ライフサイエンスコーパス: skin tumor

1 infectious cause of this highly vascularized skin tumor.

2 el cell carcinomas, a primary neuroendocrine skin tumor.

3 ecessary and sufficient for the promotion of skin tumors.

4 correlation and the quality of diagnosis in skin tumors.

5 s and 7,12-dimethylbenz(a)anthracene-induced skin tumors.

6 ore resistant to chemical carcinogen-induced skin tumors.

7 time consuming histopathologic diagnosis of skin tumors.

8 he de novo development of chemically-induced skin tumors.

9 They are also resistant to developing skin tumors.

10 he development or progression of UVR-induced skin tumors.

11 educed PS dosages have been shown to develop skin tumors.

12 nduced epidermal hyperplasia and spontaneous skin tumors.

13 RNA-21 (miR21) in basal cell carcinoma (BCC) skin tumors.

14 concentrations of HA only in the context of skin tumors.

15 ressed with Gli1 in human hair follicles and skin tumors.

16 enhanced apoptosis in UVB-exposure-mediated skin tumors.

17 correlation and the quality of diagnosis in skin tumors.

18 and a predisposition to medulloblastomas and skin tumors.

19 argeted tissue processing and examination of skin tumors.

20 adiation, only 60% of CD1d-/- mice developed skin tumors.

21 ve and have a high susceptibility to develop skin tumors.

22 omising approach for photodynamic therapy of skin tumors.

23 ared to either normal skin or slower growing skin tumors.

24 dritic cells, were required for rejection of skin tumors.

25 ntly observed in the p53 gene of nonmelanoma skin tumors.

26 formation of secondary benign and malignant skin tumors.

27 normal DNA damage responses, and spontaneous skin tumors.

28 of GLI in mice is sufficient to induce these skin tumors.

29 t 2% the amount of pure BP required to cause skin tumors.

30 time consuming histopathologic diagnosis of skin tumors.

31 particularly in those with previous actinic skin tumors.

32 or enhance the growth of chemically induced skin tumors.

33 the contribution of follicular stem cells to skin tumors.

34 duced p53 mutations, immune suppression, and skin tumors.

35 mmatory response were less likely to develop skin tumors.

36 ocess associated with mutational hotspots in skin tumors.

37 llular levels of Fancd2-Ub, are resistant to skin tumors.

38 tely one-third of premalignant and malignant skin tumors.

39 am formulation is successfully used to treat skin tumors.

40 ischemia and for the growth of autochthonous skin tumors.

41 s used as an antitumor agent, mainly against skin tumors.

42 PRAK promotes the growth and progression of skin tumors.

43 where gene deletion reduced the incidence of skin tumors.

44 tify papillomavirus expression in any of the skin tumors.

45 lls or their ability to reconstitute primary skin tumors.

46 ound that although 100% of WT mice developed skin tumors after 45 weeks of UV irradiation, only 60% o

47 However, they did not develop skin tumors after chronic UVB irradiation.

48 ight, and all Pol eta-deficient mice develop skin tumors after UV irradiation, in contrast to the wil

49 Heterozygous Er/+ mice develop spontaneous skin tumors and are highly sensitive to tumor-promoting

50 Krt17) protein, which is induced in basaloid skin tumors and co-polymerizes with Krt5 in vivo, delays

51 ant p53 protein in UV-induced murine primary skin tumors and cultured cell lines was constitutively p

52 ar tumors at higher CTL/tumor ratios than in skin tumors and demonstrated comparable ex vivo effector

53 creatic, breast, prostate, and squamous cell skin tumors and ependymoma, although there was significa

54 gens, benzo(a)pyrene and urethane, to induce skin tumors and lung tumors, respectively.

55 re monitored for the occurrence of malignant skin tumors and other malignant tumor types for a period

56 For UVB-induced murine skin tumors and papillomas, regression is known to invol

57 erexpression in the malignant progression of skin tumors and suggest that Aurora-A may be an importan

58 romotes proangiogenic stimuli in UVB-induced skin tumors and suggest that endogenous enhancement of I

59 acteristics associated with aggressive human skin tumors and that this protein may be an important mo

60 of 33 weeks of TPA promotion, the number of skin tumors and tumors >1.5 mm in diameter per mouse in

61 efore UV exposure resulted in both 56% fewer skin tumors and tumors that were 70% smaller.

