ライフサイエンスコーパス: tumor promoter

1 lphorbol-13-acetate, a well-known mouse skin tumor promoter.

2 aB in the induction of MnSOD by cytokine and tumor promoter.

3 lin-35/Rb acts as a soma-autonomous germline tumor promoter.

4 r that acts as both a tumor suppressor and a tumor promoter.

5 d to function as both a tumor suppressor and tumor promoter.

6 with most observations identifying pERK as a tumor promoter.

7 -O-tetradecanoylphorbol-13-acetate, a potent tumor promoter.

8 ophic gastritis, and is considered a gastric tumor promoter.

9 rcinoma (HCC) development, acting as a liver tumor promoter.

10 with 12-O-tetradecanoylphorbol-13-acetate, a tumor promoter.

11 functions either as a tumor suppressor or a tumor promoter.

12 Therefore, it is likely to act as a tumor promoter.

13 BC1 alternatively as a tumor suppressor or a tumor promoter.

14 PBRM1 can operate as a tumor suppressor or tumor promoter.

15 c) mimic mutant (MnSOD(K68Q)) functions as a tumor promoter.

16 been hypothesized that miR-221 may act as a tumor promoter.

17 d that NF-kappaB functions as an independent tumor promoter.

18 d skin carcinogenesis in mice treated with a tumor promoter.

19 ) has been suggested to switch TGF-beta to a tumor promoter.

20 nverts TGF-beta from a tumor suppressor to a tumor promoter.

21 switch of TGF-beta from tumor suppressor to tumor promoter.

22 itor, but in malignant cells it may act as a tumor promoter.

23 sis, acting as both a tumor suppressor and a tumor promoter.

24 2-O-tetradecanoylphorbol-13-acetate (TPA) as tumor promoter.

25 ittermate controls, even without exposure to tumor promoter.

26 een shown to act as endocrine disruptors and tumor promoters.

27 tate-13-acetate (PMA) are known to be potent tumor promoters.

28 monstrating that CDK4 replaced the action of tumor promoters.

29 arious carcinogens, inflammatory agents, and tumor promoters.

30 tivation but also transformation response to tumor promoters.

31 rboxylase (ODC), can be modulated by oxidant tumor promoters.

32 necessary to predispose tissues to secondary tumor promoters.

33 r diacylglycerol (DAG) and the phorbol ester tumor promoters.

34 s approach those of the potent phorbol ester tumor promoters.

35 the phorbol esters, they are not first-stage tumor promoters.

36 th the activity of the compounds as complete tumor promoters.

37 erin is a novel target for the phorbol ester tumor promoters.

38 th regulatory activity of these non-TPA-type tumor promoters.

39 at inhibition of apoptosis is a mechanism of tumor promoters.

40 ester tumor promoters and other potent skin tumor promoters.

41 hose activity is stimulated by several other tumor promoters.

42 r diacylglycerol (DAG) and the phorbol ester tumor promoters.

43 l differences with the typical phorbol ester tumor promoters.

44 osphatase inhibitors are often considered as tumor promoters.

45 rmation in either the presence or absence of tumor promoters.

46 Like PMA, the complete tumor promoter 12-deoxyphorbol 13-tetradecanoate induced

47 initiator dimethylbenz-anthracene and/or the tumor promoter 12-O-tetradecanoyl-13-acetylphorbol on mi

48 diation followed by repeated exposure to the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate.

49 of Aurora-A alone or in combination with the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA

50 on followed by repetitive application of the tumor promoter 12-O-tetradecanoylphorbol 13-acetate.

51 ) mRNAs were induced to higher levels by the tumor promoter 12-O-tetradecanoylphorbol acetate (TPA) a

52 levels in P- cells following exposure to the tumor promoter 12-O-tetradecanoylphorbol acetate than in

53 ne accumulation following treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

54 ration (6 versus 24 hours) when treated with tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

55 in JB6 skin epidermal cells treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

56 characterized protein kinase C activator and tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

57 rative response following treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

58 ly affected after topical treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

59 The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

60 was observed after acute treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA

61 We report that tumor promoter 12-O-tetradecanoylphorbol-13-acetate expo

62 However, treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate indu

63 n down-regulate AP-1 activity induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, ins

64 erated epidermal thinning in response to the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, phe

65 ay, expression of COUP-TF strongly inhibited tumor promoter 12-O-tetradecanoylphorbol-13-acetate-indu

