ライフサイエンスコーパス: tumor promotion

1 1 and IL-6 levels, which have been linked to tumor promotion.

2 O-tetradecanoylphorbol-13-acetate (TPA) skin tumor promotion.

3 ls in human tumors, plays important roles in tumor promotion.

4 nvolved in hormone release, mitogenesis, and tumor promotion.

5 s that c-src plays an important role in skin tumor promotion.

6 thway and that it plays an important role in tumor promotion.

7 uirement for AP-1-dependent transcription in tumor promotion.

8 known but not the mechanism of DMBA-mediated tumor promotion.

9 ng that NF-kappaB activation is required for tumor promotion.

10 with wild-type littermates after 23 weeks of tumor promotion.

11 2) expression plays an important role in UVB tumor promotion.

12 tion of COX-2 plays a functional role in UVB tumor promotion.

13 -induced signal transduction associated with tumor promotion.

14 giogenesis, and they may even have a role in tumor promotion.

15 NF-alpha is important to the early stages of tumor promotion.

16 tors play in specific biological pathways of tumor promotion.

17 effect against both stage I and stage II of tumor promotion.

18 TPA-caused changes that are associated with tumor promotion.

19 ts protein kinase C (PKC), a key mediator of tumor promotion.

20 ed capillary formation and thereby aid in KS tumor promotion.

21 nteract with alcohol and tobacco exposure in tumor promotion.

22 nt in curry, suppresses tumor initiation and tumor promotion.

23 del for studying the mechanism of late-stage tumor promotion.

24 other erbB family members in the process of tumor promotion.

25 uppressed, suggesting involvement of PKD1 in tumor promotion.

26 y initiated cells die early in the course of tumor promotion.

27 hich is considered to play a crucial role in tumor promotion.

28 lonic secondary bile acids relevant to colon tumor promotion.

29 y in cell proliferation, differentiation and tumor promotion.

30 ation of TIMP-1, as observed in patients, on tumor promotion.

31 l-autonomous contributions were required for tumor promotion.

32 turn ERK functions from tumor suppression to tumor promotion.

33 that prolactin is etiologically important in tumor promotion.

34 suppression are also required for mutant p53 tumor promotion.

35 h advantage allowing clonal expansion during tumor promotion.

36 2)), important mediators of inflammation and tumor promotion.

37 ously unrecognized mechanism of AHR-mediated tumor promotion.

38 o many adverse biological effects, including tumor promotion.

39 E7 oncogene (K14-HPV16-E7), show E7-enhanced tumor promotion.

40 dation leads to uncontrolled cell growth and tumor promotion.

41 , an important mediator for inflammation and tumor promotion.

42 t this modulation is potentially involved in tumor promotion.

43 own to be mitogenic and therefore capable of tumor promotion.

44 onal markers and other novel markers of skin tumor promotion.

45 conventional as well as novel biomarkers of tumor promotion.

46 nown to progress through a step often called tumor promotion.

47 ked to increased epithelial apoptosis during tumor promotion.

48 uggest that NQO2 protection might be against tumor promotion.

49 velopment and pathological processes such as tumor promotion.

50 r clonal expansion of initiated cells during tumor promotion.

51 r (EGFR) in modulating Stat3 activity during tumor promotion.

52 rane translocation, whereas the inhibitor of tumor promotion 12-deoxyphorbol 13-phenylacetate, which

53 and theaflavins may further explain the anti-tumor promotion action of these tea constituents.

54 ber of genes with no apparent direct role in tumor promotion also sustain deletion as a result of chr

55 is usually dysregulated at some point during tumor promotion, an early stage of carcinogenesis.

56 a new paradigm for cancer cell survival and tumor promotion and a mechanistic link between ssDNA, DS

57 SASP), a pro-inflammatory response linked to tumor promotion and aging.

58 sively as an in vitro model for the study of tumor promotion and anti-tumor promotion, to study the a

59 ever, the potential role of JNK in mediating tumor promotion and carcinogenesis is unclear.

60 te to a variety of human disorders including tumor promotion and carcinogenesis.

61 t genes provides a novel strategy to inhibit tumor promotion and carcinogenesis.

62 w, we discuss the mechanisms of MSC-mediated tumor promotion and evaluate cell-stromal interactions b

63 critical event in cancer pathogenesis, with tumor promotion and immune evasion proving dominant in c

64 te an important role for macrophages in lung tumor promotion and indicate that these cells have disti

65 duced signal transduction may be involved in tumor promotion and induction of apoptosis.

66 on of cyclooxygenase-2, which is involved in tumor promotion and inflammation, were dose-dependently

67 morigenesis, albeit with variable degrees of tumor promotion and latency.

68 r AP-1 (activator protein-1) is required for tumor promotion and maintenance of malignant phenotype.