62 is overexpressed in chemically-induced mouse skin tumors, and its overexpression (but not accelerated

63 s are elevated in transformed keratinocytes, skin tumors, and psoriasis.

64 protect against sunburn, delay the onset of skin tumors, and reduce ultraviolet-B-radiation-induced

65 uced levels of skin hyperplasia, spontaneous skin tumors, and tumor progression activity compared to

66 Galectin-3 was increased in TSC-related skin tumors, angiomyolipomas, and lymphangioleiomyomatos

67 Although skin tumors are highly immunogenic, exposure to UV radia

68 These results suggest that hamartomatous TSC skin tumors are induced by paracrine factors released by

69 Our results indicate that more skin tumors are induced in Hipk2+/- and Hipk2-/- mutants

70 , whereas larger, aggressive, and metastatic skin tumors are less likely to respond.

71 purify a CSC-like cell population from early skin tumors arising from treatment with 7,12-dimethylben

72 F inhibitors is the stimulation of cutaneous skin tumors, arising in about 30% of patients receiving

73 ently low in chemically and UV-induced mouse skin tumors as well as in human cutaneous squamous cell

74 in decreased incidences and multiplicity of skin tumors as well as malignant progression to SCC.

75 rcoma protuberans (DFSP) is a rare malignant skin tumor associated with a characteristic chromosomal

76 ult mice conditionally ablated in PS1 and in skin tumors associated with the loss of PS1.

77 l concentrations of NO were only produced by skin tumor-associated Ms though ocular tumor-associated

78 nogen-induced tumorigenesis, as they develop skin tumors at an increased rate.

79 at assessed itch and pain intensity of their skin tumors at the time of excision.

80 pt, we used this method to differentiate two skin tumors, basal cell carcinoma (BCC) and Merkel cell

81 MO-MDSCs isolated from B16 melanoma and from skin tumor-bearing ret transgenic mice also expressed hi

82 f cSCC, to determine the function of Cav1 in skin tumor biology.

83 ance its power in revealing the mysteries of skin tumor biology.

84 n is normally a hallmark of DMBA-TPA-induced skin tumors, but 70% of carcinomas from Pten+/- mice do

85 tch-deficient murine fibroblasts or in human skin tumors, but are not up-regulated in RK3E cells tran

86 of caspase 3-positive cells in nonmalignant skin tumors by 87% or 72%, respectively, and in squamous

87 against ultraviolet radiation (UVR)-induced skin tumors by activating p53 via the stress mitogen-act

88 Paradoxically, the regression of skin tumors by CTL transfer therapy required NO producti

89 tion also dramatically reduced the number of skin tumors (by approximately 80%) produced following pr

90 ffectively reduces the incidence and size of skin tumors caused by UVB exposure.

91 Deletion of tak1 gene in skin tumors caused the accumulation of ROS and increased

92 in DU145 and PC3 prostate cancer cells and a skin tumor cell line derived from EphA1/A2 knockout mice

93 Screening of mouse skin tumor cell lines for differentially expressed genes

94 In Gli1-transgenic mice, infiltrating skin tumor cells expressed active, unphosphorylated beta

95 atient, molecular analyses demonstrated that skin tumor cells had the donor genotype and harbored a T

96 malignant progression of chemically induced skin tumors compared with WT mice.

97 ta is essential for the development of mouse skin tumors containing Ras mutations and can cooperate w

98 ined whether ablation of TAK1 in preexisting skin tumors could cause an increase in ROS and result in

99 C terminus, associated with the hypertrophic skin tumor cylindromatosis, disrupt the USP domain, acco

100 or-suppressor gene disorder characterized by skin tumors, cystic lung disease and renal cell carcinom

101 We discovered that skin tumors derived from epidermal expression of oncogen

102 roles in TSC tumorigenesis, we screened TSC skin tumor-derived cells for altered gene and protein ex

103 8 transposition-induced prostate, breast and skin tumors detected tissue-specific and shared data set

104 Nonpigmented skin tumors, determined clinically and dermoscopically,

105 Unlike most mouse models, Zmiz1-induced skin tumors develop rapidly and in the absence of promot

106 These data show that Mek1 is important for skin tumor development and that Mek2 cannot compensate f

107 3 and cyclin D2 play opposite roles in mouse skin tumor development and that the suppressive activity

108 reas homozygous deletion of SIRT1 suppresses skin tumor development but sensitizes the B6 mice to chr

109 nsulin-like growth factor-I (IGF-I)-promoted skin tumor development by 73% in BK5.IGF-1 transgenic mi

110 ly, CDK6 overexpression results in decreased skin tumor development compared with wild-type siblings.