66 effect of 1,25-(OH)2D3, and conversely, the tumor promoter 12-O-tetradecanoylphorhol-13-acetate not

67 nown to be induced by cytokines and the skin tumor promoter 12-tetradecanoylphorbol-13-myristate (TPA

68 Here, we found that PEITC blocks tumor promoter (12-O-tetradecanoylphorbol-13-acetate or

69 ive to the proliferative effects of the skin tumor promoter, 12-0-tetradecanoylphorbol-13-acetate (TP

70 hyperproliferation following exposure to the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TP

71 sly that skin tumor formation induced by the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TP

72 Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TP

73 2 deregulation drives dysplasia, and loss of tumor promoter 53 is a cooperating genetic event that po

74 oncomitant application of a carcinogen and a tumor promoter (7,12-dimethylbenz[a]anthracene (DMBA) an

75 -1) has been shown to be responsible for the tumor promoter action of UV light in mammalian cells.

76 chanisms by which phorbol esters, a class of tumor promoters, activate the 9E3 gene and its chemokine

77 Dioxin, a potent tumor promoter, activates the aryl hydrocarbon receptor

78 on of the integrin alphavbeta6, switching on tumor promoter activity through activation of TGFbeta an

79 ipts and has been suggested to function as a tumor promoter, although little is known regarding the m

80 mportance of RUNX1 in solid tumors both as a tumor promoter and a suppressor.

81 g on the concentration, HYAL1 functions as a tumor promoter and as a suppressor and provides a basis

82 in which expression is both up-regulated by tumor promoter and down-regulated by TAM67.

83 ironment, stromelysin-1 can act as a natural tumor promoter and enhance cancer susceptibility.

84 In these assays, LMP1 functioned as a weak tumor promoter and increased papilloma formation.

85 erimental studies indicate that ethanol is a tumor promoter and may promote metastasis of breast canc

86 of TNBC, POGZ exerted a dual role, both as a tumor promoter and metastasis suppressor.

87 These results establish copper as a tumor promoter and reveal that varying levels of copper

88 acral melanoma and implicate LZTR1 as a key tumor promoter and therapeutic target.

89 synthesized by keratinocytes in response to tumor promoters and are produced at very high levels in

90 the intracellular receptor of phorbol ester tumor promoters and asbestos is a putative tumor promote

91 cells (HMVECs) in an environment that avoids tumor promoters and complex matrices.

92 the nucleus, death receptors can function as tumor promoters and might be therapeutic targets.

93 activated by the prototypical phorbol ester tumor promoters and other potent skin tumor promoters.

94 ology of the receptors for the phorbol ester tumor promoters and the second messenger diacylglycerol

95 Bile acids are intestinal tumor promoters and their concentrations have to be tigh

96 nd 'second-hand' cigarette smoke components, tumor promoters and thrombin, differentially stimulate t

97 ponse to many growth factors, oncogenes, and tumor promoters and to changes in polyamine levels.

98 own to work as both a tumor suppressor and a tumor promoter, and current knowledge does not provide s

99 Some reports link PDEF to tumor promoter, and others show tumor-suppressing functi

100 Okadaic acid is a tumor promoter, and the structural A subunit of PP2A is

101 B activation induced by inflammatory agents, tumor promoters, and carcinogens.

102 Numerous factors, including mitogens, tumor promoters, and cytokines have been found to stimul

103 xpression is rapidly increased by cytokines, tumor promoters, and growth factors and is markedly enha

104 Androgens, such as testosterone, are strong tumor promoters, and work with the AR to augment the eff

105 reatment with a tumor initiator and repeated tumor promoter applications, transgenic mice expressing

106 TGF-beta from a potent growth inhibitor to a tumor promoter are not fully understood.

107 ted the induction of heme oxygenase-1 by the tumor promoter arsenite in a chicken hepatoma cell line,

108 early stages of cancer progression and as a tumor promoter at later stages.

109 OA is a tumor promoter but also induces apoptosis in some tumor

110 results, we conclude that TPA is not only a tumor promoter, but also induces apoptosis in breast can

111 Herein, we show that the skin tumor promoter butylated hydroxytoluene hydroperoxide (B

112 idence shows that CD95 is also emerging as a tumor promoter by activating nonapoptotic signaling path

113 onvert TGF-beta from a tumor suppressor to a tumor promoter by causing the upregulation of AGR2, whic

114 onvert TGF-beta from a tumor suppressor to a tumor promoter by causing the upregulation of AGR2, whic

115 or by inhibiting motility and in others as a tumor promoter by enhancing survival.