69 bset of AP-1-dependent genes is required for tumor promotion and may be targeted for cancer preventio

70 synthase-2, and other genes associated with tumor promotion and metastasis.

71 n (STATs), particularly Stat3, in mouse skin tumor promotion and multistage carcinogenesis.

72 een suggested that autophagy plays a role in tumor promotion and progression downstream oncogenic pat

73 ic Ha-ras codon 12 mutation is important for tumor promotion and progression.

74 inflammation and volume of CAs, hallmarks of tumor promotion and progression.

75 ction, which in turn could have a bearing on tumor promotion and progression.

76 pression through p38alpha inactivation leads tumor promotion and progression.

77 ave recently emerged as important players in tumor promotion and progression.

78 ht be functionally significant parameters of tumor promotion and progression.

79 been considered to play an important role in tumor promotion and progression.

80 n of genes regulating susceptibility to lung tumor promotion and pulmonary chemopreventative agents t

81 e complex role of the necroptotic pathway in tumor promotion and suppression and in metastasis.

82 ckade of TAM influx in this setting disrupts tumor promotion and sustains a more durable therapeutic

83 basal epithelial cells leads to spontaneous tumor promotion and that up-regulation of both mitogenic

84 C (PKC) isozymes have been widely linked to tumor promotion and the development of a metastatic phen

85 4/80(+)Foxp3(+) macrophages are important in tumor promotion and the induction of T reg cell conversi

86 ator protein 1 (AP-1) has a critical role in tumor promotion, and blocking of tumor promoter-induced

87 ing cell growth, differentiation, apoptosis, tumor promotion, and carcinogenesis.

88 cluding cell proliferation, differentiation, tumor promotion, and cell death.

89 opic responses, including liver hypertrophy, tumor promotion, and induction of genes encoding drug-me

90 ta1-responsive genes, which are required for tumor promotion, and through mediating TGF-beta1-induced

91 , and thus, diminished epidermal response to tumor promotion, and ultimately, two-stage skin carcinog

92 ggest that the gene dosage of Ki-ras affects tumor promotion at an early stage of mammary tumor progr

93 establishment, thus also implicating DEK in tumor promotion at later stages.

94 d AP-1 activation is known to play a role in tumor promotion, both p38 and ERK could be potential tar

95 BxD27 mice are sensitive to TPA skin tumor promotion but carry the C57BL/6 allele of Psl1.

96 cal retinoids exhibit suppressive effects on tumor promotion, but have no effect on tumor initiation.

97 cts of PKCdelta overexpression on mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate

98 essential downstream effectors of mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate

99 ene were examined for responsiveness to skin tumor promotion by 7,12-dimethylbenz[a]anthracene and TP

100 Although the mechanisms involved in colon tumor promotion by a HFML diet are not fully known, our

101 hyperplasia contributes to the mechanism of tumor promotion by butylated hydroxytoluene (BHT), we hy

102 Using Car(-/-) mice, we have here examined tumor promotion by chronic treatment with PB in drinking

103 TGF-beta signaling from tumor suppression to tumor promotion by engaging Notch signaling and activati

104 of CD98hc and provide a novel mechanism for tumor promotion by integrins.

105 gest cell cycle disregulation contributes to tumor promotion by NTBI in this liver cell model.

106 genes is targeted by TAM-67 when it prevents tumor promotion by OA.

107 Importantly, tumor promotion by p53-deficient MSCs was abolished by a

108 The role of oxidants in the mechanism of tumor promotion by peroxisome proliferators remains cont

109 Furthermore, tumor promotion by phenobarbital was completely inhibite

110 aling has been shown to be required for skin tumor promotion by phorbol ester, studies were undertake

111 activities could potentially play a role in tumor promotion by PPs.

112 izes the responsiveness of wa-1 mice to skin tumor promotion by the phorbol ester, 12-O-tetradecanoyl

113 mice were found to be very resistant to skin tumor promotion by TPA after initiation with 10 nmol DMB

114 ecrosis factor (TNF)alpha levels during skin tumor promotion by TPA, and this increase may be linked

115 However, despite being resistant to skin tumor promotion by TPA, PKCdelta transgenic mice elicite

116 ted to PKCdelta-mediated suppression of skin tumor promotion by TPA, the irreversible inhibitor of OD

117 were evaluated for sensitivity to mouse skin tumor promotion by TPA.

118 essed at sufficient levels can suppress skin tumor promotion by TPA.

119 link heterogeneity in TGF-beta signaling to tumor promotion by tumor stromal cells.

