethylbenz[a]anthracene (DMBA) and enhanced proliferation following exposure to 1

79 th the carcinogen dimethylbenz[a]anthracene (DMBA) and maintained on HFD.

80 inogens, and 7,12-dimethylbenz[a]anthracene (DMBA) is a model PAH widely used to study tumorigenesis.

81 or initiator 7,12-dimethylbenz[a]anthracene (DMBA) resulted in a significant increase in the number o

82 he model PAH 7,12-dimethylbenz[a]anthracene (DMBA) results in pre-B cell apoptosis.

83 d 3 doses of 7,12-dimethylbenz[a]anthracene (DMBA) to initiate mammary cancer.

84 nsgene with 7, 12-dimethylbenz[a]anthracene (DMBA) treatment followed by phorbol 12 myristate 13-acet

85 100 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) twice a week for 4 weeks (complete carcinogenesis

86 ocultures to 7,12-dimethylbenz[a]anthracene (DMBA), a prototypic PAH, down-regulated nuclear Rel A an

87 7,12-Dimethylbenz[a]anthracene (DMBA), a prototypical polycyclic aromatic hydrocarbon, a

88 l carcinogen 7,12-dimethylbenz[a]anthracene (DMBA), AIB1 deficiency protected the mammary gland, but

89 carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), to which mice carrying defective nucleotide excis

90 induced with 7,12-dimethybenz[a]anthracene (DMBA), whereas the Wistar Furth (WF) strain is susceptib

91 or initiator 7,12-dimethylbenz[a]anthracene (DMBA)-induced apoptosis both in vivo epidermis and in vi

92 eported that 7,12-dimethylbenz[a]anthracene (DMBA)-induced bone marrow toxicity is p53-dependent in v

93 roscopy of a 7,12-Dimethylbenz[a]anthracene (DMBA)-induced hamster cheek pouch model of oral squamous

94 use model of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis we found a marked a

95 f SP against 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat breast carcinogenesis, and further stu

96 efractory to 7,12 dimethylbenz[a]anthracene (DMBA)-induced skin tumorigenesis and these mice displaye

97 itiated with 7,12-dimethylbenz[a]anthracene (DMBA).

98 carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA).

99 totypic PAH, 7,12-dimethylbenz[a]anthracene (DMBA).

100 essive agent 7,12 Dimethylbenz[a]anthracene (DMBA).

101 t carcinogen 7,12-dimethylbenz[a]anthracene (DMBA).

102 d by the PAH 7,12-dimethylbenz[a]anthracene (DMBA).

103 ototypic PAH 7,12-dimethylbenz[a]anthracene (DMBA).

104 e model PAH, 7,12-dimethylbenz[a]anthracene (DMBA).

105 ponse to the 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate mouse skin ca

106 sing the 7,12-dimethylbenz(alpha)anthracene (DMBA)/12-O-tetradecanoylphorbol-l3-acetate (TPA) multist

107 sis protocol (dimethylbenz[alpha]anthracene (DMBA) initiation with 12-ortho-tetradecanoylphorbol-13-a

108 development (7,12-dimethylbenz[a]anthracene, DMBA), and find these mice to be resistant to tumorigene

109 ediated immune response to topically applied DMBA.

110 e an appropriate oncogenic stimulus, such as DMBA treatment, to reveal their increased susceptibility

111 Injecting anti-IL-1alpha Ab before DMBA applications significantly (P < 0.04) decreased the

112 skin treatment with dimethyl benzanthracene (DMBA) and tetradecanoyl-phorbol acetate (TPA).

113 romoter model using dimethyl benzanthracene (DMBA), followed by repeated treatments of 12-O-tetradeca

114 s tumors in 9,10-dimethyl-1,2-benzanthracene(DMBA)-initiated mice.

115 Both DMBA and TCDD caused a dramatic increase in the amount o

116 tumor incidence and reduced latency in both DMBA-induced and MMTV-Erbb2/Neu mouse mammary tumor mode

117 K14E5 mice treated with both DMBA and TPA to induce large numbers of papillomas had a

118 intrinsic apoptotic pathway is activated by DMBA and that the ultimate death signal is a DMBA metabo

119 tal of 25 mice), and 94% of those induced by DMBA (a total of 16 mice) possessed a -CAA- to -CTA- mut

120 Pancreatic adenocarcinomas induced by DMBA in rats express markers consistent with a ductal ph

121 it to levels much lower than that induced by DMBA.