116 hepsin L (CTSL) is often thought to act as a tumor promoter by enhancing tumor progression and metast

117 ng a tumorigenic mutagen, sunlight acts as a tumor promoter by favoring the clonal expansion of p53-m

118 suggest that inorganic arsenic may act as a tumor promoter by perturbing key signaling transduction

119 by inhibiting Wnt signaling and acting as a tumor promoter by preventing induction of p53.

120 f the angiogenic switch, RhoB functions as a tumor promoter by sustaining endothelial Akt signaling,

121 Arsenic shares many properties of tumor promoters by affecting specific cell signal transd

122 exposure to both cigarette smokes and/or to tumor promoters can lead to tumorigenesis.

123 studies have shown that structurally diverse tumor promoters can modulate protein kinases involved in

124 e importantly, this is the first report of a tumor promoter capable of inhibiting senescence in a rec

125 Treatment with a tumor promoter caused the heavily damaged epidermal cell

126 sm of such effects may involve inhibition of tumor promoter-caused cellular, biochemical, and molecul

127 vation induced by pro-inflammatory cytokine, tumor promoter, cigarette smoke, and endotoxin.

128 rative response following treatment with the tumor promoter compared to non transgenic littermates.

129 tive stress can be considered as a bona fide tumor promoter, contributing to the initiation and progr

130 TGFbeta1) can act as a tumor suppressor or a tumor promoter depending on the characteristics of the m

131 GF-beta1) can act as a tumor suppressor or a tumor promoter depending on the characteristics of the m

132 her an epithelial cell growth inhibitor or a tumor promoter, depending on the cellular context.

133 g-term treatment of cells with phorbol ester tumor promoters down-regulates the expression of many PK

134 mors did, suggesting that PKCdelta acts as a tumor promoter downstream of oncogenic K-ras while actin

135 age of tumorigenesis, but it can switch to a tumor promoter during neoplastic progression.

136 vidence that Cav-1 does indeed function as a tumor promoter during prostate carcinogenesis, rather th

137 catenin in HCC to establish it as a compound tumor promoter during the progression of the disease.

138 orylation of histone H3 (H3ph) is induced by tumor promoters (EGF, UV and TPA) and immediate early ge

139 such mice no longer required treatment with tumor promoters for tumors to develop.

140 und a significant reduction in the levels of tumor promoter GPs at the end of 4th week during 4-week

141 NF-kappaB activation induced by carcinogens, tumor promoters, growth factors, and inflammatory stimul

142 ha in cancer in which inflammation acts as a tumor promoter has yet to be investigated.

143 nverting TGF-beta from a tumor-suppressor to tumor-promoter has not been identified.

144 C (the commonly recognized pathway for these tumor promoters), (ii) a contribution involving tyrosine

145 s complex role as an RNA-binding protein and tumor promoter, impacting RNA processing, splicing, and

146 changes from that of a tumor suppressor to a tumor promoter; improvements are needed in our understan

147 is, paradoxically, it also seems to act as a tumor promoter in advanced cancer leading to metastasis.

148 e demethylase KDM3A as a new, miR-regulated, tumor promoter in Ewing Sarcoma.

149 ervations indicate that ROCK activation is a tumor promoter in human cutaneous SCC and acts via mecha

150 The data suggest that tamoxifen might be a tumor promoter in human endometrium.

151 echanisms underlying the AR functioning as a tumor promoter in inducing prostatic oncogenesis still r

152 implicated as both a tumor suppressor and a tumor promoter in many solid epithelial cancers.

153 ll, our study shows that MZB1 is a potential tumor promoter in melanoma and could be explored as a ta

154 several cancers, plexin B1 may function as a tumor promoter in melanomas not driven by c-Met activati

155 genetic obesity is a potent bona fide liver tumor promoter in mice.

156 as a tumor suppressor in some contexts and a tumor promoter in others.

157 tudies reveal a novel role for Reg3beta as a tumor promoter in pancreatic adenocarcinoma through the

158 PBRM1 is a tumor promoter in prostate cancer, contributing to migra

159 Cyclooxygenase-2 (COX-2; Ptgs2) acts as a tumor promoter in rodent models for colorectal cancer, b

160 to determine whether TLR4 played a role as a tumor promoter in sporadic colon cancer.