111 ed studies examining the effect of gender on skin tumor development following equal doses of UVB.

112 o contribution of individual p38 isoforms to skin tumor development has not been elucidated.

113 ssessed the effect of p38delta deficiency on skin tumor development in vivo by subjecting p38delta kn

114 ullizygous mice are completely refractory to skin tumor development induced by a variety of carcinoge

115 ect, rather than sensitize, K14.COX2 mice to skin tumor development induced by an initiation/promotio

116 pha knockout mice were highly susceptible to skin tumor development involving oncogenic Ras.

117 a reduction in IKKalpha expression promotes skin tumor development is currently unknown.

118 -)) mice are more susceptible to TPA-induced skin tumor development than wild-type mice.

119 e assessed the effect of Stat3 deficiency on skin tumor development using the 2-stage chemical carcin

120 -deficient mice were completely resistant to skin tumor development when DMBA was used as the initiat

121 of CD8(+) T cells plays a protective role in skin tumor development whereas CD4(+) T cells have the o

122 hibit moderate hyperplasia, with spontaneous skin tumor development within 5 weeks of birth.

123 rived VEGF-A was essential for initiation of skin tumor development, both spontaneously and UV-light

124 keratinocyte proliferation is essential for skin tumor development, EP2-mediated signaling pathways

125 involvement of the Gli2 repressor domain in skin tumor development, we overexpressed the Gli2DeltaN2

126 (GPCR), EP2, plays important roles in mouse skin tumor development.

127 t ODC is post-transcriptionally regulated in skin tumor development.

128 itor of ATM and Rad3-related (ATR), promoted skin tumor development.

129 nor the indirect activation of CDK2 enhanced skin tumor development.

130 at each receptor may play a distinct role in skin tumor development.

131 lin D3 and cyclin D2 overexpression in mouse skin tumor development.

132 PA)-induced epidermal hyperproliferation and skin tumor development.

133 s, indicating a unique role of C/EBP beta in skin tumor development.

134 role in the protumorigenic action of PGE2 in skin tumor development.

135 icient in Stat3 were completely resistant to skin tumor development.

136 6 or 4.5 to 12 kJ per m2) were monitored for skin tumor development.

137 sion in the epidermis dramatically inhibited skin tumor development.

138 f COX-2 and elevated prostaglandin levels in skin tumor development.

139 suggest that JNK1 is a crucial suppressor of skin tumor development.

140 ation but differ in apoptosis activation and skin tumor development.

141 This decreased incidence of skin tumors did not reflect differences in epidermal dev

142 Survival without a skin tumor differed over the four groups (p < 0.0001) an

143 pha production by plasmacytoid DC (pDC) from skin/tumor draining lymph nodes and the cross-priming of

144 CD103(+) DC from the skin/tumor draining lymph nodes of the immunized mice ap

145 mmary tumors driven by the PyMT oncogene and skin tumors driven by the SmoM2 oncogene arose with acce

146 rated and increased formation of nonmelanoma skin tumors during chemical carcinogenesis.

147 ee mice, which had a high risk of developing skin tumors during the next several months, were then tr

148 ndings suggest that pathologists involved in skin tumor evaluation should be encouraged to learn derm

149 Ge et al. now show that skin tumors exhibit merged chromatin profiles from disti

150 On the other hand, the intestinal and skin tumors exhibited microsatellite instability but kep

151 e remarkably resistant to the development of skin tumors following exposure to a tumor initiator and

152 is a rapidly progressing potentially lethal skin tumor for which early diagnosis is critical.

153 omas (SCCs) are heterogeneous and aggressive skin tumors for which innovative, targeted therapies are

154 , we have investigated the susceptibility to skin tumor formation by forced expression of CDK4.