122 ent and susceptibility to tumor induction by DMBA.

123 kines and growth factors, is up-regulated by DMBA and contributes to inflammation and carcinogenesis.

124 d CK2 and downstream targets AhR and Slug by DMBA induces EMT; EGCG can inhibit this signaling.

125 Progenitor suppression by DMBA, therefore, occurs with minimal effects on the gene

126 that IL-1alpha is induced by a carcinogenic DMBA dose and contributes to DMBA-induced inflammation a

127 al exposure of SENCAR mice to a carcinogenic DMBA dose indeed triggers significant increases in mouse

128 Cyp1b1 deletion did not affect circulating DMBA and metabolites.

129 we examined the role of IL-17 in the classic DMBA/TPA-induced skin carcinogenesis model.

130 Remarkably, SP cleared DMBA-induced rat mammary tumors, which was clearly confi

131 Conversely, DMBA/TPA-induced tumor formation was greatly attenuated

132 A549 cell lysates were found to convert DMBA-3,4-diol to the corresponding o-quinone.

133 viously shown that PEMs from mice bearing D1-DMBA-3 mammary tumors (T-PEM) are deficient in inflammat

134 impaired in macrophages from mice bearing D1-DMBA-3 tumors.

135 t be partially responsible for the decreased DMBA-induced mammary tumor initiation and progression in

136 pical chemical [9,10-dimethylbenzanthracene (DMBA) and phorbol 12-myristate 13-acetate (PMA)] applica

137 en treated with 7,12 dimethylbenzanthracene (DMBA) or UVB, they develop skin tumors, including some c

138 f Min mice with 7,12-dimethylbenzanthracene (DMBA) doubled both tumor multiplicity and size within 20

139 igenesis, using 7,12-dimethylbenzanthracene (DMBA).

140 ubjected to the 7,12-dimethylbenzanthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate two-stage ski

141 with the carcinogens dimethylbenzanthracene (DMBA) or 2,3,5,7-tetrachlorodibenzo-p-dioxin (TCDD), was

142 duced photoproducts, dimethylbenzanthracene (DMBA) carcinogenesis was investigated because this agent

143 s ability to prevent dimethylbenzanthracene (DMBA)-induced mammary cancers, presumably by inhibiting

144 er, upon exposure to dimethylbenzanthracene (DMBA), the vhl heterozygous fish showed an increase in t

145 N,N-Dimethylbenzylamide (DMBA) was used as a switchable solvent and converted to

146 .g. 7,12-dimethylbenz[a]anthracene-3,4-diol (DMBA-3,4-diol) and benzo[g]chrysene-11,12-diol).

147 nd 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione) potently inhibited (IC(50) values 3-5 mi

148 ve 7,12-dimethylbenz[a]anthracene-3,4-dione (DMBA-3,4-dione), which was trapped in situ as its mono-

149 High-dose DMBA cytotoxicity may be associated with p53-independent

150 c cancer precursor lesions induced by either DMBA or mutant Kras was greatly reduced in rpS6(P-/-) mi

151 PRAK deficiency in mice enhances DMBA-induced skin carcinogenesis, coinciding with compro

152 atricellular protein osteopontin facilitates DMBA/TPA-induced cutaneous carcinogenesis most likely th

153 Abs developed more H-ras mutations and fewer DMBA-specific cytotoxic T lymphocytes.

154 ld (P = 0.001) 24 h and 48 h after the fifth DMBA exposure, respectively.

155 se in serum was evident 24 h after the first DMBA application, whereas that in skin required five DMB

156 Compared with control fish, DMBA-treated vhl heterozygous fish also showed an increa

157 Five DMBA applications (200 nmol each) caused a statistically

158 lication, whereas that in skin required five DMBA doses and became statistically significant (P < 0.0

159 both wild-type and Mek2-null mice following DMBA/TPA treatment.

160 hts into the requirement of genotoxicity for DMBA-induced immunosuppression in vivo and highlights th

161 of myeloid progenitors (6 h) occurs only for DMBA.

162 Rats were phenotyped for DMBA-induced mammary carcinomas and genotyped using micr

163 tly, we reported that CYP1B1 is required for DMBA-induced lymphoblastoma formation in vivo.

164 bolite (DMBA-DE) is probably responsible for DMBA-induced immunosuppression.

165 CD4(+) T cells from DMBA contact-sensitized mice preferentially produced int

166 n of Rel A or c-Rel rescued BU-11 cells from DMBA-induced apoptosis.