161 These results establish NTBI as a tumor promoter in T51B rat liver epithelial cells.

162 mice, whereas phenobarbital was an effective tumor promoter in the c-myc single transgenic mice.

163 , increased PPAR gamma signaling serves as a tumor promoter in the mammary gland.

164 r tumor promoters and asbestos is a putative tumor promoter in the respiratory tract, we hypothesized

165 revised model wherein Axin2 acts as a potent tumor promoter in vivo.

166 ity suggests that these compounds may act as tumor promoters in estrogen-responsive tissues.

167 al phorbol esters represent the paradigm for tumor promoters in mouse skin, it is now clear that diff

168 transactivation of NF-kappaB is inducible by tumor promoters in P+ but not in P- JB6 cells.

169 some proliferators (PPs) act as nongenotoxic tumor promoters in rodents.

170 y bile acids have long been postulated to be tumor promoters in the colon; however, their mechanism o

171 is after treatment with different classes of tumor promoters, including 12-O-tetradecanoylphorbol-13-

172 e (P+) JB6 cells substantially inhibited the tumor promoter induced activation of Erks1 and 2 and of

173 We have shown that tumor promoter induced activation of the transcription f

174 The phorbol ester tumor promoter induced higher mitogenic and angiogenic a

175 Because skin tumor promoters induced epidermal ornithine decarboxylas

176 cal role in tumor promotion, and blocking of tumor promoter-induced activation of AP-1 inhibits neopl

177 ssing mice results in dramatic inhibition of tumor promoter-induced AP-1 luciferase reporter activati

178 of a dominant negative c-jun (TAM67) blocked tumor promoter-induced AP-1 transactivation and neoplast

179 ct from fresh apple peel extract may inhibit tumor promoter-induced carcinogenesis and associated cel

180 a purified compound of anthocyanin inhibits tumor promoter-induced carcinogenesis and tumor metastas

181 -NH(2)-kinases (JNK) play a critical role in tumor promoter-induced cell transformation and apoptosis

182 y, we investigated the influence of InsP6 on tumor promoter-induced cell transformation and signal tr

183 al cell line is a well established model for tumor promoter-induced cell transformation and was used

184 Thus, MSK1 is required for tumor promoter-induced cell transformation through its p

185 transgenic mouse skin was less sensitive to tumor promoter-induced inflammation, with reduced angiog

186 ovel transformation suppressor that inhibits tumor promoter-induced neoplastic transformation and the

187 ically susceptible (P+) or resistant (P-) to tumor promoter-induced neoplastic transformation exhibit

188 cell lines provide a cell culture model for tumor promoter-induced neoplastic transformation ideally

189 e transcription factor AP-1 is important for tumor promoter-induced neoplastic transformation, the in

190 iants suggests a role for HMG-Y in mediating tumor promoter-induced neoplastic transformation.

191 cal activity or decreasing calorie intake on tumor promoter-induced Ras-MAPK and PI3K-Akt pathways.

192 In JB6 cells, knockdown of Srx abolishes tumor promoter-induced transformation and enhances cell

193 The inhibition of AP-1 and tumor promoter-induced transformation in JB6 cells occur

194 When tested for activity in inhibiting tumor promoter-induced transformation in JB6 P+ cells, t

195 Transactivation of AP-1 is required for tumor promoter-induced transformation in mouse epidermal

196 bited RSK2-mediated ATF1 transactivation and tumor promoter-induced transformation of JB6 Cl41 cells.

197 ues for a requirement of induced AP-1 in the tumor promoter-induced transformation process.

198 sfected P+ cells rendered cells resistant to tumor promoter-induced transformation, indicating that e

199 To test the hypothesis that Pdcd4 inhibits tumor promoter-induced transformation, stable cell lines

200 1 transactivation or ODC activity suppressed tumor promoter-induced transformation.

201 ame dose range as seen for the inhibition of tumor promoter-induced transformation.

202 n factors might contribute to the process of tumor promoter-induced transformation.

203 minal kinase domain in JB6 cells resulted in tumor-promoter-induced neoplastic transformation in a ma

204 radecanoylphorbol-13-acetate (TPA)-type skin tumor promoter, induces a signaling pathway leading to t

205 ift of TGF-beta from a tumor suppressor to a tumor promoter; inhibitors of TGF-beta signaling might b

206 -treated women, the impact of tamoxifen as a tumor promoter is small.

207 sts that susceptibility of skin to exogenous tumor promoters is dependent on age.