155 in in basal epidermal cells are resistant to skin tumor formation by the 7,12-dimethylbenz(a)anthrace

156 MIF leads to a loss of control of epithelial skin tumor formation in chemical skin carcinogenesis, wh

157 MIF leads to a loss of control of epithelial skin tumor formation in chemical skin carcinogenesis, wh

158 We have found previously that skin tumor formation induced by the tumor promoter, 12-O

159 e describe an inducible mouse model in which skin tumor formation is initiated by activation of an en

160 ions of Smad4-mediated signals in repressing skin tumor formation through the TGFbeta/BMP pathway, wh

161 Arsenic enhances skin tumor formation when combined with other carcinogen

162 the p53(R172H) allele resulted in increased skin tumor formation, accelerated tumor progression, and

163 2 transcriptional activity serves to promote skin tumor formation, thereby indicating a suppressor ac

164 mice results in a significant inhibition of skin tumor formation.

165 of ultraviolet light B-induced, VAT-promoted skin tumor formation.

166 indicating a suppressor activity of ATF2 in skin tumor formation.

167 epidermis, and suppressed chemically induced skin tumor formation.

168 KSR1, KSR1 is obligate for v-Ha-ras-mediated skin tumor formation.

169 ceptibility toward epidermal hyperplasia and skin tumor formation.

170 ocol, DKO mice showed a significantly higher skin tumor frequency and multiplicity compared with cont

171 ma (MCC) is a rare and deadly neuroendocrine skin tumor frequently associated with clonal integration

172 arcinoma (MCC) is a malignant neuroendocrine skin tumor frequently associated with the Merkel cell po

173 We grew fibroblast-like cells from 29 TSC skin tumors from 22 TSC subjects and identified germline

174 all MT mice developed spontaneous malignant skin tumors from 3 months to 13 months of age.

175 lected 101 consecutive IVD and EVD images of skin tumors from a private dermatology practice from Mar

176 T1 levels are significantly reduced in human skin tumors from Caucasian patients, a population at hig

177 103 matched benign, malignant and metastatic skin tumors from genetically heterogeneous mice to demon

178 We find that skin tumors from mice lacking Nfatc1 display reduced Hra

179 h lesions were observed within either dorsal skin tumors from plasminogen-deficient mice or footpad t

180 allele-specific alterations at these loci in skin tumors from the same backcross animals.

181 proteolytic products are elevated in vivo in skin tumors from transgenic mice overexpressing Dsg2.

182 Skin tumors from transgenic mice showed a dramatic incre

183 , and Stat5 were constitutively activated in skin tumors generated by the two-stage carcinogenesis re

184 quamous-cell carcinomas, occurrence of other skin tumors, graft function, and problems with sirolimus

185 ssociated leukocytes, suppressed established skin tumor growth and colitis-associated tumorigenesis,

186 Here, we show that CsA promotes primary skin tumor growth in immune-deficient mice and keratinoc

187 cal effects of mtDNA mutations in UV-induced skin tumors, hairless mice were irradiated to produce tu

188 ynthesis and promote the formation of benign skin tumors in conjunction with chemical carcinogens.

189 ealed a uniformly accelerated development of skin tumors in Egr1-null mice (P < 0.005).

190 n and prevented the development of malignant skin tumors in female mice with chronically UVB-damaged

191 Following UVB irradiation, the formation of skin tumors in K5.Stat3C mice was accelerated and both t

192 Inducing skin tumors in mice with a keratinocyte-restricted loss

193 ll types known to support the development of skin tumors in mice.

194 ad range of tumors as well as in TPA-induced skin tumors in mice.

195 stic models of human breast, pancreatic, and skin tumors in mice.

196 s required for gastrointestinal, breast, and skin tumors in murine models.

197 ributed to increased benzo(a) pyrene-induced skin tumors in NQO1-null mice.

198 d CXCR2 null keratinocytes formed only small skin tumors in orthotopic skin grafts to CXCR2 intact ho

199 a deficiency alone had no effect, UV-induced skin tumors in pol eta-deficient mice developed 4 weeks

200 to factors that influence the development of skin tumors in response to UV irradiation.

201 It also occurs in basaloid skin tumors in situ.

202 dermal sarcoma virus (WDSV), induces benign skin tumors in the infected fish and replicates near 4 d

203 re the primary targets for the initiation of skin tumors in this model system.

204 VB radiation led to the development of fewer skin tumors in vIL-10 mice than in WT controls, and vIL-

205 or Stat3 in driving malignant progression of skin tumors in vivo.