167 DNA adduct analysis of keratinocytes from DMBA-initiated CD34KO mice revealed that DMBA was metabo

168 Further, DMBA sensitization raised Mut H-ras epitope-specific CTL

169 Furthermore, DMBA-3,4-dihydrodiol-1,2-epoxide, a DNA-reactive metabol

170 significantly higher ( approximately 50%) in DMBA-treated congenics homozygous and heterozygous for t

171 e molecular events that precede apoptosis in DMBA-treated 70Z/3 cells, a pre-B cell line.

172 ndent pathway for activation of apoptosis in DMBA-treated pre-B cells.

173 cated a greater number of apoptotic cells in DMBA-treated skin and papillomas from osteopontin-null v

174 ed that the number of proliferating cells in DMBA/TPA-treated mouse skin were higher in the KO mice.

175 pithelial to mesenchymal transition (EMT) in DMBA-treated NF-kappaB c-Rel-driven mammary tumor cells

176 enhances the expression of genes involved in DMBA metabolism and increases DMBA-induced DNA damage in

177 (-/-) mice, implicating the CXCR3 pathway in DMBA/TPA-induced epidermal inflammation and proliferatio

178 activation that plays a predominant role in DMBA-initiated skin carcinogenesis.

179 ve compound 7l was also estimated in-vivo in DMBA induced mammary tumor in female Sprague-Dawley rats

180 r incidence, body weight and tumor volume in DMBA-induced rats.

181 rigenesis and these mice displayed increased DMBA-induced apoptosis in epidermal keratinocytes compar

182 es involved in DMBA metabolism and increases DMBA-induced DNA damage in keratinocytes.

183 nation generated specific CTLs and inhibited DMBA-induced tumor initiation, growth, and progression i

184 In HepG2 human hepatoma cells, DBM inhibited DMBA- and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-ind

185 ed mammary cancers, presumably by inhibiting DMBA activation, and was highly effective.

186 e of the 7-oxa-7,8-dihydro-RAs in inhibiting DMBA-initiated and TPA-promoted mouse-skin papillomas.

187 um-based N,N-dimethylbenzylamine complex (La(DMBA)(3)) as a precatalyst is reported.

188 are induced by carcinogenic chemicals, like DMBA, could be a means of preventing skin cancers caused

189 oduce the appreciable amounts of bone marrow DMBA dihydrodiol epoxide DNA adducts present in wild-typ

190 The ability to measure DMBA-3,4-dione formation in A549 cells implicates the AK

191 DMBA-3,4-dihydrodiol-1,2-epoxide metabolite (DMBA-DE) is probably responsible for DMBA-induced immuno

192 LCs efficiently metabolized DMBA to DMBA-trans-3,4-diol, an intermediate proximal to

193 nocytes expressing activated Ha-Ras to mimic DMBA-initiated epidermis, ODC and CDK4 protein levels we

194 Moreover, DMBA-trans-3,4-diol application bypassed tumor resistanc

195 ype littermates were initiated with 100 nmol DMBA and then promoted twice weekly with 5 nmol TPA.

196 sis protocol using repetitive application of DMBA alone was applied.

197 adducts formed after topical application of DMBA are sufficient to account for the tumor-initiating

198 f IFN-gamma following topical application of DMBA, whereas IL-17 was elevated in C3H/HeJ mice.

199 adducts formed after topical application of DMBA.

200 epared mono- and bis-thioether conjugates of DMBA-3,4-dione.

201 45a were injected with a single i.p. dose of DMBA at 10-14 days of age.

202 In wild-type mice, this dose of DMBA induced a >5-fold increase in Gadd45a transcript in

203 Increasing the initiating dose of DMBA to 400 nmol resulted in tumor development in the CD

204 lls to DMBA-induced apoptosis at the dose of DMBA we used contributes to the delayed tumorigenesis of

205 treated in three arms of different doses of DMBA alone or followed by hormone administration.

206 munosuppression is p53-dependent at doses of DMBA that produce immunosuppression in the absence of cy

207 induced by both bay-region diol epoxides of DMBA lead to the mutation at codon 61 of H-ras and, cons

208 bolically formed bay-region diol epoxides of DMBA, and we have also analyzed mutations in the H-ras g

209 t CYP1B1 is responsible for the formation of DMBA dihydrodiol epoxides in the bone marrow.

210 sis may, therefore, arise from generation of DMBA metabolites by Cyp1b1 in the developing tumors.