208 morigenesis, as either a tumor suppressor or tumor promoter, is complex and may be dependent upon the

209 arsenite and suggest that arsenite acts as a tumor promoter largely by usurping this growth factor si

210 A single topical application of tumor promoters led to significantly elevated levels of

211 lasia and increased the levels of mouse skin tumor promoter marker ornithine decarboxylase, and (4) e

212 In both cell lines and primary tumors, promoter methylation was associated with loss of

213 ic instability remains a key element in this tumor promoter model.

214 for the first time that senescent cells are tumor promoters, not tumor initiators, and that they sti

215 gen 9,10-dimethyl-1,2-benzanthracene, or the tumor promoter O-tetradecanoylphorbol-13-acetate.

216 beta (TGF-beta) from a tumor suppressor to a tumor promoter occurs frequently during mammary tumorige

217 HS-2), which can be induced by oncogenes and tumor promoters, occurs during colon carcinogenesis by e

218 mparing PPs with other growth regulators and tumor promoters of known activity.

219 lloma-producing 308 mouse keratinocytes, the tumor promoter okadaic acid, a serine-threonine phosphat

220 The effects of the non-phorbol ester type tumor promoter okadaic acid, a serine-threonine phosphat

221 r tumor promoter phenobarbital, and the skin tumor promoters okadaic acid and thapsigargin.

222 For example, treatment of cells with the tumor-promoter okadaic acid, an inhibitor of certain typ

223 The stimulating effect of tumor promoters on cell spreading requires activation of

224 stigated the effects of several non-TPA-type tumor promoters on COX-2 expression in immortalized mous

225 r hyaluronidase (e.g., HYAL1) functions as a tumor promoter or as a suppressor.

226 Bcl-3 thus functions as a tumor promoter or suppressor, depending on the cellular

227 gs indicate that Gadd45a functions as either tumor promoter or suppressor, is dependent on the oncoge

228 role in cancer, acting as context-dependent tumor promoter or suppressor.

229 lates the beta subunit of CCT in response to tumor promoters or growth factors that activate the Ras-

230 in response to Ras expression or exposure to tumor promoters or to growth factors, and have been impl

231 -dependent functions that can translate into tumor-promoter or -suppressive functions.

232 is expressed in response to growth factors, tumor promoters, or cytokines.

233 Given the role of TPA as a skin tumor promoter, our findings provide additional support

234 t differ in their transformation response to tumor promoters; P+ cells form anchorage-independent col

235 The tumor promoter palytoxin has been found to activate the

236 talized on the unique properties of the skin tumor promoter palytoxin, which does not activate protei

237 cellular lipid metabolism, the rodent liver tumor promoter phenobarbital, and the skin tumor promote

238 In contrast to palytoxin, the TPA-type tumor promoter phorbol 12,13-dibutyrate and the non-TPA-

239 show that a macropinocytosis activator, the tumor promoter phorbol 12-myristate 13-acetate (PMA), en

240 hat are either sensitive or resistant to the tumor promoter phorbol 12-myristate 13-acetate (PMA).

241 by treatment of cells with the phorbol ester tumor promoter phorbol 12-myristate 13-acetate and the l

242 ibitor actinomycin D (50 micrograms/ml), and tumor promoter phorbol ester (TPA); (100 nM) were tested

243 is and in mouse skin upon treatment with the tumor promoter phorbol-12-myristate-13-acetate (PMA).

244 y a carcinogen (cigarette smoke condensate), tumor promoters (phorbol myristate acetate and okadaic a

245 alyzed Tspo transcriptional responses to the tumor promoter, phorbol-12-myristate 13-acetate (PMA), i

246 Exposure of cells to serum, lipids, or the tumor promoter PMA suppressed formation of these complex

247 genic signaling in response to serum and the tumor promoter PMA was dependent on TRBP phosphorylation

248 lica may act mechanistically as a mitogen or tumor promoter, rather than a genotoxic carcinogen, in t

249 beta (TGF-beta) from a tumor suppressor to a tumor promoter remains incompletely understood.

250 length c-jun promoter via the proximal jun1 tumor promoter-responsive element (TRE)-like promoter el

251 Our results support a tumor promoter role for LHPP phosphohistidine phosphatas

252 s have suggested tumor suppressor as well as tumor promoter roles for them.

