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

23 racene/12-O-tetradecanoylphorbol-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 Although DMBA did not directly cause apoptosis in pre-B cells, do

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 7,12-Dimethylbenz(a)anthracene (DMBA), but not benzo(a)pyrene (BP), depletes BM hematopo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 100 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) twice a week for 4 weeks (complete carcinogenesis

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

85 7,12-Dimethylbenz[a]anthracene (DMBA), a prototypical polycyclic aromatic hydrocarbon, a

86 etabolite of 7,12-dimethylbenz[a]anthracene (DMBA), a widely studied experimental prototype for the p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 ediated immune response to topically applied DMBA.

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

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

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

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

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

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

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

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

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

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

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

120 majority of murine mammary tumors induced by DMBA.

121 ent and susceptibility to tumor induction by DMBA.

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

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

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

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

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

127 Cyp1b1 deletion did not affect circulating DMBA and metabolites.

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

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

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

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

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

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

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

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

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

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

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

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

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

141 e exposed to the PAH dimethylbenzanthracene (DMBA) or 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 the host-strain's underlying propensity for DMBA-induced ovarian neoplasms, our studies underscore t

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

164 1B1, and not AhR activation, is required for DMBA-induced pre-B-cell apoptosis.

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

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

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

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

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

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

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

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

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

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

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

176 del that mEH is a key genetic determinant in DMBA carcinogenesis through its role in production of th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 adducts formed after topical application of DMBA.

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

202 45a were injected with a single i.p. dose of DMBA at 10-14 days of age.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 n of the ultimate carcinogenic metabolite of DMBA, the 3,4-diol-1,2-epoxide.

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

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

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

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

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

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

228 nitiated tumorigenesis via the regulation of DMBA metabolism.

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

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

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

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

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

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

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

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

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

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

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

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

241 otent in effecting pre-B-cell apoptosis than DMBA, whereas the potent AhR agonist 2,3,7,8-tetrachloro

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

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

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

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

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

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

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

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

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

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

252 The DMBA 3,4-dihydrodiol metabolite was more potent in effec

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 They were also resistant to DMBA-mediated toxicity.

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

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

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 cer chemoprevention study was conducted with DMBA-treated female Sprague Dawley rats.

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

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

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

293 ontributes oxidative signaling not seen with DMBA.

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

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