211 ansformation by oncogenic ras (a hallmark of DMBA initiation) or TPA exposure induced all CXCR2 ligan

212 H-ras mutation is normally a hallmark of DMBA-TPA-induced skin tumors, but 70% of carcinomas from

213 Additionally, the genotoxic impact of DMBA on human keratinocytes was significantly increased

214 , this study substantiates the importance of DMBA dihydrodiol epoxide generation at the site of cance

215 et genes responsible for TAM67 inhibition of DMBA-TPA-induced tumorigenesis.

216 sed epidermal turnover, leading to a loss of DMBA-initiated label-retaining keratinocytes.

217 MBA) are well known but not the mechanism of DMBA-mediated tumor promotion.

218 previously been implicated as a mediator of DMBA/TPA-induced skin carcinogenesis.

219 Cyp1b1 metabolism of DMBA and endogenous oxygenation products may each affect

220 ol-1,2-epoxide, a DNA-reactive metabolite of DMBA, was sufficient to upregulate p53, induce caspase-9

221 els further increased in the mitochondria of DMBA/TPA treated mice, and this increase was much greate

222 mice was treated with one dose of 10 nmol of DMBA.

223 plays an important role in the prevention of DMBA skin tumorigenesis and that this is associated with

224 prove to be beneficial in the prevention of DMBA-induced cutaneous tumors.

225 expression of Nfatc1 suppresses the rate of DMBA/TPA-induced skin tumorigenesis.

226 nitiated tumorigenesis via the regulation of DMBA metabolism.

227 Gel shift analysis showed suppression of DMBA-induced NF-kappaB activation by resveratrol.

228 ithelial marker E-cadherin on the surface of DMBA-induced in situ cancers.

229 After 16 weeks of DMBA-treatment, Cav-1 null mice showed a 10-fold increas

230 Coexpression of c-Rel and CK2, or DMBA exposure induced the aryl hydrocarbon receptor (AhR

231 itchable solvent and converted to protonated DMBA form by the addition of dry ice.

232 cyclooxygenase 2) differed in two respects; DMBA responses were low and BP responses declined extens

233 ice using fetal liver LC-precursors restores DMBA-induced tumor susceptibility.

234 r to subjecting them to a standard two-stage DMBA/12-O-tetradecanoylphorbol-13-acetate cutaneous carc

235 mice were subjected to a standard two-stage DMBA/TPA cutaneous carcinogenesis protocol, the percenta

236 d carcinoma formation induced by a two-stage DMBA/TPA protocol, while littermate controls developed b

237 st tumor-resistant phenotype in the standard DMBA/PMA 2-stage carcinogenesis model of skin papilloma

238 hereas treatment with resveratrol suppressed DMBA-induced ductal carcinoma.

239 results suggest that resveratrol suppresses DMBA-induced mammary carcinogenesis, which correlates wi

240 roximately 10-fold greater tumor burden than DMBA/TPA-treated WT-controls.

241 mammary epithelium to a greater extent than DMBA exposure alone.

242 ce in NQO2-/- mice but to a less extent than DMBA.

243 We also demonstrated that DMBA activated PKR, an interferon-inducible protein kina

244 vo immune function studies demonstrated that DMBA-induced splenic immunosuppression is p53-dependent

245 ing caspase inhibitors, we demonstrated that DMBA-mediated pre-B cell apoptosis is dependent on activ

246 logical analysis of the tumors revealed that DMBA induced ductal carcinomas and focal microinvasion i

247 rom DMBA-initiated CD34KO mice revealed that DMBA was metabolically activated into carcinogenic diol

248 Our laboratory has shown that DMBA-induced splenic immunosuppression is CYP1B1- and mi

249 These results suggest that DMBA activates p53 in a CYP1B1- and mEH-dependent manner

250 vicins in H-ras mutations at codon 61 in the DMBA and DMBA/TPA models, respectively, as well as a sig

251 In the DMBA-induced tumour model, Bcl11a deletion substantially

252 rial membrane potential did not occur in the DMBA/stromal cell-induced pathway, cytochrome c release

253 A model; however, CXCR3 was important in the DMBA/TPA model where gene deletion reduced the incidence

254 phenylcarbazone (DPC) and extracted into the DMBA phase.

255 d to increase nebulization efficiency of the DMBA phase.