206 evelop spontaneous tumors and have increased skin tumor incidence after treatment with dimethylbenz(a

207 was also up-regulated in TPA or UVR-mediated skin tumors including papillomas, spindle cell tumors, a

208 Basaloid skin tumors, including basal cell carcinoma (BCC) and ba

209 squamous cell skin carcinoma (SCC) and rare skin tumors, including Merkel cell carcinoma (MCC) and d

210 ylbenzanthracene (DMBA) or UVB, they develop skin tumors, including some characteristic of overexpres

211 ble ex vivo effector function to CTLs within skin tumors indicating that ocular tumor progression was

212 effective therapeutic target for preventing skin tumor induced by aberrant Pten signaling.

213 ed to control SKH1 hairless mice in terms of skin tumor induction and extracellular matrix changes oc

214 nlike the usual resistance of this strain to skin tumor induction.

215 In addition, injection of Stat3 decoy into skin tumors inhibited their growth.

216 Deletion of Stat3 prior to skin tumor initiation with 7,12-dimethylbenz(a)anthracen

217 Kras mutations in lung and Hras mutations in skin tumors is determined by local regulatory elements i

218 seborrheic keratosis, the most common of all skin tumors, is dependent on acutely transforming retrov

219 transgenic population developed spontaneous skin tumors, mainly squamous cell papillomas.

220 Pbeta deficiency also led to greatly reduced skin tumor multiplicity and size, providing additional e

221 The DFMO treatment did not affect the skin tumor multiplicity of PKCdelta transgenic mice.

222 (-/-) mice where a high number of UV-induced skin tumors occurred that were characterized by aggressi

223 Thirteen cell lines established from skin tumors of mice expressing either the E6 or E7 oncop

224 strate that the levels of PS and EGFR in the skin tumors of PS1(+/-)/ PS2(-/-) mice and the brains of

225 L-1beta) in chronically UVB-exposed skin and skin tumors of wild-type mice but less effective in IL-1

226 ulted in mice with a high risk of developing skin tumors over the next several months in the absence

227 sed the number of nonmalignant and malignant skin tumors per mouse by 44% and 72%, respectively.

228 ed the number of non-malignant and malignant skin tumors per mouse induced by 12-O-tetradecanolyphorb

229 sed the number of nonmalignant and malignant skin tumors per mouse induced by 12-O-tetradecanolyphorb

230 XN1 that underlies a benign versus malignant skin tumor phenotype.

231 Skin tumors produced by polyaromatic hydrocarbons, such

232 yperplasia and increased the levels of mouse skin tumor promoter marker ornithine decarboxylase, and

233 capitalized on the unique properties of the skin tumor promoter palytoxin, which does not activate p

234 Given the role of TPA as a skin tumor promoter, our findings provide additional sup

235 canoylphorbol-13-acetate, a well-known mouse skin tumor promoter.

236 cid (OA) is a prototypical non-phorbol ester skin tumor-promoting agent that works by inhibiting prot

237 iption (STATs), particularly Stat3, in mouse skin tumor promotion and multistage carcinogenesis.

238 BxD27 mice are sensitive to TPA skin tumor promotion but carry the C57BL/6 allele of Psl

239 signaling has been shown to be required for skin tumor promotion by phorbol ester, studies were unde

240 mor necrosis factor (TNF)alpha levels during skin tumor promotion by TPA, and this increase may be li

241 However, despite being resistant to skin tumor promotion by TPA, PKCdelta transgenic mice el

242 tributed to PKCdelta-mediated suppression of skin tumor promotion by TPA, the irreversible inhibitor

243 synthesis inhibitor, pentoxifylline, during skin tumor promotion completely prevented the developmen

244 n PKC epsilon transgenic mice on DFMO during skin tumor promotion has not been reported before in the

245 ivation may be a critical event during mouse skin tumor promotion, possibly through regulation of ker

246 ventional markers and other novel markers of skin tumor promotion.

247 o 12-O-tetradecanoylphorbol-13-acetate (TPA) skin tumor promotion.

248 thesis that c-src plays an important role in skin tumor promotion.