253 tin receptor (alpha(v)beta(3)-integrin) as a tumor promoter seems well established, and, consequently

254 the intermediate derivatives and most potent tumor promoters, showed patterns of translocation typica

255 Finally, we observed that a tumor promoter significantly induced FACL4 expression.

256 Tumor promoters stimulate the selective expansion of ini

257 Tumor promoters such as 12-O-tetradecanoylphorbol-13-ace

258 regulator for cell transformation induced by tumor promoters such as EGF and TPA.

259 ailed molecular analysis revealed that known tumor promoters such as pituitary tumor-transforming gen

260 Tumor promoters such as the phorbol ester 12-O-tetradeca

261 agents (such as TNF-alpha and endotoxin) or tumor promoters (such as phorbol ester and okadaic acid)

262 ng topical applications in the presence of a tumor promoter, such as, for example, sunlight.

263 Tumor promoters, such as 12-O-tetradecanoylphorbol 13-ac

264 When cells were stimulated with tumor promoters, such as epidermal growth factor (EGF) o

265 iferation and cell transformation induced by tumor promoters, such as epidermal growth factor or 12-O

266 Phorbol ester tumor promoters, such as phorbol 12-myristate 13-acetate

267 12-O-Tetradecanoylphorbol-13-acetate-type tumor promoters, such as phorbol 12-myristate 13-acetate

268 regulated by cytokines, growth factors, and tumor promoters, such as the protein kinase C (PKC) acti

269 However, DNA2 may also function as a tumor promoter, supporting cancer cell survival by count

270 These findings expand our understanding of tumor promoter/suppressor inter-relationships and downst

271 horbol 12,13-dibutyrate and the non-TPA-type tumor promoters thapsigargin and okadaic acid do not app

272 a tumor suppressor, with uSTAT1 acting as a tumor promoter that acts by elevating resistance to Fas-

273 Palytoxin is a novel skin tumor promoter that does not activate protein kinase C.

274 Thapsigargin is a non-phorbol ester-type tumor promoter that elevates the intracellular Ca2+ (Ca(

275 llfish toxin, okadaic acid (OA), is a potent tumor promoter that induces expression of the proto-onco

276 ndrostane receptor (CAR), a well-known liver tumor promoter that mediates toxic bile acid signaling,

277 proliferators (PPs), which are rodent liver tumor promoters that cause gross alterations in cellular

278 treated with certain apoptotic agents (i.e., tumor promoters that inhibit type 1 and 2A protein phosp

279 deoxycholic acid (DCA) are well-established tumor promoters that may exert their pathologic actions

280 way and add the PPs to the growing number of tumor promoters that modulate signaling proteins.

281 Because SIRT1 may function as a tumor promoter, these results suggest that SIRT1 should

282 we have shown that YBX1 could function as a tumor promoter through phosphorylation of its Ser-165 re

283 ved in the switch in response to TGFss1 from tumor promoter to tumor suppressor through the reprogram

284 ell neoplastic transformation induced by the tumor promoter TPA or epidermal growth factor (EGF).

285 dogenous PKC isoforms with the phorbol ester tumor promoter TPA, and also the effects of TPA on genet

286 e reaction stimulated by the phorbol diester tumor promoter, TPA.

287 hat the EGF receptor (EGFr) was activated in tumor promoter treated mouse epidermis.

288 In addition, Stat3 activation in tumor promoter-treated epidermis and in skin papillomas

289 reased levels of CS and activity of Ch-ST in tumor promoter-treated epidermis were accompanied by inc

290 he activity of Ch-ST in normal epidermis, in tumor promoter-treated epidermis, in epidermis during wo

291 in-alpha/SPPR1 was examined in untreated and tumor promoter-treated mouse skin, hair follicles, and s

292 The cytokine tumor promoter tumor necrosis factor (TNF)-alpha transac

293 and our perspective on their dual roles, as tumor promoter versus tumor suppressor, in cancer.

294 ex-specific germline activity of the ovarian tumor promoter was found to be dependent upon somatic fa

295 ected with wild-type c-jun or treated with a tumor promoter, were more sensitive to PEITC-NAC-mediate

296 ly, we demonstrate that NLRX1 functions as a tumor promoter when expressed in 4T1 tumor cells using g

297 lies, OVO-B positively regulated the ovarian tumor promoter, while OVO-A was a negative regulator of

298 phorbol-13-acetate (TPA) is widely used as a tumor promoter with organotropy in skin and esophagus.

299 ochlorine pesticide that is a rodent hepatic tumor promoter, with inconclusive carcinogenicity in hum

300 Herein, we report a novel tumor promoter, ZBTB46, which is negatively regulated by