256 Comparison of the DMBA-treated ovaries with the contralateral control orga

257 sis revealed that resveratrol suppressed the DMBA-induced cyclooxygenase-2 and matrix metalloprotease

258 lase (mEH)-dependent, demonstrating that the DMBA-3,4-dihydrodiol-1,2-epoxide metabolite (DMBA-DE) is

259 Both observations imply that the DMBA-induced tumor precursor cells are drawn from the st

260 Application of in vivo stress using the DMBA/TPA skin carcinogenesis protocol revealed that comb

261 These data indicate that this DMBA animal model gives rise to ovarian lesions that clo

262 Thus, DMBA treatment of c-Rel-transformed mammary tumor cells

263 nhanced sensitivity of Brca2 mutant cells to DMBA-induced apoptosis at the dose of DMBA we used contr

264 a carcinogenic DMBA dose and contributes to DMBA-induced inflammation and volume of CAs, hallmarks o

265 LCs efficiently metabolized DMBA to DMBA-trans-3,4-diol, an intermediate proximal to oncogen

266 Each progenitor responded equally to DMBA and BP in congenic mice expressing the PAH-resistan

267 Exposure to DMBA and TPA activated p53 and decreased MnSOD expressio

268 ells in allergic contact hypersensitivity to DMBA and that CD4(+) T cells have an inhibitory role and

269 ) mice, allergic contact hypersensitivity to DMBA was reduced compared with wild-type (WT) C3H/HeN mi

270 were far more sensitive than control mice to DMBA/TPA treatment, exhibiting a 10-fold increase in the

271 Lkb1(+/-) mice are highly prone to DMBA-induced squamous cell carcinoma (SCC) of the skin a

272 ency period of tumor development relative to DMBA-treated animals.

273 ll mice were found to be highly resistant to DMBA-induced carcinogenesis.

274 C-deficient skin was relatively resistant to DMBA-induced DNA damage.

275 K14-survivin mice were resistant to DMBA-induced keratinocyte apoptosis.

276 e marrow, are almost completely resistant to DMBA-induced skin carcinogenesis compared with their wil

277 ted gene, C/EBP delta, were not resistant to DMBA-induced skin tumorigenesis, indicating a unique rol

278 They were also resistant to DMBA-mediated toxicity.

279 Paradoxically, few genes responded to DMBA, whereas 12 times more responded to BP.

280 e deficient of BRCA2, were more sensitive to DMBA-induced apoptosis, than were Brca2+/+ mouse cells a

281 of TC-PTP increased epidermal sensitivity to DMBA-induced apoptosis and it decreased TPA-mediated hyp

282 ecific Lkb1 deletion are also susceptible to DMBA-induced SCC and develop spontaneous SCC with long l

283 Moreover, before the development of tumors, DMBA-treatment induced severe epidermal hyperplasia in C

284 ge chemical carcinogenesis experiments using DMBA as the tumor initiator and TPA as the promoter, K5.

285 m previous skin carcinogenesis studies using DMBA as the initiating agent, Ras mutations where found

286 In vitro, DMBA-3,4-diol was oxidized by AKR1C4 to the highly react

287 Moreover, in vivo DMBA treatment led to increased incidence of B cell mali

288 ely resistant to skin tumor development when DMBA was used as the initiator and TPA as the promoter.

289 significantly increased tumor frequency with DMBA + TPA when compared with their wild-type littermate

290 cells with fluasterone after induction with DMBA or TCDD failed to decrease enzyme activity, indicat

291 and WT mice treated with TPA thrice or with DMBA followed by TPA for 11 weeks showed a similar incre

292 ontributes oxidative signaling not seen with DMBA.

293 nesis, mice were treated once topically with DMBA followed by twice weekly with PMA for 32 weeks.

294 Nod2(-/-) mice treated with DMBA and maintained on HFD gain significantly more weigh

295 rived at the N10 generation was treated with DMBA, and the COP homozygous rats developed 1.5 +/- 0.3

296 , and the female offspring were treated with DMBA.

297 ls isolated from wild-type mice treated with DMBA/TPA restored wild-type levels of epidermal prolifer

298 A series of trans-(FcC(2n))Ru(2)(Y-DMBA)(4)(C(2m)Fc) with n, m = 1 and 2 and Y-DMBA as N,N'

299 al studies indicate that the (-C(2n))Ru(2)(Y-DMBA)(4)(C(2m-) fragments are among the most efficient m

300 -DMBA)(4)(C(2m)Fc) with n, m = 1 and 2 and Y-DMBA as N,N'-dimethylbenzamidinate or N,N'-dimethyl-(3-m