249 K5-Gli2DeltaN2 mice developed a variety of skin tumors resembling human trichoblastomas, cylindroma

250 inuation of UVB exposure before the onset of skin tumors results in the disappearance of p53 mutation

251 uninvolved skin from tumor-bearing mice, and skin tumors showed a statistically significant decrease

252 sis of K5CDK4 and K5Myc epidermis as well as skin tumors showed that keratinocyte proliferation is me

253 ancer response in association with distorted skin tumor stem cell signaling and population dynamics,

254 Skin tumors subsequently developed with concomitant stro

255 ked down-regulation in colorectal, lung, and skin tumors, suggest its use as a biological marker in c

256 fresh tumor samples and cells grown from TSC skin tumors, suggesting that increased epidermal prolife

257 and within a high percentage of cells within skin tumors suggests a non-stem cell pro-survival role f

258 via PKCdelta to epidermal ODC induction and skin tumor suppression appear to be independent.

259 Epidermal cell differentiation and skin tumor suppression were caused by a p53-dependent tr

260 model, we previously identified at least 13 skin tumor susceptibility (Skts) loci in a large intersp

261 One locus, skin tumor susceptibility 5 (Skts5) on chromosome 12, sh

262 Skin tumor susceptibility 5 (Skts5) was identified as a

263 in mouse and STK15 in human) as a candidate skin tumor susceptibility gene.

264 sage, but that manifestation of Tgfb1-linked skin tumor susceptibility in M. musculus NIH/Ola x (M. s

265 We demonstrate that skin tumor susceptibility is altered by Tgfb1 gene dosag

266 effects of germ-line variants that influence skin tumor susceptibility loci on the patterns of somati

267 and congenic mouse strains to map the major skin tumor susceptibility locus Skts1 within a genetic i

268 sculus NIH/Ola)F1 backcrosses, to identify a skin tumor susceptibility locus, Skts14, on proximal chr

269 nt mice showed at least a 2-fold increase in skin tumor susceptibility over their littermates.

270 ts keratinocyte stem cell proliferation, and skin tumor susceptibility, and is a candidate stem cell

271 of previously unknown genetic loci affecting skin tumor susceptibility.

272 opic hair follicle development and increased skin tumor susceptibility.

273 loci mapped in this study are distinct from skin tumor-susceptibility loci identified previously.

274 ective in reducing the number of UVB-induced skin tumors than 5-FU treatment alone.

275 found to develop a twofold greater number of skin tumors than Ikkalpha(+/+) mice after chronic UVB ir

276 diation in mouse skin and are lower in human skin tumors than in normal skin.

277 with a human prostatic tumor line, forming a skin tumor that produces a high blood titer of prostate-

278 ulatory role for Krt17 in Hh driven basaloid skin tumors that could impact additional tumor settings,

279 Remarkably, 100% of the skin tumors that developed in K5.Stat3C transgenic mice

280 Skin tumors that form spontaneously in ODC/Ras double tr

281 ple squamous-carcinoma-like locally invasive skin tumors that grow rapidly for a few weeks before spo

282 Seborrheic keratoses (SKs) are common benign skin tumors that share many morphological features with

283 The 2.4% incidence of skin tumors, the most common neoplasms, was 1.58-fold gr

284 rtant role in the development of UVB-induced skin tumors through its effects on both survival and pro

285 mulation of ROS and increased apoptosis, and skin tumors totally regressed within 5 to 10 days.

286 In the mouse skin and skin tumors, UVB radiation downregulates E-cadherin.

287 2 receptor is involved in the development of skin tumors was unknown.

288 cidence of malignancy (excluding nonmelanoma skin tumors) was determined in these 1886 patients and c

289 tumor-promoting event in the development of skin tumors, we determined the effects of IL-12-deficien

290 s predominated within ocular tumors, whereas skin tumors were primarily infiltrated by CD11b(+)Gr-1(-

291 By the early 20th century, malignant skin tumors were produced in laboratory animals by repea

292 emarkably, the incidence and multiplicity of skin tumors were reduced in mice that received MnTE-2-Py

293 re resistant to CTL transfer therapy whereas skin tumors were sensitive.

294 d and both the incidence and multiplicity of skin tumors were significantly greater than wild-type co

295 -/-) mice rapidly develop chemically induced skin tumors, whereas CYP27B1(-/-) and wild-type mice do

296 ation of proapoptotic Smac/DIABLO protein in skin tumors; whereas treatment with resveratrol resulted

297 Exceptions included skin tumors, which displayed increased multiplicity in w

298 PA as the promoter, K5.Stat3C mice developed skin tumors with a shorter latency and in much greater n

299 t mice develop aggressive chemically induced skin tumors with enhanced CAF activation.

300 can determine the phenotype of Hh/Gli-driven skin tumors, with high-level signaling required for deve