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 cylindroma pulmonary metastases from primary skin tumors.

4 lls or their ability to reconstitute primary skin tumors.

5 ecessary and sufficient for the promotion of skin tumors.

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

7 ore resistant to chemical carcinogen-induced skin tumors.

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

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

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

11 nduced epidermal hyperplasia and spontaneous skin tumors.

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

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

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

15 correlation and the quality of diagnosis in skin tumors.

16 and a predisposition to medulloblastomas and skin tumors.

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

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

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

20 time consuming histopathologic diagnosis of skin tumors.

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

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

23 They are also resistant to developing skin tumors.

24 normal DNA damage responses, and spontaneous skin tumors.

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

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

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

28 correlation and the quality of diagnosis in skin tumors.

29 argeted tissue processing and examination of skin tumors.

30 omising approach for photodynamic therapy of skin tumors.

31 formation of secondary benign and malignant skin tumors.

32 time consuming histopathologic diagnosis of skin tumors.

33 particularly in those with previous actinic skin tumors.

34 or enhance the growth of chemically induced skin tumors.

35 the contribution of follicular stem cells to skin tumors.

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

37 mmatory response were less likely to develop skin tumors.

38 ocess associated with mutational hotspots in skin tumors.

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

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

41 am formulation is successfully used to treat skin tumors.

42 ischemia and for the growth of autochthonous skin tumors.

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

44 PRAK promotes the growth and progression of skin tumors.

45 where gene deletion reduced the incidence of skin tumors.

46 tify papillomavirus expression in any of the skin tumors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 f cSCC, to determine the function of Cav1 in 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 Genetic ablation of alpha3 in established skin tumors caused their rapid regression, indicating th

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

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

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

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

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

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

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

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

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

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

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

104 8 transposition-induced prostate, breast and skin tumors detected tissue-specific and shared data set

105 Nonpigmented skin tumors, determined clinically and dermoscopically,

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

107 Skin tumors developed preferentially within the cutaneou

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

109 3 and cyclin D2 play opposite roles in mouse skin tumor development and that the suppressive activity

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 6 or 4.5 to 12 kJ per m2) were monitored for skin tumor development.

138 sion in the epidermis dramatically inhibited skin tumor development.

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

140 PA)-induced epidermal hyperproliferation 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 of the alpha3 integrin subunit fail to form skin tumors during two-step chemical tumorigenesis, indi

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

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

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

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

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

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

155 senescence, which might be of importance for skin tumor formation and cellular aging of keratinocytes

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

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

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

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

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

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

162 Arsenic enhances skin tumor formation when combined with other carcinogen

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

164 2 transcriptional activity serves to promote skin tumor formation, thereby indicating a suppressor ac

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

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

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

168 epidermis, and suppressed chemically induced skin tumor formation.

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

170 ceptibility toward epidermal hyperplasia and skin tumor formation.

171 etradecanoylphorbol-13-acetate (TPA)-induced skin tumor formation.

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

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

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

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

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

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

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

179 103 matched benign, malignant and metastatic skin tumors from genetically heterogeneous mice to demon

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

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

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

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

184 Skin tumors from transgenic mice showed a dramatic incre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 It also occurs in basaloid skin tumors in situ.

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 w specific thresholds is sufficient to block skin tumor initiation, promotion, and progression.

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

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

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

221 regulator of the keratinocyte secretome and skin tumor microenvironment and as a potential therapeut

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

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

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

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

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

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

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

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

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

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

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

233 Skin tumors produced by polyaromatic hydrocarbons, such

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 Skin tumors subsequently developed with concomitant stro

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

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

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

257 World Health Organization classification of skin tumors suggests the elimination of cases with BRAF

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

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

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

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

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

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

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

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

285 2 receptor is involved in the development of skin tumors was unknown.

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

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

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

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

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

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

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

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

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

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

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

297 e tumor suppressor CYLD and develop multiple skin tumors with diverse histophenotypes.

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

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

300 Gata6 ablation increases the total number of skin tumors yet decreases the proportion of SG tumors.