120 hesis inhibitor, pentoxifylline, during skin tumor promotion completely prevented the development of

121 Prostratin's lack of tumor promotion, coupled with its ability to block viral

122 dies that the effect of dietary fat on colon tumor promotion depends not only on the amount of fat bu

123 Tumor promotion disrupts intercellular relations to allo

124 urther understand the mechanism of action of tumor promotion during early neoplastic progression of h

125 r-suppressive roles may appear to morph into tumor-promotion during cancer progression.

126 However, the tumor promotion effects of (+/-)-anti-5-methylchrysene-1

127 tumor promotion studies, to examine the anti-tumor promotion effects of EGCG and theaflavins at the m

128 However, the mechanisms that mediate B[a]PDE tumor promotion effects remain unclear.

129 cancer model may be well suited for studying tumor promotion events that precede p53 disruption.

130 asia are conventionally used markers of skin tumor promotion, first, we assessed the effect of GE on

131 nithine decarboxylase (ODC) induction during tumor promotion following a single initiating event [i.e

132 epsilon transgenic mice on DFMO during skin tumor promotion has not been reported before in the prev

133 non-small-cell lung cancer, but its role in tumor promotion has not been studied.

134 he effects of chronic microbial infection on tumor promotion have not been studied in the context of

135 CAR activation is a mechanism of xenobiotic tumor promotion; however, the effects of chronic microbi

136 d in a highly significant protection against tumor promotion in 7,12-dimethylbenz(a)anthracene-initia

137 TNF-alpha is a critical mediator of tumor promotion in a number of experimental cancers.

138 paB)-dependent transcription is required for tumor promotion in cell culture models and transgenic mi

139 macologically preventing NET release reduced tumor promotion in Dicer1(+/-) mice, suggesting NETs pro

140 at of TPA in stage I or mezerein in stage II tumor promotion in dimethylbenz(a)anthracene-initiated S

141 hin invasive breast carcinomas contribute to tumor promotion in large part through the secretion of S

142 er, the mechanistic basis for EPHA2-mediated tumor promotion in lung cancer remains poorly understood

143 Retinoic acid (RA) inhibits tumor promotion in many models in vivo and in vitro, amo

144 horbol 12-myristate 13-acetate (PMA)-induced tumor promotion in mice and is in clinical trials as an

145 ormation in mouse epidermal JB6/P+ cells and tumor promotion in mouse skin carcinogenesis.

146 ignificant suppression of ATR expression and tumor promotion in the context of ATR haploinsufficiency

147 romal IL-6 production, which is required for tumor promotion in the epithelial compartment.

148 R-mediated effects, may be more important in tumor promotion in the rat liver.

149 sessed the protective effect of silymarin on tumor promotion in the SENCAR mouse skin tumorigenesis m

150 esis that induced osteopontin is involved in tumor promotion in vivo, osteopontin-null and wild-type

151 ed for P+ cell transformation as well as for tumor promotion in vivo.

152 most antioxidants afford protection against tumor promotion, in this study, we assessed the protecti

153 Selenium treatment during tumor promotion increased hepatic GPx4 expression and re

154 The role of inflammation in carcinogenesis, tumor promotion, invasion, and metastasis is viewed as b

155 In this system, tumor promotion is a critical step in the generation of

156 during the CAC model confirms that enhanced tumor promotion is dependent on HGF-Met signaling in muc

157 t is not known whether phorbol ester-induced tumor promotion is due to activation or depletion of PKC

158 Together, our findings suggest that liver tumor promotion is enhanced by an impaired metabolic det

159 is, but information about their role in lung tumor promotion is limited.

160 The transition from tumor suppression to tumor promotion is mediated by a tumor-induced shift in

161 TPA-induced, organ-specific tumor promotion is not correlated with the distribution

162 However, the role of JNK activation in tumor promotion is not yet defined.

163 etradecanoylphorbol-13-acetate (TPA)-induced tumor promotion is still not well understood even though

164 Considering the important role of AP-1 in tumor promotion, it is possible that blocking UV-induced

165 ptional complex implicated in the process of tumor promotion, its role in the pathogenesis of human t

166 ges were polarized towards wound healing and tumor promotion M2-type.

167 eloid-derived suppressor cells (MDSCs) favor tumor promotion, mainly by suppressing antitumor T cell

168 n of ODC would be a sufficient condition for tumor promotion, mice with high levels of ODC expression

169 haracterized, the mechanisms involved in the tumor promotion of PAHs remain elusive.

170 evidence that ANGPTL2 can function in either tumor promotion or suppression, depending on what cell t

171 dissect the tumor promotion paradigm orchestrated by PM(2.5) inhalat

172 of the molecular events occurring during the tumor promotion phase of photocarcinogenesis could lead

173 The tumor promotion phenotype and the enhancement of metasta

174 on may be a critical event during mouse skin tumor promotion, possibly through regulation of keratino

175 xceptionally high protective effects against tumor promotion, primarily targeted against stage I tumo

176 se data suggest that JNK2 is critical in the tumor promotion process.

177 though protein kinase C (PKC) is involved in tumor promotion/progression and cytoskeletal remodeling,

178 e is known about the molecular mechanisms of tumor promotion/progression in mammary carcinogenesis.

179 the important roles of AP-1 and NFkappaB in tumor promotion/progression, these results suggest that

180 ors and eosinophil-derived growth factors in tumor promotion/progression.

181 Because we did not use a tumor-promotion protocol to induce tumors, most of the q

182 anism by which the EGFR mediates TPA-induced tumor promotion-related signal transduction.

183 The mechanisms underlying the RFA-induced tumor promotion remain largely unexplored.

184 cular mechanisms underlying ethanol-mediated tumor promotion remain unknown.

185 ic carcinogens, but the role of CAR in liver tumor promotion remains unexplored.

186 includes tumor promotion-sensitive (P+) and tumor promotion-resistant (P-) cells, is a well-establis

187 ppears to be an important contributor to the tumor promotion-resistant phenotype in JB6 cells.

188 lines highly sensitive and resistant to skin tumor promotion, respectively.

189 necessary for but also sufficient to confer tumor promotion response.

190 reby delaying AP-1 activation and inhibiting tumor promotion, resulting in reduction of tumors in MnS

191 rtain if this novel Helicobacter sp. plays a tumor promotion role in hepadnavirus-associated tumors i

192 cinogenesis, especially in transformation of tumor-promotion sensitive epithelial cells has not been

193 uced anchorage-independent transformation in tumor-promotion sensitive JB6 mouse skin P+ cells but no

194 mouse epidermal cell system, which includes tumor promotion-sensitive (P+) and tumor promotion-resis

195 nes were stably transfected into a JB6 mouse tumor promotion-sensitive (P+) cell line: a luciferase r

196 In this study, we utilized the tumor promotion-sensitive JB6/P+ cells to identify AP-1-

197 porter cell line maintained the phenotype of tumor promotion sensitivity and was able to report basal

198 onally high protective effect during stage I tumor promotion, showing 74% protection against tumor in

199 With regard to stage II tumor promotion, silymarin showed 26, 63, and 54% protec

200 teps in carcinogenesis that occur during the tumor promotion stage.

201 sts a functional role for MAPK activation in tumor promotion stimulated by oxidants and other agents.

202 en used extensively as an in vitro model for tumor promotion studies, to examine the anti-tumor promo

203 previously developed for carcinogenicity and tumor promotion studies.

204 erapy-induced senescence as a culprit behind tumor promotion, suggesting that elimination of senescen

205 a, similarly induced cell transformation and tumor promotion, suggesting the contribution of molybden

206 been implicated in both tumor initiation and tumor promotion, the amplification of ROS by this pathwa

207 l cycle progression, cell proliferation, and tumor promotion, the precise roles of specific isoforms

208 Changes that occur during tumor promotion, the rate-limiting phase of multistep ca

209 that Smad3 may be required for TPA-mediated tumor promotion through inducing TGF-beta1-responsive ge

210 mulated cells and its inhibition may lead to tumor promotion through induction of proto-oncogenes suc

211 Tumor promotion through, but regulation above, the level

212 tegies aimed at shifting their function from tumor promotion to fostering antitumor immunity.

213 characterized mouse epidermal cell model for tumor promotion, to a low concentration of arsenite (<25

214 el for the study of tumor promotion and anti-tumor promotion, to study the anti-carcinogenesis effect

215 Inhibitors of AP-1 have been shown to block tumor promotion, transformation, progression and invasio

216 ay play in skin growth, differentiation, and tumor promotion, transgenic mice were generated that ove

217 te an unexpected interphase role for Mad1 in tumor promotion via p53 destabilization.

218 Enhanced tumor promotion was associated with decreased hepatic ex

219 ells in the hair follicles, after which time tumor promotion was begun.

220 r protein-1 (AP-1), which is associated with tumor promotion, was reduced in MnSOD transgenic mice ov

221 To determine E2 effects on tumor promotion, we developed an intraperitoneal mouse x

222 t the stage specificity of silymarin against tumor promotion, we next assessed its effect against bot

223 yl inositol 3-kinase (PI3K)/Akt signaling in tumor promotion, we next determined the effect of topica

224 h in omega-6 fatty acids increased the colon tumor promotion, whereas diets containing fish oil high

225 e high in omega-6 fatty acids increase colon tumor promotion, whereas diets rich in omega-3 fatty aci

226 as found in the skin of wild-type mice after tumor promotion with 12-O-tetradecanoylphorbol-13-acetat

227 n of the mechanism by which TAM-67 can block tumor promotion without affecting hyperplasia will be im